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OMBR - Clinical Occupational Medicine IV Part A
OMBR - Clinical Occupational Medicine IV Part A
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This slide lecture is part of the third lecture in clinical occupational medicine. The first part here concerns itself specifically with pulmonary disease. The second part later on will address infectious disease and noise-induced hearing loss. Pulmonary disorders, as we all know, are quite common and important in occupational medicine. We'll go through the major ones, and the real focus here will be on work-related asthma, along with some other immunological disorders, and the pneumoconiosis, particularly silica, asbestos, and coal, with a smattering of other disorders and diseases such as hypersensitivity, pneumonitis, beryllium lung disease, and lung cancer. We'll finish up with occupational tuberculosis. Work-related asthma is now, in the United States, the most common occupational lung disease. It's supplanted the pneumoconiosis, although we still see those fairly extensively. And it's useful to differentiate work-related asthma into two sets. One is what gets termed occupational asthma, or specific work-related asthma. And this is new-onset asthma that is specifically related to occupational exposures. And it can be through exposure to allergens in the workplace, or through heavy exposures to irritants, forming a RADS-type picture. This is differentiated from work-exacerbated asthma, which is pre-existing asthma. In other words, someone has already been sensitized to an asthmagen. They go into the workplace, and either they're re-exposed to some of these allergens, or they may be exposed to nonspecific irritants that trigger the asthma. But primarily from a worker's compensation standpoint, their asthma was not caused by exposure in the workplace. It's just been exacerbated and become more symptomatic because of current workplace exposures. So for occupational asthma, particularly immunologic asthma, it's useful to think in terms of two sets of allergens or antigens that cause this asthma. The first set are the high molecular weight allergens. These have certain characteristics, obviously. They weigh more and are at a higher molecular weight. But mainly, these are the traditional, classic IgE-mediated responses that lead to type 1 or immediate hypersensitivity reactions. And they're readily tested for either by RAST or IgE testing, or by skin prick testing, as the allergists do. And they generally lead, as do many IgE responses, to immediate asthmatic response. That is, coming into contact with the allergen causes symptoms after about 30 minutes to an hour or so. And many of these over on the right-hand side are kind of classic large molecular weight allergens that come either from animals or plants. In other words, organic materials and matter, such as animal dander, pollens, in the case of occupational cases, wood dusts, molds, or enzymes used for detergents. The low molecular weight allergens get a little bit more tricky. These are oftentimes industrial chemicals, which are often very small. And the thought is that they oftentimes complex with plasma proteins to form antigen-haptin complexes. And they proceed possibly by other mechanisms that aren't IgE-mediated responses, but have inflammatory mechanisms that might be through more cell-mediated immune-type reactions, such as T-cell reactions. The problem there is that they're oftentimes harder to diagnose because IgE isn't elaborated. You don't have readily available or very specific tests. And because of the fact that these may not proceed through IgE-mediated mechanisms, we oftentimes see delayed asthmatic responses, which don't occur for 6, 8, 10 hours. The main examples of these are industrial chemicals, such as the isocyanates, which are used in spray paints, such as on cars, colophony and fluxes, biocides, epoxy materials, and other small molecules that cause asthma with a prolonged exposure. Briefly on the next couple of slides, we'll look at the clinical presentations, the early response characteristic more of the high molecular weight antigens, and the late response characteristic more of industrial chemicals and low molecular weight. These graphs represent FEV1, taken before and after challenge with an inhaled antigen. The top graph is representative of a classic immediate hypersensitivity response, in which immediately after the challenge, within about an hour or so, the FEV1 has dropped from the baseline 100 to about 60% of the baseline, with a slow recovery following over several hours. The second or middle panel is characteristic of the late response. This can be more seen, as we mentioned in the last slides, with isocyanates or low molecular weight allergens. And as you can see, there's no response across the first several hours, and it's not until 6 to 8 hours that the tested individual drops the FEV1 back down to about 50-60% of the initial control. So that's representative of a late response. And the third panel is a combination early and late response, which may occur with some allergens as well. This slide shows a pair of more unusual responses. The bottom panel is a cyclic response to Western Red Cedar. This is done across days rather than hours. And the reason for this is because Western Red Cedar antigen is sequestered by macrophages and then intermittently released at 12-24 hour bursts, which accounts for the drop in FEV1 across several days. Bisinosis is in the top. This is less of an asthmatic response, and it is more like a CLPD type of response, in which new exposure to cotton dust allergens causes a slow progressive drop in FEV1 with a slow rebound, at least initially. Later on in the course of the disease, this becomes fixed and stable, and more like a CLPD type of picture. Having covered the mechanisms of allergic asthma in the previous slide, this slide moves on to cover irritant-induced asthma. This is reactive airways that results from a single high-dose exposure, and as such is termed Reactive Airways Dysfunction Syndrome, or RADS. These do not take place via the immunologic basis, but in general are workers who are hospitalized or seen in the ED at least for inhalation of severe irritant materials, such as chlorine or acid fumes. Many cases we see are hypochlorite fumes from mixing bleach and ammonia, oftentimes in a confined space. Three to six months out, despite the fact that there's no allergic mechanism, these are workers who still exhibit wheezing, reactivity to nonspecific simulants, such as dust or cigarette smoke, and respond to bronchodilators. They're generally treated the same as other asthmatics with bronchodilators, inhaled corticosteroids, and similar medicines. Additionally, it looks and acts like asthma and responds to the same, although it's non-immunologic and instead is the consequence and sequela of a severe irritant exposure. Work-exacerbated asthma, which we saw at the beginning of this slide set, is worsening of pre-existing asthma, in other words, in workers who were sensitized such as pollens or animals. In many cases, the trigger may be re-exposure to the allergen, for example, if they go into work in animal care, but more often they're reacting to nonspecific irritant exposures such as chemical vapors, dust, cigarette smoke, hot or cold air, and airborne particulates, including also stimuli like cold air or exercise. With these individuals, they tend not to be able to file or claim a workers' compensation case because the asthma is considered to be a pre-existing condition and most often they're best dealt with through ADA mechanisms, in other words, considering that they have a disability or impairment so that they can function without triggering their asthma. Moving on to the evaluation of work-related asthma. Of course, the history becomes paramount and you want to have a history of shortness of breath and wheezing in relationship to exposures. You want