It's my great pleasure to introduce Dr. Carl Wurz, who has drastically understated himself in the bio that he posted online for us. He graduated Kirksville College of osteopathic medicine. Residency trained in internal medicine and occupational environmental medicine fellow of the college of. Of of our college, it is also the chair of the commercial. Driver medical examiner course, he is here to speak today on several topics, beginning with occupational pulmonology. But, thank you, thank you very much. Thanks for that kind introduction. So, we're going to blast through the occupational diseases. Problem is, I've all pulmonology is a 3 year fellowship. There is actually. I mean, it's probably sub fellowships now in occupational pulmonary diseases, but people that are already boarded and pulmonology. We're going to cover it all in an hour, so I'm trying to summarize 4 hours of. Of 4 years of didactic education, we're going to go through all all these things. Let's just go ahead and do them because we've got, we got to keep moving. 1 of the things we know, Dr. Jesus are under reported. 1 of the questions, I mean, there's people that will argue that, you know, adult onset asthma is usually a specific cause and an awful lot of them are work related. Not all those get captured as work related problems. As I move through time, the 1 of the 1 of the things is difficult is that the disease is the same, whether it's were caused or not were caused. Um, when the entry things is that if you go to non industrialized populations, you'll see much less of certain of, like, occupational asthma was adult onset. So, there may be some connection there a little bit about. We're talk a little bit about dust accumulation in the lungs and some of the dust accumulation diseases usually usually lumped together to call them. We typically talk about coal dust and silica. We often will talk about asbestos in that same group. There are another page of little tiny ones that could also occur, but it's just deposits in the lungs. Much of the larger the particle is the further up your airway. It's going to be captured. So, at the very top of the lungs, you'll, you'll capture the upper airways in the back of the throat. You capture things greater than about 10 microns or micro meters. Trachea will get catch the 3 to 7 micro meter stuff and then getting all the way down into the alveoli will be the much smaller particles in the 3 to 0.5 to 3 micro meter or micron. Diameter and this is aerobic diameter. Now, clearance is of all these from all these levels is by the mucociliary escalator. Although, if you kind of think about it, the things that get all the way down the alveoli are actually below the mucociliary escalator system. So, if they get all the way down there, it takes a while to get them back up and there's macrophages involved and other things like that. Accumulation depends on a lot of things. Different people have different accumulation rates and it's probably some genetic thing that we don't fully understand, but we know it's different in different people. And the biologic response can vary between individuals. So there's all those things can make this little complicated puzzle out. So, talk a little bit of I want to talk briefly about. The basic diagnostic testing 1 of the reasons I include this specifically is that while we're not expecting people who are an occupational medicine practice to be, like, you know, we're doing their own MRI, MRI, PET scan to the brain. That's kind of beyond what we do. Many people do their own spirometry. It's an, it is considered an appropriate office skill in occupation medicine practice and you'll be doing your own interpretation. So you need to kind of know what's going on. Basic spirometry, you have a device, the patient glows into a tube. In the old days, I would have talked about a dry rolling seal, bellows thing that would move. When you do that, it would move a pen on a chart. We've now, all that's now been automated and computerized. Generates 2 different kinds of flows of diagrams. The 1 kind of on the lower right hand corner is the volume time tracing. That's what I grew up with, with my dry rolling seal spirometer and a pen graph that you had to do. Which gives you a lot of information, but the up on the upper right hand corner, you'll see a flow volume loop, which gives you additional information. If you're going to do spirometry in 2022, you need to be comfortable. Working with both of these graphs to identify both abnormalities and disease states. Super basic, a review of spirometry, we talk about the forced vital capacity, which is how much did the person blow out before they couldn't blow out anymore. And this shows kind of that line, just it's the top of the plateau of that person's volume time curve. The other thing we're interested in is how fast can they blow out the air? And so we look at that, we measured that. It's called the FEV1, the forced extra volume in 1 second. This part is standardized across the planet. And then, so you go out 1 second, draw the line across and you get a number and that would give you the FEV1. The machine does all this for you now, but you need to kind of understand what it's trying to get at. There are a lot of other measurements you can make, FEF25, FEF50, FEF75, there's a lot of different measurements you can do also that you can resolve from this. But the basics, the ones that everybody agrees on are useful and are interpretable, is the FEV1 and the ratio between the 2. Calculator ratio, you start with the best FEV1 and the best FVC. You then calculate, just divide, so divide the FEV1 by the FVC in liters or whatever the unit of measure is for your system. You express as a percentage. The ratio, if you kind of think about it, the ratio corrects the airflow if