to also be careful to ask about delayed responses. Oftentimes, in the case of delayed responses, they come back from work and they start wheezing in the late evening hours or at night and it gets blamed on the cat or some other type of home trigger. These people may not improve away from work according to what you normally think of in the evaluation of work-related disorders. Is there a history of pre-existing asthma? Is this a work-related exacerbation of asthma? There are signs of other immediate hypersensitivity reactions such as rhinitis, nasal polyps or atopy in some form. Keep in mind the differential for asthma. For example, some individuals may have vocal cord dysfunction, upper airway disorders and some others may have COPD. In other words, they've got fixed obstructive lung disease which is acting or behaving like asthma and it's reversible. I know this sounds really pitifully stupid to even mention at this course in a lecture but you can't have occupational asthma unless you have asthma. The very first point in the workup of occupational asthma is to demonstrate airways obstruction and demonstrate reversibility by giving them a bronchodilator. If they have normal airway flow and they've been away from work for some time and they don't have a trigger for their asthma you could consider nonspecific inhalation challenge such as methacholine challenge but first demonstrate asthma before you start calling it occupational asthma. Use of diagnostic tests becomes essential for the demonstration of work-related asthma. You can try to accomplish this in several ways. Spirometry and especially if you're able to get it cross-shift spirometry meaning at the beginning of a work week, say Monday morning and at the end of the day or at the end of the work week you should be able to see a drop of about 10-12% in FEV1 across a work shift or an exposed shift. This is a good metric for the diagnosis of occupational asthma because it demonstrates a drop occurring across someone's shift. The problem here again with some of the low molecular weight allergens is that you could miss a delayed response which may not happen at the end of the work shift but might happen into the evening or the nighttime hours. Additionally you can have the worker keep a peak flow diary we'll see an example on the next page. This should show improvements on weekends and holidays and oftentimes you want to have the worker have a running period where they're away from work for a while to get a kind of a baseline peak flow measurement and then try and see whether or not you have a drop when they return to work. IgE antigen testing can be useful remember from the previous slides that it's better for those who have low molecular weight antigens particularly biologicals and in many cases such as isocyanates there's going to be a very large percentage of false negative results because the testing isn't particularly good or sensitive for it. In the United States bronchoprovocation testing is oftentimes not available in Canada it becomes the gold standard where you can put somebody in an inhalation chamber give them a dose or exposure to the suspect material and see a definitive drop in FEV1 again considered the gold standard but not necessarily available here. Peak flow measurement is dealt with in a little more detail here again it's helpful to have the worker away from work for a week to 10 days followed by 2-3 weeks return to work and exposure to the suspect antigen make sure that they're exposed to the suspect agent at work on return. And here's a typical recording of peak flow measurements it's oftentimes easy enough to eyeball what happens rather than look at the numbers specifically so here around day 2 and day 9 these look like weekends with the solid circles filled in which the worker is at home possibly for 2 days and note that there's a baseline in the 600s with the open triangles which represent time at work you can see this jagged or sawtooth pattern which is indicative of a drop in peak flow occurring at work so this is good evidence that there is some type of asthmagen or asthma trigger occurring at the workplace. Peak flow measurements been considered quite important in the diagnosis and evaluation of potential occupational asthma there are of course some criticisms of it one is that people may falsify their result a couple of ways to get around this there are now some recording peak flow meters that have a little chip that can take the records of the measurements and download them into the computer and then graph them out so that it's not it's useful to get concurrent spirometry and measurements of FEV1 at the same time peak flow is going on and of course the last problem is that there's demonstrable association with the workplace but it doesn't clearly identify the agent and if one or more suspect agents are in use it won't necessarily identify which one is causing it however on the flip side you do have some demonstration of association with the workplace vis-a-vis the home and noting also some other problems in the workup of work related asthma for sensitizer induced asthma antigenic tests may demonstrate that there's specific IGE but it doesn't demonstrate airway sensitization so you want to combine positive tests with their presence in the workplace and demonstration of the workplace ability to cause a drop in FEV1 commercial tests may not have all of the appropriate antigens particularly again with low molecular weight allergens which may precede by these non-IGE mediated mechanisms cell mediated immunity and late responses and so some of the testing particularly if you're looking at chemical allergens may not give you the full answer as to causation specific bronchoprovocation testing we mentioned before is considered the gold standard because you're applying a specific sensitizer to the testing of the worker but it's really done mainly in Canada there's only a few centers in the US mainly concerned with a specific of research it can be expensive it's time consuming you have to put the patient in the hospital etc. etc. and long periods outside of work may reduce the sensitivity there's some other questions associated with it is that the conditions may not simulate what happens at work and what happens if you get the wrong agent so while we call it the gold standard it's really done very little in the demonstration of occupational asthma at least in the United States there's a few important take home points related to the management of work related asthma one is that sensitization is immunologic and idiosyncratic and it may occur at levels that are below the permissible exposure level so adherence to the PEL doesn't mean that workers cannot become sensitized more importantly is that once these workers are sensitized they may react at very small doses a tenth or one hundredth below the PEL or the REL orders of magnitude below it and that very very small amounts may trigger an asthmatic attack because of the immunologic response being amplified so in these cases personal protective equipment such as respirators may not be protective even if they're 99.9 percent effective a few small molecules can induce an asthmatic episode so in these cases you really want to recognize sensitizer induced asthma and in most cases remove the worker early such that they don't develop a fixed obstructive pattern or develop very difficult to treat asthma from being continuously exposed in irritant induced asthma it's a little bit easier to work with there what you're really trying to do in those cases are just reduce the exposures if there's dust clean up the workshop if there's cigarette smoke get rid of it if there's hot or cold air available you may want to transfer the worker and get them away from the source of their irritants and here's why I mention again that ADA considerations rather than compensation considerations may come into effect. Acute inhalation injury I'm only going to mention in passing as this was