they've got a low total lung capacity. That's what the ratio gets you to. So, if they've got some restrictive disease, the FEV1 alone may still show that restrictive disease, whereas the ratio will correct for that. So, predicted values, we can do at least 2 hour and probably, I could do probably a 3 to 4 hour discussion of this topic of predicted values. We're not going to, we're going to spend 1 slide on this. Basics today is it's based upon. Gender, age, height in stocking feet, and something about ethnicity, and I've got stars next to both gender and ethnicity because it's functionally your gender during puberty. And we'll talk about that more on Friday morning. And then the ethnicity thing is its own very deep rabbit hole that we're not going into as far as, you know, there's different data sets have different ways of breaking this down, which can get very complex. And so, if you're, if I'd been here 3 years ago, I would have been saying, you should really go to use the NHANES data set that's based all the United States and most people still use. Today, 1 of the questions, what do you do with people that are polyethnic? And this becomes quite confusing, like, what data set do I use for Obama? For Barack Obama, I mean, his mom was white. From Europe, his dad was from Africa. There's no data set for that. So that's where this has become super. Infusing 1 of things I always recommend is because you can use a predictive equation. You figure out how what the percent predicted is for that individual. Always be careful if you get FEV1 or FEC that are greater than 130% of predicted be suspicious. Always go back when I see over 130, I check the numbers. Because we're into the range where it's usually not physiologic or the person should have an Olympic medal for an aerobic event. I mean, and when I get above 150, 150% predicted, it is non physiologic. There are occasional individuals that really are well conditioned athletes that might get in the 130s. I've seen that a couple of times. But if you talk to a person, it's never the guy that's, you know, there's never the 350 pound guy that plays on his, that does video games. But you might every once in a while get that guy. The reason that guy won the gold medal at the Olympics is because his lungs are bigger and he could run a little farther, a little faster than everybody else. Remember Olympic medals are given to mutants. That's how that all works. Occasionally skilled, but mostly physiologic mutants. Way back when a lot of people went through their training. We talked about anything between 120 or 80%, 120% predicted is considered normal and we move on. That died in 2005. So, with the recommendation now is to use the concept of lower limit of normal, which is about the 5th, which is the 5th percentile of a normal population. So, less than that is considered abnormal. And then you look at the patterns based upon that. Keep in mind that that 5% cut off means that 5% of the population is still below that. So, just like when we look at the hemoglobin, it says the hemoglobin rating should be 13 to 17 and somebody's 17.1 or they're 12.9, we don't get excited as a clinician. The same thing applies to these cutoffs. Don't get super excited if the person is just below the cut off. That's not necessarily an abnormal finding. If they're way, because the abnormal people are way below the cut off. It's not subtle in most of the time. And the other thing I mentioned on here is the lower limit of normal for young people can be pretty high. Yeah, for like a 23 year old or 22 year old, that lower limit of normal can get up to about 85% predicted. Come back on Friday because I'll talk about this more. This is the flow chart you use. And basically, you're going to place the person in the category of normal, destructive pattern, restrictive pattern, and then you will or mix. And then you'll use these severities based on the FEV1. This is not the most current recommendation from ERS. But their current recommendation, I will argue, is unimplementable in a clinical setting. And again, we'll talk about this more on Friday, but their current recommendation, they just changed how they want to do. They don't do it by part of the test. And I don't know what it means to have a severe FEV1 and a normal FVC. I don't know how you explain that to a patient. Coming attraction, that they're severe. I mean, and then TLC would be different and residual volume would be different. It's going to be a complex discussion with your patient. This is the long version of how to do that. If you add DLCO and the total. And if you add long volumes at DLCO, you can actually be more precise. And this helps you look at things that are interstitial disease or neuromuscular problems and to help identify them more clearly. Be thoughtful when you order things. My kind of cutoff is if the basic spirometry is normal, I probably don't need long volumes. If basic spirometry is not normal, I need long volumes. And if I'm worried about something that could interfere with gas exchange, I also would like to get DLCO or some equivalent test. And if you want to be super fancy, you can think about, do you want to have automatic bronchodilator testing if it looks like if they have a low FEV1, you think it's error, they have a low ratio, you can and your PFT lab is somewhat sophisticated. You may be able to write an order that will say, you know, if the ratio is less than something, then you want them to do bronco, then you want them to do. Then you want them to do reversibility testing. Please don't use 0.7 from gold, just please don't. Again, come back on Friday, but that drives me nuts. Okay, so there's lots of literature on how to interpret pulmonary function tests. I'm not going to go into it too much today. And yes, this is the European