covered in the previous module slides. Recall that the site and severity of injury are going to be related to water solubility of gases and vapors with the high water soluble materials affecting the upper respiratory tract and the less polar more low water soluble molecules the lower airways and those include phosgene and oxides of nitrogen. And a brief reminder about the sequela of acute inhalation injury can range early from acute respiratory distress syndrome and of course as we talked about earlier development into irritant asthma or RADS along with upper airways dysfunction and PTSD a non-pulmonary sequela. The next few slides look at COPD as an occupational injury or illness. Used to be thought that COPD was related to smoking smoking and smoking and the workplace exposures had very little to do with the development of COPD but evidence across the past decade or two has indicated that chronic irritant exposures will result in obstructive lung physiology with the development of emphysematous damage to the lung and non-reversibility of airway obstruction across time. Many workers exposed to dust gases mists and vapors or combination of these will develop a productive cough after 10 or 20 years of exposure. This has been termed chronic or industrial bronchitis and if other causes such as smoking are excluded then they can be put down to an occupational source of good evidence that prolonged exposure across a working life will result in this type of chronic bronchitis. And here in this slide we can put some numbers on the proportion of COPD attributable to work. It's a little bit easier to trace now that smoking has in general declined although amongst many workers at risk they may still continue to smoke but about one-fifth overall of COPD is probably attributable to work in inhalations of gas dust and vapors as we mentioned before. Once you cut out smoking it's close to about a third as the attributable fraction of COPD from exposure at work and variety of particularly dust generating occupations such as coal mining, quarrying, or hard rock mining and work around concrete products may expose workers to long-term high concentrations of inhaled dust which may or may not be fibrogenic as the case of coal and silica but may set up a prolonged irritation in the lungs. The ATS some years back came out with a statement from which these numbers are taken that outlines the occupational contribution to airways disease burden particularly with COPD. Moving on from obstructive airways diseases, asthma and COPD, we'll move to the restrictive lung disease. This is primarily interstitial fibrotic lung disease from inhalation of fibrogenic dusts in particular and namely asbestos, silica, and coal. So asbestos or asbestiform minerals is the broad brush designation for a number of hydrated magnesium silicates that come in fibrous form and they can be taken and woven into cloth or made into insulation. There's two main varieties and I think really only the big differentiation between amphiboles and the serpentine asbestiform minerals is important for the boards. The amphiboles are straight and needle-like and come under the names of tremolite, amasite, and crocidolite, which isn't here, but in the main have been considered more fibrogenic and with more potential to cause cancer. Crocidolite being the main serpentine or curly material and while in the past it has been considered to be less fibrogenic, it still remains and is a carcinogen and fibrogenic asbestiform mineral. There's a huge variety of workers at risk from exposure to asbestos, beginning with the miners and ranging on to people who used it for pipe fitting and insulation, military personnel at and after World War II, especially in the Navy where it was used for insulation on ships, sustained very large high doses of asbestos inhalation, and currently because it's been so ubiquitous and used in buildings, ships, and a variety of other materials, asbestos remediation workers who have to tear out and replace the material remain at risk in these days. Asbestos will cause both parenchymal and pleural disease. Focusing first on the pleural disease, we see one of the favorite board trivia type questions, which is the first manifestation of asbestos-related pleural disease, and that is to say a pleural effusion, which can occur with a latency of approximately 10 years or slightly less, and for trivia buffs this is the most common effect within the first 20 years. Again, used to be at least a common board question. Rounded atelectasis, which is also related to pleural effusion and to some pleural thickening, can also be seen in the early years, and then more commonly appearing are pleural plaques, which generally have a latency of at least 10 years and oftentimes more like 15 to 20 years, and these can be calcified. They are not malignant on their own. In other words, they do not develop into mesothelioma, but they serve as a marker for significant asbestos exposure. So the presence of pleural plaques generally indicates that a worker has had significant long-term asbestos exposure across the course of at least 15 years and probably longer. Here's a chest x-ray with the typical appearance of asbestos-related pleural plaques in central lung zones. These are either anterior or posterior, so you're seeing them lying across the field of vision. The diaphragmatic plaque over on the left side, or the patient's right, is less visible in this, but is also calcified, and you can see some increased intensity on this picture. Following on from the pleural disorders, asbestosis is the main parenchymal disorder related to asbestos inhalation. This is interstitial fibrosis of the lungs, and generally has a mean latency of at least 20 to 25 years. A couple of take-home points for this. It's predominantly in the lower lung zones, which is distinct from silicosis and COL, which are generally in the upper lungs, one way of differentiating them, and they have linear or curved or irregular scarring that oftentimes look like curly B-lines. This is different from the rounded opacities of silica and COL, and of course there's a, because of the fibrosis and fibrotic lung disease, there's a decrease in total lung capacity, restrictive lung disease, with the fibrosis causing a decrease in diffusion capacity. This is a good inclusive chest x-ray pointing at both pleural and parenchymal disease in asbestosis. In the central and lower lung zones, you can see the interstitial fibrosis, and again linear or irregular opacities, kind of typical of pulmonary fibrosis in general, but also again occurring in the lower zones. In the lower lobe on the patient's right side is the large pleural plaque. You can see a few more over on the patient's left as well, and this slide also does a good job of showing pleural thickening, not plaques, but blunting of the costophrenic angles bilaterally, which will occur with severe pleural thickening as well as the development of pleural plaques. Moving on from the parenchymal disease are the two cancers caused by asbestos, mesothelioma and bronchogenic cancer of the lung. Mesothelioma has a high association with a history of asbestos exposure. It's a very, very rare cancer otherwise, and so appearance of a mesothelioma should prompt a search for some asbestos exposure in the past. Now, of interest as opposed to the other asbestos lung diseases, mesothelioma exposures may be short in duration and low intensity. There have been cases of workers who worked during high school at steel mills for their summer jobs, or Navy personnel who were drafted in World War II, spent some time in the shipyards fitting or building ships, and 30, 40, 50 years later developed mesothelioma, so a prior history need not be prolonged or of many years duration for the development of mesothelioma. It has the longest latency of any asbestos-related disease and usually doesn't occur until about 30 years following exposure, but it can go on up to about 50 years. Generally