spelling, so I didn't spell any of it wrong. So other diagnostic testing we do is chest x-rays, staying basic, right? There's something called the ILO classification system. The International Labor Organization has this classification system for the presence of pneumoconiosis on chest x-rays. The person that does this is called a B-reader. If you're a licensed physician from anywhere on the planet, you too can become a B-reader if you so choose. You have to come to Morgantown, more or less, and take a test. It is a hard test to pass. I failed it twice. And it really requires you to be—what you have to be is really focused on what are the allowed abnormalities on an x-ray and have eyes that can look at the x-ray and fix it when they take the picture orally. And that's what I have a hard time with, is I'm not visual enough to, like, undo the fact that they under-penetrated this x-ray and then see what would be left in my brain. They talk about small—the profusion is the magic word of small opacities. And if there's large opacities, those are identified as well, to identify the presence of one of the pneumoconiosis. Here are some pictures. These are the actual standard pictures. So you compare the patient's x-ray to the standards that are produced by the International Labor Organization. You can buy a set of them. They're now available both analog and digital. A new set of standard films will be coming out any moment now. They will be digitally acquired. Right now, these are all analog films from the 1950s, is what they're using as their standards. There will someday soon be digitally acquired standard films, and that process is ongoing. And it wouldn't surprise me if tomorrow we get an announcement that it's been released. And you can see what you basically look at is look at the spaces between the ribs, and you've got—in the 1-1, there's a little bit. In the 2-2, there's more. In the 3-C, there's a lot. Then the lower right-hand corner, you can see an A lesion, because these small opacities will grow together and will form—will make large opacities. And it's all—this is all—it's a fibrotic disease. These are all—this is scar tissue in the lungs, and the scar tissue growing together and making less and less and less of their lungs is functional for gas exchange. That's really what this disease process is. So this is the form that's used. It is rather cryptic how it's done. And, I mean, you can learn—you can figure it out. It's not super hard to figure out, but there are codes and boxes. The whole idea was get everything on one piece of paper for a reader to be able to do it so they don't have to have, you know, a 12-page report. It's all check boxes on there. And if you—if this is something that you do at all, it's worth spending time to understand the form and what all the boxes mean. Some of them, if you're the ordering physician, some of those are boxes you have to respond to. Like, if they call it cancer, you have to do something about that. You can't ignore that. And so that's where they do the quality of the film. Here they interpret for the presence of small and large pneumoconiotic opacities. Down there are the symbols, which are in a mix. They're in Franglish. I don't know how to say that. They're sort of English and sort of French. If you look at what the letters actual are, because it's not always English, but it's not always French either. But you have to know that if you're going to order these things, you need to know what those are. So you don't, like, you know, they click CA, you don't realize that's cancer. Or, you know, PX for pneumothorax. And you had to kind of know. In the middle is a part about several changes, which really only applies to asbestosis or asbestos. It doesn't really apply to silica or coalmine dust. And it's on the same form, so you'd use one form for all research studies. Okay, next, we're done with the diagnostic testing. Any quick questions on diagnostic testing? Okay, let's move into diseases. So for occupational, so the occupational asthma, step one, 100% of the time, is diagnose asthma. You can't have occupational asthma if you don't have asthma. And a lot of people, they have a little trouble breathing, and they have some workplace exposure, and they come in to me with a diagnosis of occupational asthma. They've never had pulmonary function tests. They've never had bronchoprevocation. You've never finished the diagnosis of asthma, and yet they've already got the occupational label attached to it. So, as you're well aware, there's two ways to diagnose asthma. You can do reversibility with bronchodilator and show that that changes, or you can do bronchoprevocation. Most places use methylcholine. You may use, there's histamine, there's polder. There's some other choices for bronchoprevocation that are used in some parts of the country. Whatever it is you can do there, hold the bronchodilators, give them sequentially larger doses of that thing, and if it's positive at a level that's meaningful, because eventually everybody will react, but if it's positive at a meaningful level, then now I've diagnosed asthma or reactive airways. Now I can look at what the causation is. But this is the first step, and it does amaze me the number of people that I would see when I was at the university that came in for occupational asthma that no one ever diagnosed asthma. The person said, I think I have a hard time breathing when I'm at work, and that became occupational asthma. And that's not, you gotta do asthma, you gotta diagnose real asthma first. So first question is, do I have asthma? We got past that. Now the question is, what's the causation? I really, this is the one where you spend, this is the hour-long history you take from the patient of what's the timing of their exposure and their symptoms? How