presents, as you see in this slide, with evidence of a mass, oftentimes asymptomatic initially until it's too late for the patient, and the five-year survival is very poor, under 10%. It responds very poorly to any cancer modalities, including extensive surgery to debulk it and to chemotherapy. Bronchogenic lung cancer, as I mentioned, is the other malignancy related to asbestos disease. This can be all types. It can be squamous cell, adenocarcinoma, and small cell carcinoma of the lung. Its latency is a bit less than in mesothelioma, and the mean latency for development is about 25 years. Highlighted here are the relative risks for development of lung cancer with smoking and asbestos alone, so these are non-asbestos exposed smokers or non-smoking asbestos workers, which have relative risks of 10 and 5, respectively. Lung cancer is one of the more interesting cases from the epidemiologic standpoint in that smoking and asbestos exposure appear to have a synergistic relationship, and so the relative risk for lung cancer with both these exposures is about 50 or very, very high. Don't be trapped by the boards if someone asks you what the risk or synergy between smoking and mesothelioma is. There is no synergy between that since cigarette smoking does not appear to be a cause of mesothelioma. Asbestos is a known human carcinogen for other locations of cancers. In the respiratory tract, it can cause laryngeal cancer. It can translocate across the GI tract and from swallowed particles, for example, out of the respiratory tree can then proceed to cause colon cancer, and again translocating across the digestive system can cause peritoneal mesothelioma and renal cell cancer. One association not here, which is probably growing in strength of association, is a association with ovarian cancer also. Next of the fibrotic occupational pulmonary diseases, silicosis. Silica or silicon dioxide is the most abundant mineral in the Earth's crust, and fundamentally we're talking about inhalation of crystalline silica, which usually comes in the form of quartz or two other fused materials from high heat, cristobalite or tritamite. Amorphous silicates such as glass or diatomaceous earth, which are non-crystalline, are generally non-toxic and don't cause silicosis, but if they're fired or fused at high temperature, it can convert them to crystalline silica. There's a very extensive list of occupations exposed to crystalline silica, and recall that silicosis worldwide is still the most prevalent occupational pulmonary disorder. This is the frequency of its use in the developing world, for example in mining and construction, quarrying and foundry work, and a huge variety of other tasks that mainly occur in factories and related work in the developing world. The natural history of silicosis with ongoing exposure progresses from simple silicosis into confluent opacities and fibrosis, and down to progressive massive fibrosis. Simple silicosis is characterized by small rounded nodules which are less than one centimeter in diameter, and with the onset of more and more of these opacities and fibrosis come decreased lung volumes, reduced FVC, and reduced total vital capacity, along with reduced diffusion capacity or gas exchange with progressive cases. This occurs across years, and a couple of other points to remember about silicosis, both simple and complex, is that it yields an increased risk of bacterial pulmonary disorders, including an increased risk for tuberculosis and for bacterial infections, particularly anaerobic infections. So if there's a upper lobe infiltrate or the possibility of a pulmonary abscess, you want to think infection occurring in the setting of silicosis. It's also been demonstrable that silica is associated with autoimmune disorders and collagen vascular disease, particularly scleroderma, and the evidence has been much better across the past 10 years in favor of association of silica exposure with these disorders. Simple silicosis, if exposure continues, will progress to reticular nodule fibrosis. You get conglomeration of these small opacities into larger fibrotic masses. These can pull up some of the lung and form emphysematous bully as well, and as we'll see in the next couple of slides with x-rays, this leads to what's called a characteristic angel wing fibrosis occurring at the apices to the mid-lung zones. You can also see eggshell calcification in some of the hilar nodes. Here's a set of x-rays of silicotic nodules, particularly the x-ray on the left-hand side in the mid and upper lung zones. You can see the outline of what look like a lot of puff balls, which are less than a centimeter in diameter. These are more and better outlined over on the right-hand side x-ray, but they show fundamentally the same set of nodules as seen in simple silicosis. And just briefly reiterating a few facts about progressive massive fibrosis. This is rapid confluence of these silicotic nodules into large fibrotic masses. This then leads to progressive respiratory insufficiency from poor gas transfer, can develop into respiratory insufficiency and core pulmonality, and can be fatal if exposure goes on and if left untreated. These are the confluent nodules of progressive massive fibrosis or complex silicosis. You can see the angel wing opacities as described in the mid and upper lung zones, and very little in fact of the small nodules that we saw in the previous x-rays because these have all become confluent. The other point to notice is down in the lower lung zones at the bases where there's evidence of emphysematous changes from the lungs being pulled upwards by the fibrosis in the mid lung zones. And this is a CT of a similar type patient with a confluent right upper lobe fibrotic mass along with calcifications within the masses which are naturally occurring with silicosis. They serve as a nidus for calcification. Of course what you want to think of here is to exclude the possibility of lung cancer and watch this very closely and carefully because silica is well as a class 1 carcinogen for the lung and therefore this is a patient at greater risk for the development of lung cancer in addition to the fibrotic masses found here. I mentioned before that silicosis is the most common occupational lung disease in the developing world, but we also need to take care that we don't miss it. Here in the United States, coal miners are exposed to a combination of coal dust and silica because of the nature of the mining. And this is a section from a recent MMWR that shows the resurgence of progressive massive fibrosis in coal miners occurring in the Appalachian states going from a low of about 0.5% prevalence up to recent times in which a nearly 10-fold increase in prevalence has been seen in PMF in this group of workers. In addition to simple silicosis and PMF, there's also an entity known as acute silicosis. This is relatively rare and comes from high-dose exposures. This is direct injury to the lung from inhalation of crystalline quartz, and it resembles pulmonary alveolar proteinosis, essentially mass outpouring of proteinaceous fluid into the lungs in response and can be fairly rapidly fatal. Picture here is from the Gauley Bridge Hawks Nest Tunnel in West Virginia, which was dug in the early 1930s through a sandstone mountain without benefit of wet drilling and which killed several hundred workers as a consequence of acute and progressive, rapidly progressing, increased silicosis and fibrosis across the time it was being dug. It was America's worst industrial disaster at that time. Silica has now been classified as a group 1 lung carcinogen by IARC since 1997, so this is a known human carcinogen and group 1. Amorphous silica, as we mentioned, glass or diatomaceous earth is not classifiable for carcinogenicity, but crystalline silica is very distinctly carcinogenic. Coal worker's pneumoconiosis is very similar to silicosis and is, of course, the consequence of prolonged coal dust exposure and mining. Picture