do they go together? Are there potential triggers we can figure out? Are there known irritants in their workplace? AOEC has an asthmagen list, which I've found quite helpful. It's actually pretty coherent, and they make that available on their website. That's not behind, at least last time I looked, it was not behind a paywall. So you can see that as a public service that they do. I'm also curious, if they have medications help, have they noticed that there's a time for recovery? This helps me figure out, is this really asthma? Is it really hypersensitive pneumonitis? Is it really, there's five or six other ones we're gonna talk about in just a few seconds, and that helps. I may also want to do testing. Now I listed IgE, skin or patch testing, all of which are reasonably well available in the United States. Now, if one of those is positive, I'm kind of done. It just got a whole lot easier. I mentioned functional testing. The problem is in the US, for whatever medical financial reason, it's super hard to get this testing done. There's one or two places that will sort of do it. Most of them won't interact with insurance or workers comp at all. Outside the US, this is done a lot. The problem is you almost have to bring the person in like to the hospital, and then we're gonna expose them this morning in our exposure chamber, and then we're gonna watch them for a period of time, maybe measure pulmonary function tests, an hour afterwards and three or 20 minutes afterwards, an hour afterwards, six hours afterwards. And then yeah, but you gotta keep in the hospital because they may have a late phase reaction and they may get in real big trouble at two o'clock in the morning. So you gotta, that's why it's really hard to pull this off in the US. In other parts of the world, in Canada, South America, this is done much more commonly. There are three different kinds of asthma. This is Carl's taxonomy. That's, I'm Carl. This is my taxonomy. There's allergic and irritant. Everybody agrees with our types of asthma. An allergic one has an immunologic react mechanism. Irritant is direct irritation of the airways. If you ever go outside when it's cold, I don't mean when it's like 30, I mean when it's like minus 20, your airways will react. And that's, so that's an irritant effect. It's not, you're not allergic to the cold. You react, it's a mechanical reaction of your airways. Smoke often is in that category as well. RADS or reactive airway dysfunction syndrome, I include it as an asthma because it's kind of the same thing. Huge exposure to something and now their airways are twitching, they react to everything. That's RADS or reactive airway dysfunction syndrome. Usually it requires a big exposure. Most of the ones I've seen or that I've personally diagnosed are following fires or an explosion or something that's like a fire because the person's getting a huge dose of stuff right now. And then they have a sensitivity to kind of everything. The good news is this typically burns out after three to five years, but not 100% of the time. So it's maybe 70% of the people, five years out, they're pretty much back to normal. But this can be a real problem during that five years, being able to get the person back into work. I've had people that just going outside when it's in the winter was a huge, they were fine in the summer, then the cold air comes and just getting out to their car to drive to work, just shut them down, they couldn't breathe. So it can be a real problem. This is a list of common asthmagens that are known to be in many workplaces. There are many, many, many more. This is the super, the most common ones. And all of these are ones that at some point or another I have dealt with clinically, especially the top one, the animal handler, which was, I did a lot of that for a while. So I talked about RADS. This is, people argue over whether RADS exists or not. I believe it does. These are the diagnostic criteria that go with it and can't do anything wrong with your airway before, big exposure, rapid onset of symptoms. It doesn't have to be, and so it's not like you got, I get exposed and six weeks later, I first had trouble breathing. It's gotta be pretty fast. You have to, testing for out, testing looks like asthma and either a positive methylcholine challenge. And then I exclude other diseases. They're all very reasonable criteria. We're gonna move into bisinosis. This is the one that actually, this is the oldest, most famous one of our occupational lung diseases. This is sometimes called brown lung, sometimes called Monday morning fever. This has to do with exposure to people that work in the cotton industry. It's uncommon in the United States at this point, although it is one of the OSHA standards that has driven a lot of our occupational health stuff in the United States. So people can flip symptoms and there can be pulmonary impairment that can become permanent if the exposure continues. The weird, the Monday morning fever thing is people, on Monday, people have a hard time. By Friday, they're doing pretty okay. Then the weekend comes, they go home and they get unexposed for a couple of days. They come back on Monday and it's back again. This is, as I said, this is very common in that industry. It has to do with the carding. I will use the words, I can't 100% explain. The people that card and work with certain parts of the cotton plant, between it being on a plant and it being going into a mill. You're not gonna see this disease in people that are making clothes out of already made fabric. That's not a problem. Where this is, this is the people that are taking the cotton bowl and turning it into yarn, into thread that they can then make other things out of. That's the people at risk. The price, precise cause, they still fight over that. But it definitely occurs. It also can happen with flax. I mentioned cotton dust and hemp. We don't have a big enough room here, but if I had a room with 50 people and I said, who's wearing something that's made from hemp? Somebody's gonna put their hand up. And so this is because this, and that is a US domestic industry. So we may start seeing bisonosis in hemp workers, not people, not the marijuana side, but the clothing and other uses for hemp world. This is one of the things, we monitor the workers with spirometry. This is one of the, this is the reason why there are NIOSH certified spirometry technicians. Is to do, to provide the workforce to test people for this disease. Diagnosis is mostly by history and the OSHA cotton dust standard is all right there if you wanna read more about it. If you do spirometry in your office and you have the opportunity, I would encourage you to take the NIOSH spirometry course. It's two to three days. And if you wanna understand spirometry better, it's a pretty good way to do that. Next one in our parade of occupational lung diseases is hypersensitivity pneumonitis. It's got a couple of other names. One of them is extrinsic allergic alveolitis. That was its most recent change, but they seem to call it both now. I didn't understand. They've confused me with their attempt to argue over what they should call this disease. So it's an immunologically modulated inflammation of the lung parenchyma after inhaling, after breathing in an allergen. I'm sorry, an antigen. And the most common things that does this is the organic materials. So things around farms are the most likely to get people in trouble with this. And it is officially a type three hypersensitivity reaction for people who are keeping score. There's lots of microbial things that'll do this. So the most common one is what they call farmer's lung. And this is not the silo fillers, silo emptiers. This can be the silo. Fillers just almost get involved in this, but this is often like moldy hay is where you'll get to this kind of a product. The silage sometimes, although not if it's done properly. Animal proteins. So bird fanciers lung is in this category and the low molecular weight industrial chemicals, the isocyanates primarily are also can get people involved with hypersensitive humanitis. So these are not uncommon things. You'll see that like for farmers, it's up to 12% of the population of farmers. Mushroom workers, it's like 20% of the people. Bird hobbyists up to 20% or 21%. And methyl isocyanates about 5% of the workers in those industries will develop hypersensitivity pneumonitis over time. Decreasing exposure can definitely help with this, but it is not perfect. The diagnostic criteria. So there are common radiographic changes. Sometimes you have normal pulmonary function testing and hypoxia at rest or with exercise are certainly clear. There's certainly something going on at that point. There are some, what they call minor criteria. So bronchoalveolar lavage, inhalation challenge or histopathology sometimes can be, can tell you what's going on. If you see, these are complicated patients to work up. I probably wouldn't do one alone. I'd probably get a pulmonologist involved to help me because some of the testing that they may need is stuff I can't do. Like I don't do BALs, that's above my pay grade. So that's the one group. And whenever I have to prepare for this, I make up, because these two diseases get, these three diseases really get confused in my own brain. Now I live in West Virginia. We have lots of coal mining. I can tell you everything you want to know about black lung and probably more than that. We have relatively little farming. We're not a farming, everyone's with somebody that basically keeps cows, that makes beef. But there's very, very little farming in my area. If you're in a different area, these diseases may be very different where you are. So this is the ODTS, it's interesting because it's a non-infectious febrile illness, which already is going to make doctors weird about this. Because we have, fever's got to be from infection, right? And it follows exposure to bacterial or fungal species. There's probably some common thing on the cell wall of the thing that's getting us infected, but it's not completely elucidated at this point. This is way more common than hypersensitivity pneumonitis. This is a more common thing. It's in the summer months, usually younger people. And the things may have to do with this lipopilosaccharide in the cell walls, maybe, and that occurs in gram-negative bacteria cell walls. Organic dusts have this stuff in it. So remember, this is where this loops around on itself. So bisonosis is one of these, maybe. Swine workers, farmer's lung. And when they look, when they tried using endotoxin inhalation, it does develop symptoms and they develop lab changes. So maybe that's the problem. Again, this is, the problem is it's hard to get humans that say, yeah, I want to go, give me the worst flu ever and maybe I'll die from it, is a hard thing to get through the IRB. So a little bit about pneumoconiosis. There's several kinds of pneumoconiosis that are shown on this chart. So the left-hand side in the green box shows things that can cause progressive massive fibrosis. That's what PMF is. The middle ones cause fibrosis, but no progressive massive fibrosis. It doesn't progress to that. And the right-hand side is the mimics. I rarely see, I actually look at x-rays for NIOSH. They're supposed to be from coal miners. I rarely see baritosis or stenosis. I do see viral pneumonias. And a kid that had chickenpox pneumonia when they were like a year old, and I'm now looking at their x-ray and they're like 19, and it looks like they've got horrible state. The second, you know, two slash two or two