over on the right side shows the cellular changes in the lung parenchyma that come with coal dust inhalation. There's formation of coal macules with macrophage recruitment, scarring, and fibrosis, and there's very little normal lung parenchyma. Maybe if you look at the top of the slide, there's a little bit, but you can see how the alveolar cells have become markedly thick and fibrotic and distorted, and this is going to, of course, then lead to restrictive lung disease and poor DLCO and gas transfer. Many coal workers will develop also emphysema and chronic bronchitis from the chronic dust inhalation, and because there's oftentimes mining through silica rock, coal workers can develop kind of a combination of silicosis plus coal worker's pneumoconiosis. So coal worker's pneumo progresses much the same as silicosis, starting out as a simple pneumoconiosis, again, with rounded opacities on the chest X-ray. It's oftentimes mild. Sometimes in early stages can be more of an obstructive than a restrictive pulmonary disorder, but essentially similar to silicosis, it can advance to progressive massive fibrosis. And as you saw, the MMW report of coal miners in Appalachia, PMF, has been on the progressive increase across the past several years. Coal dust can also induce rheumatologic or immunologic disease, and there's an entity called Kaplan syndrome, which looks much like rheumatoid nodules within the lung and can be accompanied by rheumatoid stigmata on the fingers and hands, for example. So to move on to some other similar entities as pneumoconiosis, cobalt can induce a condition called hard metal disease. Cobalt is used to make machine tools, in other words, tools that have to machine other types of steel. And so what you want is the hardest metal to machine these materials that you can make. So tungsten carbide steel, to which cobalt has been added, forms this hard metal. Cobalt is an immunologic reactor, and its inhalation will cause a fibrosis with an immunological component. It forms these giant cells, which leads to a giant cell interstitial pneumonitis on biopsy. So I think the key here is just to remember to associate cobalt with this immunologic reaction and giant cell interstitial pneumonitis. A brief word or two about the ILO classification of pneumoconiosis. This is what the B Reader program in the United States encompasses if one is trained and takes a certification exam by NIOSH. The principal purpose of the ILO classification is to increase reliability in epidemiologic investigations, in other words, to describe the progression of pneumoconiosis, both asbestos, silica, and coal. And its secondary purposes have been sort of co-opted from the primary purpose, and this is legal classification and its other uses in surveillance exams. Now, so that those of you taking the board exam for the first time, don't get nervous. Nobody is going to throw you an X-ray and ask you to B Read it. So basically, underlying point is to relax. It just helps to know about the classification because you might be asked about that. Opacities in the ILO system are classified by their size and shape, which you see at the top. And these are rounded opacities, which are recorded as P, Q, and R. And irregular or linear opacities classified as S, T, and U. Most importantly, and what you'll normally see in the reports, is the profusion of opacities, in other words, the extent or density that they appear within the lung there. And this ranges on a scale from 0, which is essentially normal or of bare few opacities, all the way to 3, which is very extensive opacities that obscure the pulmonary vessels in some of the architecture. And so the reading you tend to get is based on comparison with a series of standardized films. And the films of a patient are then graded as 1, 2, or 3, and with a kind of a borderline designation. So you may see a 1, 0, which is that the patient's X-ray lies between a grade 1 profusion and a 0 profusion, or a 1, 2, which would be in the opposite direction. So that's what the scales and readings mean. And beyond that, I think that it's, at least for the purposes of the boards, we need not go further into this. Moving on into other occupational lung disease, we cover hypersensitivity pneumonitis, or HP, sometimes called extrinsic allergic alveolitis, or EAA, which also describes the pathophysiology of it. It can have an unusual or confusing clinical presentation. And a lot of typical cases are often mistaken for the flu or pneumonia. They may present with fever and a cough. A chest X-ray shows pulmonary infiltrates, and it gets treated as a community-acquired pneumonia. The worker stays home from work and, therefore, out of exposure for a while. And when it becomes recurrent, when the worker returns to work or several episodes happen, then that can raise a suspicion that this is HP and not a simple infectious process. HP, though, rather than being infectious, is a hypersensitivity reaction to a variety of primarily biological materials. And these generally include mainly molds and atypical bacteria. So in the case of farmer's lung, thermophilic actinomyces, which grow on chaff or silage, along with micropolyspora, also growing in those areas. Pigeon breeder's lung has been termed that because of allergy to bird antigens. Woodworkers can develop allergies to wood dust. There's a variety of other biological materials, mainly things like mold, as well as bacteria that grow in metal working fluids, things like atypical mycobacteria, to which workers who are exposed will elaborate an IgG reaction and a typical hypersensitivity reaction, type 3 or sometimes type 4 reaction. There's a number of clinical findings and manifestations of HP, which also are not specific to the disorder and therefore make the diagnosis somewhat difficult. Granulomatous changes and fibrosis can be seen on chest X-rays and CT scans. Also, as we'll see in a subsequent slide, ground glass opacities resulting from the alveolitis can be helpful in the diagnosis. If they undergo bronchial alveolar lavage for diagnosis, there's usually a lymphocytic infiltration. In a lot of these cases, we'll elaborate IgG antibodies to some of the antigens we looked at at the previous slide. These are oftentimes known as precipitants and can be obtained through standard IgG or HP panels. There's a small warning about that, though, which is to say that there can be a number more people sensitized or exhibiting positive IgG than is the case with specific people who develop, go on to develop the disease. So, for example, in panels related to the antigens in farmers' lung, about 40% or 50% of farmers may have positive IgG antibodies, whereas only a few may be ill from HP. High-resolution CT scanning is particularly useful in the diagnosis of HP. And typical findings, although not purely pathognomonic, are those shown here, which are ground glass opacities, those small whitened areas, most particularly notable in the posterior lung zones, but essentially throughout the lung fields, particularly on the patient's left side. And these are fundamentally the result of alveolar inflammation. Next is beryllium lung disease. Beryllium is an extremely light metal. Its atomic number is four, and it comes in for heavy use, particularly in the aerospace industry as well as in the nuclear industry. It's very, very light. In any attempt to save weight on metals, beryllium becomes a useful metal to use. Its main problem is that it causes a granulomatous lung disease that's difficult to distinguish from sarcoidosis, and we'll see that in the next couple of slides. Workers affected with beryllium lung disease may exhibit kind of a slow onset of dyspnea and cough, followed by, or accompanied by, anorexia, fatigue, and weight loss. Note is made here also that it's a IR group 1 carcinogen, but principally will be concerned with the granulomatous lung disease. Here are the clinical findings of beryllium lung disease. Chest X-ray will exhibit interstitial