slash three chest x-ray with black lung is almost always a viral pneumonia. And a lot, because I think I talk to these, because I would end up, I'm the, what do we do? This guy called in with a question. I don't know what to do. Give it to worms. That's always what happens. And so I ended up talking to these guys and almost always I say, there should be this 19 year old says, I've worked in the mine for three days. How do I have two slash two pneumoconiosis on my x-ray? And he's right, you can't. I mean, pneumoconiosis is not that fast. And so when I said, do you ever, do you remember being in the hospital when you were a kid? And they usually said, no, I don't remember anything like that. I was like, okay, great. Go ask your mom. So far, where I have feedback, I'm about 80% where they had, they were bad enough. They had, it's usually chickenpox pneumonia. Looks just like it on an x-ray. And it'll confuse your, if you're doing a surveillance system, it confuses your surveillance program. Not super common, but you'll definitely see. I've seen that a number of times. They're sick though. Hold on. I didn't remember that. No, no, no, no. If they had it when they were, but they could have had it when they were six months old. I mean, they're usually sick enough to be in the hospital. That's completely correct. They're usually in the hospital with this, but that's not, but I don't remember where I was when I was six months old. So we're going to focus on the ones in the green box, the ones that can go on to PMF because they're the ones we're most likely to see in occupational setting. The basic mechanics of this is you inhale things faster than you can clear them. Every one of us has a slightly different rate that we can clear things from our lungs. And as long as our exposures stays equal to or less than what we can clear, we're good. And when we get exposures that are greater than what we can clear, then we get disease because we've got residual, that stuff, silica mostly, that stays in your lungs and your lungs start reacting to it. And if you can't clear it, it's just like TB and it walls it off, makes a little granuloma. And if you do that once, you're fine. If you do that thousands of times, it's a problem or millions of times. So the big player is silica, not silicone. I always have to say that to people. Asbestos will do this also. And let me talk about that. So silicosis, think of people who are working with or creating or working with fresh fractured silica. That's really where the money is. So it's the sandblaster. It's not the sand he puts in a sandblaster. It's not the beach. You go to the beach all year long, you'll never get silicosis. It's the fact he takes the sand, runs it into some metal thing, and then that sand grain breaks in half. That exposed surface is what caused the reaction in your lungs, is the exposed surface is now ready to react. So people doing miners, people using concrete saws that don't turn on the water. All the concrete saws in the last 20 years all have a place to put water to them. If you don't do that, you ever see the guys on the highway that just disappear in this cloud when they're cutting the concrete? That person is putting themselves at risk for silicosis, especially if they're not in a respirator. The well drillers and frackers are a big problem now in my area. The foundry people, especially sand mold, and when you get into that, I have to ask them exactly how to get it off. Simple silicosis, small changes on the x-ray, just the little ones, they haven't grown together yet. And the symptoms can vary quite a bit. Complicated is when those little opacities have grown together and made big opacities, and they can look just like a tumor or TB or something big. You can see core pulmonology in these folks. So these are some big opacities. These are unfortunately pictures from my clinic where I see these people way too often. And acute silicosis is a different disease. It's alveolar proteinosis. It really is different. And it's not fibrotic. It's in huge exposures. It's fast and clinically looks like TB, like six months of exposure at the right workplace. And you may have people that are symptomatic. Half-life for the one thing that I don't want to talk is this Hawk's Nest incident. The half-life from arrival at the jobs, they were going down into the South in like 1900 and recruiting workers to come up and work at this, to make this tunnel in West Virginia. And it was go, go, go, go, go, go fast. And they were, their half-life from arrival till day was about 16 months for most of those people that they recruited to come up and work. And initially they thought it was all TBs. The doctors wouldn't touch them. There's no autopsies. And then somebody finally got brave enough to do one. And he cut through the lungs and he's like, hey, this is like cutting through sandpaper. This is the, what you can see in this x-ray, if you look real carefully, is you can see a silicotic nodule. That can be one that you can see that also with acute silicosis in addition to the lung changes. And this person, if you look, they've got pretty ratty looking lungs. It's not, that's not normal pneumoconiosis. That is more the, there's fluid in there. It's kind of that, that arc around the top of their apices of their lungs. This is Hawk's Nest. There's at least a hundred deaths and probably more like 500 deaths. And I said, it was a super short half-life for the people that went to work there because they figured out that if they cut without turning the water jets on, they had the water jets, the equipment had them, but it slowed down the drilling. And it was more important to them to be drilling faster because the grit from the sand made the drill more effective and made the people more ill and dead. So that, so