infiltrates along with hyaluronidinopathy, making this difficult to distinguish from sarcoidosis. If you put them on a spirometry machine, they will exhibit primarily restrictive lung disease, although sometimes you can see obstructive or mixed, and a reduced diffusion capacity. Main hallmark of beryllium lung disease is its pathology. If you biopsy this, what you find are non-encaseating granulomatas, and these can be found primarily in the lung on biopsy or also in the skin and in other areas, such as the nose and respiratory mucosa, where the disease may be active. Beryllium disease was termed Salem sarcoid because of an outbreak of cases of evident sarcoidosis in Salem, Massachusetts, occurring in the 1940s. Further investigation of this cluster by Harriet Hardy, fundamentally one of the mothers of occupational medicine, disclosed the outbreak to be associated with a plant that made fluorescent bulbs, for which beryllium was the conductive material at the time, and therefore the association with beryllium exposure was made in these cases of putative sarcoidosis. So chronic beryllium disease is principally a genetically determined disorder. There are variants in the HLA regions that present antigen and which are permissive for the development of beryllium sensitization after exposure, although at high doses, other individuals without these genetic variants can also develop beryllium disease. Because of its genetic basis, sensitization to beryllium or any kind of exposure to beryllium need not be particularly intense or prolonged for some worker to develop beryllium disease. So for example, secretaries in the company offices in Salem, Mass., that we mentioned before, had developed beryllium lung disease, even though they weren't necessarily the ones who were in constant or frequent contact with machining beryllium or using beryllium as a conductor so that it can sensitize workers and individuals at relatively small doses or short-term. The lymphocyte proliferation or lymphocyte transformation test, LPT or LTT, is diagnostic for sensitization and workers in beryllium industries should undergo these to determine whether sensitization has occurred. This involves incubation of lymphocytes from bronchoalveolar lavage, BAL, or blood and proliferation in the presence of added beryllium, which indicates sensitization. There's a question as to whether these individuals should be continued in work if they're sensitized but haven't developed disease, but it's clear that industrial hygiene controls should be ramped up, particularly for cases of this as they should in broad-brush general terms and probably workers who are sensitized should be removed from continuing exposure. In this slide, we're revisiting chromium, which we had seen earlier in the skin lecture as a source of type IV hypersensitivity. Just to remind you of the sources of chromate use and production, it's found in a variety of alloys and used in the metal plating industry and exposure can occur on welding, cutting, or grinding metals with chromium within it. Hexavalent chromium or chromium-6 is the form that's carcinogenic to humans and this can be absorbed from the above-noted sources at work and there's clear evidence that there is an excess of lung cancer in chromate pigment production as well as the electroplating industries. This has led to its classification as a group 1 carcinogen by IARC in the 1990s. Principally noteworthy on this slide is the OSHA hexavalent chromium standard specifying for an action level of airborne chromium and it mandates baseline medical examinations along with annual medical exams for workers who are exposed at the action level for 30 days or more per year. This includes chest X-rays for evidence of incipient lung cancer. One of the more unusual clusters of occupationally-related pulmonary disease was a set of cases of bronchiolitis obliterans occurring in microwave popcorn production workers. This was termed popcorn lung and these workers developed rather severe bronchiolitis obliterans, an inflammatory disease which essentially constricts and obliterates the small bronchioles and leads to fixed obstruction with progressive hypoxemia and several of these workers came to the point of lung transplant. Investigation at the plant disclosed that diacetyl small molecule ketone, which was used as artificial buttering flavor was the associated exposure in developing these. Now these workers have to wear full protective gear if this is being used or other materials have to be substituted for that butter flavor. Just to reiterate what was on the previous slide, the cluster was seen in workers initially working with diacetyl as artificial butter flavor and there have been reports of other materials including artificial flavors, pentanedione for example, in other flavoring workers. As well, two other sources where it might be seen, diacetyl is given off and produced in coffee processing that's roasting and grinding, not necessarily use at home but use in the manufacture of coffee for sale. As well, diacetyl and some of these other flavorings have been used as flavorings in e-cigarettes so that direct inhalation of combusted diacetyl may be occurring in smokers of e-cigarettes and vaping. Moving from pulmonary disease, we'll be covering occupational infectious disease. The next set of slides are on occupational tuberculosis as a segue from pulmonary disease and on the next set of slides following this set, we'll cover blood-borne pathogens and the zoonoses. In the late 1990s, the CDC issued guidelines for reduction of TB transmission in hospitals and healthcare facilities. OSHA had released a proposed standard at about the same time but the CDC guidelines were generally adopted and so that OSHA then withdrew their standard. The CDC guidelines call for four points in the main and prevention of TB. This is early identification of infectious patients and rapid isolation of the known or suspected TB case, engineering controls to which those patients should be isolated to minimize the spread, that includes negative pressure rooms, use of PPE, in particular N95 respirators, and at the time periodic PPD testing of health care workers, which under recent guidelines issued in the last year has been somewhat diminished, and we'll point out the differences between the CDC recommendations that have been in effect for the past 20 years and the current and recent changes just in the last year. Just a few basic factoids to refresh your memory about TB spread. These are very small droplets. They can be about one micron in diameter, which means that they're carried on wind drafts, and they can reach the lower respiratory tract and alveoli because of their tiny size. Once exposed, PPD tests can be detectable from about 2 to 10 weeks after infection, and again, clarify that that represents indications of exposure and not of active TB disease. A few numbers, which you may not necessarily have to have perfectly at your fingertips, but just giving you an idea of the risk for development of active TB. An adult who tests positive with a normal chest X-ray but the exposure was indeterminate has a very low risk per year. The people you want to be after are the recent or new converters because they have an increased risk across the first year and the first several years of turning into an active TB case, as do household contacts of an active case. Other high individuals at risk are those with abnormal chest X-rays and those with HIV infection. The risks of TB transmission in hospitals are fundamentally in direct proportion to the number of TB cases who are admitted to the hospital per year. The risks are only slightly above community risks in hospitals that admit fewer patients per year. The real higher risks are in the great municipal hospitals and areas where TB might be active, so Cook County, L.A. County, Bellevue, etc. You should also remember that workers in the high-risk hospitals may oftentimes be at risk at the