that, this was one of the things that led to some, some of the litigation, some of the early regulations of like drillers and stuff like that. So a little bit about black lung. Black lung is religious silicosis in a coal miner. That's why I think about it and I see these patients all the time. There's always a little bit of silica and coal dust, but some of this, now the machines are stronger and better. They're not just mining coal, they're mining a lot of rock and the rock is what has the silica in it. And that's what gets people in trouble. Unfortunately, we made the equipment so much better that the equipment doesn't care anymore. It'll mine rock just as well as it mines coal. And now the exposures just went way up starting about 1990 was when the exposure started going up and now we're seeing all these guys with pneumoconiosis. In my, in my, like writing these evaluations, I do 15 over a three-day period. And it is not at all uncommon for me to have three or four people out of those 15 with PMF. And then I'll have another probably six or seven that have simple pneumoconiosis and a couple of people that are normal because I'm seeing all comers or some of them are truck drivers and whenever, you know, it's the exposures are different, but it's, there's way too much disease, just way, way too much. And we'll talk, we're not going to, these, the face workers that got people that actually ripped the coal from the ground are at the biggest risk, surface, the underground's worse than surface. And if they're drilling on the surface, that's the worst part there. There's a thing called Kaplan syndrome. This is interestingly, everybody, you have to know about it. It's one of those things that they put on tests because they just love it. Interestingly, when I learned about it, we talked about this as rheumatoid arthritis, pulmonary nodules being caused by silica. Okay. So we already had, and what we really think now is that what this is, is this is an increased risk of rheumatoid arthritis in people who are silica exposed. The understanding has actually changed in this disease. It does have its own characteristic findings. Asbestos. The next is the next one we think about, this is another pneumoconiosis. These are the fibers that we worry about. Keep in mind that up until the mid seventies, asbestos was the safest thing on the planet. It will not hurt you. You're good to go. In fact, you're safer. I mean, I don't, I want, I want the picture that says you are being protected by asbestos on the curtains at the movie theater. You know, but that was, that was definitely a real thing. It's still used a few places, not very many, but a few places it's still used because we don't have anything that'll take its place yet. It comes in different varieties. Serpentine is the wavy ones, probably less of a hazard pulmonary, pulmonaryly. Amphiboles are the bad, nasty, straight, they call needle-like ones. The big thing is that if you have serpentine, it's 99.5% serpentine, but that's half a percent that's not. And you just have to be aware that you're going to see complications from things that are not, there's amphibole contamination, almost all serpentine material. The Canadians will still argue with you over that, but even they are starting to come around that maybe it's not the best thing to work with. It's used for a lot of things. It's the magic mineral thing since sliced bread. And it really is efficient at what it does, as long as you keep it away from humans. And you'll find it a lot of different places. Obviously, the miners are a problem, shipbuilding. The Navy loved asbestos, I mean, really, really loved asbestos. It's sometimes used in HVAC systems, in brake pads. Interestingly, there's actually data that their brake pad exposure by, in and of itself, probably is not hazardous to the workers. I cannot tell you why that's true, but that's the, when they've done epidemiologic studies of those guys that change brake pads all day long, they don't see increases of asbestos-related diseases. Specifically mesothelioma was what they were really looking for. So health effects, the pharyngeal body is, that's what these things are in these pictures. And that's when you get the actual asbestos fiber with little macrophages, you couldn't digest it and give their lives and end up coating the thing in iron as they slowly die. Big effect we obviously worry about is mesothelioma and lung cancer. You can also see effusions. I've actually seen that more than I thought I was going to. For people that maybe have some asbestos pox, now they've got effusions. And it's from the asbestos, not from something else. Little potpourri at the end, metal fume fever. This is covered a couple of different things, caused by two things. And it's caused by zinc and by copper fumes and no other fumes. So anytime you see literature that says this is like metal fume fever, they're wrong. If they want to describe it as a flu-like illness, that's fine. Metal fume fever has two causes and no others. And just so it's copper and zinc, they're the two you need to know about. The key thing with this is flu-like symptoms, they feel like crap. Three days later, they're all better. The global antidote is drinking milk, which has absolutely no scientific basis in anything. I suspect if they didn't drink milk, instead of getting better in 72 hours, they'd get better in about three days if they didn't drink the milk. But it does matter where you are on the planet. If you ask a welder, every welder knows about this. Almost every welder's had it. The key feature here is no permanent health effects. Does not damage the lungs, doesn't cause any other end organ damage. That's a key take-home message from metal fume fever. Polyrhythmium fever is similar, but there's two of them you have to