community because the community is showing a high risk of TB infection, so that these are workers who may be at risk at home and in their outside life, as well as being at risk in the hospital. Some data from the 1990s that led the CDC to promulgate its guidelines are shown here. At that time, diagnosis of TB, active TB I should say, was delayed in nearly 50% of patients who had active TB and the diagnosis was delayed for an average of six days, and that exposed anywhere from 20-odd to 40-odd workers for every case diagnosed late, so it was distinctly a problem within hospitals. Other sites of occupational risk outside of the hospital include nursing homes. Residents of nursing homes, because of their age and perhaps coming from a time when TB was less controlled, often have a fairly high prevalence of positive skin testing and, therefore, at least of latent TB. There are some problems in the elderly, too. They don't mount a fever, for example. They may have a long-term chronic cough that's never been fully worked up or treated, and so the workers within nursing homes can have a high rate of TB skin test conversion and of latent TB. Correctional facilities also, because of the population that's cared for within them, also can have workers who convert their PPD more readily than out in the community, and if you look at compared to secretarial personnel within correctional facilities, guards have about a 60% increase in TB test conversion and medical employees have over a two-fold increase. The two-step testing algorithm is still used in initial medical surveillance in the workplace. All newly employed healthcare workers, unless they continue to have had a previously documented history of PPDs, and unless they already have a documented history of a positive PPD and treatment for the disease, should undergo initial two-step testing. What the two-step testing does fundamentally is to boost a reaction in people who may have had a latent TB infection way, way back as an infant or a child, and as such, their immunity to an antigenic challenge, i.e. the PPD, has waned. So, the first PPD is fundamentally giving them a booster to improve their immunity, ramp up their immune reaction, and if they are positive, then they will have a positive on the second step. So, the first PPD is given. Obviously, if it's positive on the first step, that worker should be evaluated for signs and symptoms of TB, a chest x-ray, and treated according to current preventive therapy if needed. If they don't have a positive PPD on the first step, they're given a second PPD one to three weeks after the first, and if both are negative, then you can assume that that worker's uninfected and they may go about having periodic screening. If they're positive on the second step, this is a boosted reaction indicative of a probable latent infection occurring sometime way in prior years, and then, again, you should determine the need for preventive therapy at that point. Briefly, a look at those with an increased risk of TB. These are oftentimes people who come from endemic areas or who visit high-prevalence countries. As we mentioned before, residents and, of course, healthcare personnel from nursing homes and correctional facilities and healthcare workers with high-risk patients. So, using tuberculin skin testing or PPD for TB detection, the baseline is used via two-step testing as we described in the previous slide. The main difference in the CDC guidelines issued in 2019 versus the previous ones issued in the past 20 years are about retest of workers. The CDC is now considering that workers who don't have active exposure or an active exposure incident need not undergo the same sort of annual surveillance that we've been used to giving and ourselves getting across time yearly in our healthcare organizations. So, the testing after exposures becomes more critical and testing routinely annually has become less critical. Now, I don't know whether the boards are going to have advanced that far yet. This guidance just came out last year and this may be kind of under the wire for appropriate inclusion on this year's board exams, but I think we all should be aware of the changes which are to really fundamentally abandon the annual examination as we had done before. So, just a kind of a warning caveat for the boards. I'm not clear where this may lead, at least on this year's boards. This slide shows the cutoffs for a positive skin test for tuberculin, and I think the basic underlying point here are that healthcare workers are in the 10-millimeter or greater cutoff for determination of latent TB infection. The 5-millimeter or much more stringent cutoff, usually for the immunocompromised, the cases in contact with an active case or those with abnormal chest x-rays. Most of you have some experience with employee health and some type of determination about what to do with workers who have had BCG in the past. So, a couple of take-home points from this slide. BCG is usually given in mass immunization programs to infants and young children, really about one to two years of age, and the protection that BCG affords after these people reach adulthood, they've reached their 20s now, it's been 20 years since the administration of BCG, is that that protection has really waned and virtually gone away. So, the assumption the CDC makes is that tuberculin skin testing is not contraindicated for persons who have had BCG vaccination, because in general, it's been a very long time ago, and that a positive reaction to tuberculin in a BCG vaccinated person is still indicative of infection if there's an increased risk for infection or if there are medical conditions, as we saw in the previous slide, that increase the risk for disease. So, says the CDC, and I'm quoting you chapter and verse from them, because your own methods may vary, your own approach to handling patients may vary, but this is the board exam, and they're going to take it from reputable sources as to what the appropriate answer for this type of question would be. The interferon gamma tests represent one way around that previous question about BCG administration, as well as supplying a more quantitative read on whether people have developed subclinical or latent TB infections. The CDC states that interferon gamma tests can be used in all circumstances in which you would normally or currently use a TB skin test, and as with TB skin tests, you want to apply it to a population in which there's increased prevalence, in other words, people who may be at high risk for converting, so that you minimize false positives and that you get a better predictive value from the test. So, it can be used in contact investigation, in recent immigrants' investigations, particularly if they have received BCG vaccine, and they can be used in TB screening for healthcare workers, and if you're doing serial evaluations in groups of people, including those at risk from their work in healthcare. The interferon gamma tests have some notable and fairly obvious advantages. It's a single visit for a blood sample, and you get results back fairly quickly, so that one of the main points that has interfered with tuberculin skin testing, the return to the clinic after 48 hours, doesn't need to happen, so you'll probably get better compliance. You don't have to worry about boosted responses because it's not a challenge with an antigen and a response. You don't get that reduced reader bias that you get with tuberculin skin testing. In other words, you don't have six people grouped around a worker's arm trying to decide whether the TST represents 9 millimeters or 11 millimeters of induration, so the problems around that interpretation may go away. And as we noted, it's based on a complete set of mycobacterial TB antigens and not on BCG, and therefore BCG vaccination in a negatively exposed worker won't give you a potential false positive. Some downsides, obviously, there's an expense associated with it, which isn't necessarily