be super careful. There's the one when they burn all the Teflon stuff in a tank, that will kill you. And then there's the other one that doesn't kill you. So I don't like that term. But the Teflon in a tank thing, that's a whole category in military triage, is the guys from burning military equipment, because they love Teflon wire in there. They get their own category of expectant. They're actually their own thing. A little bit about bronchiolitis obliterans. So this is an irreversible blood flow obstruction on the pulmonary function test. They usually have normal x-rays and normal CT scans. These can go on to be quite severe. These people can end up on oxygen or need a lung transplant. And this can follow a bunch of different exposures. Popcorn worker's lung. This is about 20-year-old information. And the bad actor here is something called diacetyl, which is the butter flavor they put on popcorn. They did a lot of corrective industrial hygiene stuff with the plants that were originally involved. If you don't expose humans to volatilized, heated diacetyl, then you're fine. They've pretty much eliminated this once they understood the disease. And there was a huge niche that spent a lot of time in this industry. There are probably other diacetyl-like things that are probably also bad for you. That's still being, I'll just say, figured out. This is the ocean respiratory protection standard. I encourage you to look at this. It's actually pretty well done. This is the one that tells you when you can use respirators. There's a questionnaire you do before first use of a respirator. It's getting shorter and shorter. Just got shorter again about six months ago, or more of it became optional, I should say. But you as the healthcare provider are allowed to add the things that they made optional back in if it's relevant to your workforce. So just keep that in mind. I've added some stuff back in. I do a lot of stuff for the fracking guys. You're not allowed to take away what they've already got, but you're allowed to add stuff. And I've added some of the stuff back in because some of the stuff they took out, like what are you going to be exposed to while you're working, kind of helps me understand what I'm doing. What kind of respirator do you think you might be using? Helps me a lot. Because the employer doesn't always tell me that. And if I at least ask the worker, oh, I use a full face, they have different concerns than if they're just using a disposable N95 in a healthcare setting, for example. And they are required to tell you what's going on in the workplace and consider other PPE. And let's see, where did we go here? The way the system works now is they have to have access to a healthcare provider somehow or another if there are problems. Because that's the way they flip the system over. So instead of asking all the questions up front, they say, well, don't try it. If you have trouble, let me know. And I will say on my part, the way I think of this is people who are in a ideal age environment and immediately danger to life and health, I'm really concerned about their being successful in the respirator. Somebody who's exposed to a tiny bit more of something over some OSHA cutoff, if they're exposed to seven units of stuff and five units of stuff is safe, I'm way less... If that person fails the respirator while they're leaving the area, they take the respirator off and they get one breath of seven units of stuff, they're not going to die from that. If it's ideal age, if they're a firefighter or something else in ideal age environment, I am way more worried they'd be successful because if they take the respirator off in that environment, they're dead and that's a bad thing. So things about toxic gases, this is one of the things that... This is a helpful thing to remember. And so air, the stuff in this room has a molecular weight of about 29. Anything with a molecular weight higher than that, more than 29, is going to settle to the floor. Anything with a molecular weight less than that is going to rise up into the sky. So if you have a helium leak, it's going to be in the sky before you can imagine. If you have a propane leak, it's going to be on the ground before you can imagine. Anything kind of around 29 is going to stay in the air. That's why CO is such a hazard because carbon monoxide at 12 plus a 16 gives you 28. So we're back in the range of what's in air. And so that's why it stays right here and mixes with it and gets us all sick. There are... When you're using... Keep in mind, respirators don't correct for an oxygen deficient environment unless you're supplied air of some sort or another. Gaseous toxins are not stopped by respirators. So vapors are not stopped by any respirator unless you get special ones with special cartridges. And there are special ones that will react to... That are chemically reactive. And the key thing for those is making sure you have a good process in place to replace the cartridges when they need to be replaced. Some of them have... They do have some that are a little colorimetric. The cyanide one actually will... I forget if it turns blue or turns pink or something, the way it can tell. The CO one does not have that. You have to replace the CO cartridge every so often based upon the exposure levels. Let's see. Do you want to do sample questions or you want to skip that? Okay. Let's do sample questions. They're in the slide set. If you want to do them. If you have any questions, let me know. Any questions about respiratory things? Okay. If you have any questions, send them in the chat and we'll try to get to them later.

occupational pulmonology

respiratory diseases

adult-onset asthma

spirometry

silicosis

asbestosis

hypersensitivity pneumonitis

bronchiolitis obliterans

workplace regulations