the same as with skin testing. We do have some limited data on conversion and the newly exposed, when and how frequently it would happen. Getting back to the question about false positives, many organizations found that they had a high rate of quote-unquote conversions that differed from their TST experience, where they had had very low prevalence in incidence of TST conversions. Suddenly, in a switch to interferon gamma test, they suddenly found they had 3, 5% positive assays, and this has to do part with the cutoffs that were used and the criteria for a positive test, and probably with screening a group that weren't at very high risk for conversion, in other words, producing those false positives. And unless it's performed right, and for some other reasons, there was some variability on repeat testing. Much of this seems to have gone away, and as we tend to test more individuals who are at truly elevated risk, in other words, high TB prevalence hospitals with follow-up of incident exposures, we're probably achieving better positive predictive value on these tests. Very briefly, the CDC's recommendations for preventive therapy will be covered in the next slides. The cutoffs for positive PPD were seen in the prior slide. Again, for the purposes of the occupational medicine boards, most of this slide doesn't have to be committed to memory. I think the real basic things to remember are that 9 months of daily INH therapy is the mainstay of treatment. This can be also cut down to twice weekly if there's directly observed therapy, and as well, 6 months therapy if 9 months can't be tolerated. Other therapies include isoniazid and rifampin or rifampin therapy for 4 months. There should be work restrictions for workers who develop active pulmonary tuberculosis, in other words, they're coughing and potentially spreading TB bacilli. They should be excluded from work until you can ascertain that they're receiving adequate therapy, which should be based on sensitivities and ensuring that they're not carrying resistant organisms. That there should be evidence of a response to treatment, i.e. that the cough is resolving, and they should have 3 AFB spheres negative within a 24-hour period after the therapy has been complete. If they discontinue the therapy before it's adequate, you have to keep them excluded. If workers have latent TB infection, in other words, non-active TB, and they only need to take preventive therapy, they don't pose a risk to other patients and they can continue work as long as they're not symptomatic. There may be those who either cannot take for medical reasons or refuse preventive therapy, cannot take INH, for example. They may also continue in work as long as they don't have symptoms of TB. All these workers should be counseled regarding the symptomatology of active TB development, cough with fever, night sweats, bloody sputum, etc., etc., and employee health should engage in periodic monitoring of these workers, perhaps yearly. There's oftentimes a questionnaire and a symptom check that they should complete annually, and that can be useful in ascertaining that they still remain without active tuberculosis and not at risk to themselves or to their patients. In the last two slides here on exposure control, mainstay of exposure control is early recognition of TB cases. You want to have a high index of suspicion. If they prove not to have TB, you can always not isolate them further, but cases that are active and suspicious should be isolated. The CDC guidelines call for engineering controls. These patients should be isolated in negative pressure isolation rooms with the air moving from the outside hallway into the room and then vented out to either the outside world or recirculated within the building with some treatment. So the ventilation from these rooms needs to be either directly exhausted to the outside or HEPA filtered if the air is partially recirculated or reentrained back into the building in order to remove TB droplet nuclei and particulates. If the air is being recirculated within the patient's room, that's not recirculated into the building, but within the room, that recirculated air needs to be UV irradiated. And of course, as with most engineering controls, the main object is to ensure that they're working and that they're continually working. So the CDC guidelines call for regularly scheduled maintenance and documentation of the effectiveness of these negative pressure rooms. So the industrial hygienists, for example, should use smoke entrainment into the rooms to demonstrate negative pressure. And lastly, although we'll talk about more detail on the respiratory protection standard, the N95 respirator is really the mainstay of protection for workers within the hospital or healthcare unit for filtering out tuberculosis particles. The N95 has 95% efficiency for 0.3 micron particles, which means that they're adequate and more than adequate for filtration of particles that are the size of TB droplet nuclei, in other words, 1 micron or thereabouts. Fit testing, as we'll see later on, is mandatory, and we'll talk about how that happens. The alternative for the N95 respirator is the powered air purifying respirator, or PAPR. These are more protective, but they're obviously more cumbersome. They call for a tight-fitting face mask or a loose-fitting hood, and they may be difficult to don or doff. So the recommendations mainly are for those at much higher risk, let's say pulmonary physiotherapists or workers in the bronchoscopy suite of high-risk, high-TB hospitals. And noteworthy is that risk within the room may persist, as droplet nuclei may still be floating around the room, so that the room has to be effectively cleared out and re-ventilated before other patients can be put in there. This ends the first section of the Occupational Medicine 4 series. This is followed by Part B, which continues on Occupational Infectious Disease and Hearing Loss.
Video Summary
This video is a slide lecture on clinical occupational medicine. It covers various topics such as pulmonary disease, infectious disease, and noise-induced hearing loss. The first part of the lecture focuses on pulmonary disease, specifically work-related asthma and pneumoconiosis. Work-related asthma is now the most common occupational lung disease in the United States and can be categorized as occupational asthma or work-exacerbated asthma. Occupational asthma is new-onset asthma specifically related to occupational exposures, while work-exacerbated asthma is the worsening of pre-existing asthma due to workplace exposures. The lecture also discusses the different types of allergens that can cause work-related asthma, such as high molecular weight allergens and low molecular weight allergens. Pneumoconiosis, on the other hand, refers to lung diseases caused by inhalation of dust particles, such as silica, asbestos, and coal. The lecture provides an overview of the clinical presentations and diagnostic tests for these pulmonary disorders. It also briefly mentions other occupational lung diseases, such as cobalt-induced hard metal disease and diacetyl-induced popcorn lung. The second part of the lecture delves into occupational infectious diseases, with a focus on occupational tuberculosis. The lecture discusses the guidelines for reducing TB transmission in healthcare facilities, including early identification of infectious patients, engineering controls, and the use of personal protective equipment. It also mentions the use of tuberculin skin testing and interferon gamma tests for diagnosing and monitoring TB infection. The lecture concludes with a brief overview of exposure control measures, such as isolation rooms and respiratory protection.
Keywords
clinical occupational medicine
pulmonary disease
infectious disease
work-related asthma
pneumoconiosis
occupational asthma
allergens
silica
asbestos
coal
occupational tuberculosis
exposure control measures
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