The second part of the clinical occupational medicine lecture follows musculoskeletal disorders and deals with occupational skin disease. One of the surprising things about occupational skin disorders are how widespread and prevalent they are, depending on whether you call musculoskeletal disorders injuries or diseases. Skin disorders are number one or number two following MSDs. There's a variety of occupations with increased risk, including agriculture, manufacturing, meatpacking, and health care amongst them. This is a very brief review of the anatomy of the skin. Technically, the skin is the largest organ in the body. Various areas of the skin are thicker or thinner, depending on the use to which they're put. Skin of the feet and the palms is very much thicker because it has to withstand abrasive forces, whereas that on the face and the eyelids can be much thinner. In the epidermis, the most superficial layer, the outer barrier, is the stratum corneum. This consists of keratinized cells with tight junctions and is quite impermeable to water-soluble substances, and it keeps a barrier against water and those materials. The flip side of this is that it can be quite permeable to oil-soluble or lipophilic materials, and these can penetrate the outer layers of the skin quite easily and get further down into the dermis. So if you're talking about occupational skin disease, you're really talking about contact dermatitis. This entity forms about 80% of all occupational skin disorders, and you can subdivide it into irritant dermatitis and allergic contact dermatitis. Irritant dermatitis is about three-quarters of all occupational contact dermatitis. Generally, the skin is red, swollen, may have crusting, blisters, scalene, vesicles, bullae, etc. If it's more chronic, then the skin can be thickened and lichenified. So as I mentioned in the last slide, most occupational contact dermatitis is irritant dermatitis, and this may be multifactorial. Rarely do people come into contact with a single irritant, but may use a number of them. These can be solvents, acids, bases, detergents, or soaps. For example, in healthcare, we'll see several examples, and people within healthcare oftentimes come into contact with a lot of soaps, cleaners, disinfectants, and also have to wear gloves. Now, any substance can be an irritant if it's in high concentration or if exposure is prolonged, and that can include water, as we'll see. I throw this up here also as a note for that irritant contact dermatitis can also be a phototoxic reaction. This is from a rather specialized medical journal in which a bartender was squeezing out limes for a party or gala fundraiser and went off on the beach before that started, and you can see the real severe irritant dermatitis with blisters and bullae that formed just as a result of contact with the sun and lime juice. There's a few predisposing factors to irritant contact dermatitis. Principally, this includes wet work. If the hands are macerated, the gap junctions in the epidermis, the integrity of the stratum corneum gets disrupted and lets a variety of materials through. pH extremes will also burn the skin, so a very acid or very alkaline materials will cause dermatitis fairly readily. Concentration, the area of skin involved, and the extent to which workers come into contact day in and day out also predict ICD. Some individual characteristics predict it. This is a typical board question. A bit of trivia in occupational medicine is that atopics have a 13-fold greater risk of irritant contact dermatitis rather than allergic contact dermatitis, and we'll see why that is in one of the next slides. Irritant and allergic contact dermatitis can be somewhat difficult to tell apart, at least initially. A couple of clues. Irritant contact dermatitis will occur directly at the contact site and is usually well-demarcated. Remember that this is direct damage to the skin and, unlike allergic contact dermatitis, is not a systemic disorder, so the areas of irritant contact dermatitis will be directly limited to the areas in which it comes into contact with the skin. Both have this inflammatory type response here for irritant dermatitis. It's a burn you can get erythema, blistering, and ulceration, as I mentioned before. Getting back to that Achmed trivia factoid on the previous slide, atopic workers are at increased risk for irritant dermatitis. This was always taught even way back when I was a resident. Now it's actually better understood on a molecular level. There's actually a loss of function mutation in atopics in a gene called the filaggrin gene, and this mutation predisposes to loss of integrity in the epidermis, and so many atopics, even if they don't develop an irritant contact dermatitis, can develop xerotic skin and other skin disorders as a consequence of this mutation. There's a big long list of materials that can cause irritant dermatitis, and I won't go through them in any detail. Fundamentally, they're just any agent that can injure the cells of the skin, so acids and alkalis vary obviously, damaging cells directly, detergents can denature protein, solvents can defat the skin, and a variety of these other materials can set up some type of irritation or cellular damage. Here's a worker who has a double or triple whammy in the development of an irritant reaction. This is a wet cement worker, and so a couple of things are operative in causing irritant dermatitis. You have a very, very alkaline pH. This has got a pH of about 10 or 11. The calcium oxides or hydroxides within the cement can cause that type of irritation with the skin and direct cellular damage. In addition, sand is in wet cement and has a rough texture. The skin will get abraded and that causes further damage. Wet work we mentioned before, cement's all wet when you're working with it, and that will macerate the skin. If you have to wear gloves and get these inside it, that also macerates the skin along with keeping the cement materials in contact with the skin. Cement also contains chromium as a hardener, and this is reactive with the skin, also causes damage. We'll see some pictures of chrome holes in the skin in a later slide. Chromium can also lead to allergic contact dermatitis and the irritant reaction and loss of integrity of the skin may actually predispose someone to getting chromium allergic contact dermatitis on top of this irritant dermatitis. Ongoing exposure to irritants will cause a chronic irritant dermatitis. These individuals may or may not have the acute erythematous irritant contact dermatitis, but continued exposure to the low-grade materials will start to damage the skin. This picture is of a worker who was a painter and washed his hands off with mineral spirits. This tended to defat the skin, get underneath the layers of the skin, and set up the kind of a damage reaction within the skin. So the skin first becomes erythematous, then it becomes dry, then it becomes hyperkeratotic and lichenified, so his hands are very, very rough chapped and keratotic. Here's a picture of the same worker on the previous slide who washed his hands off in mineral spirits. Any type of lipophilic materials or oil-soluble materials can defat the skin, so in addition to mineral spirits, cutting oils and coolants used by machinists and solvents used in a big variety of jobs, including metalworking, will also defat the skin. Milder acids and alkalis, soaps, and biocides also cause chronic irritation. Treatment of irritant contact dermatitis starts with initial simple symptomatic treatments of moisturizing creams and possibly topical steroids that reduce the acute symptoms of erythema. We're really targeting prevention, and so attempting to give people protective gloves, for example, may be useful. You want to be aware of people getting their hands macerated in gloves, and so sometimes they may have to wear cotton liners under more vapor barrier gloves. Giving people barrier creams in which lipophilic materials in particular can splash off of, and you want to avoid things like harsh soaps and avoid a lot of washing. This becomes very difficult because a lot of health care workers are going to be at risk for irritant contact dermatitis, and it becomes very difficult to get them to stop washing their hands, for example, stop wearing gloves, because a lot of health care tasks are involved with doing those actions and working with those materials. Sometimes materials can be substituted, and in other cases job rotation so that people aren't necessarily exposed constantly all the time may be useful or helpful in ameliorating irritant dermatitis. Okay, so we've covered irritant contact dermatitis, which brings us up next to allergic contact dermatitis. So ACD is a type 4 hypersensitivity reaction, so this is a systemic reaction brought on by sensitization to an allergen or antigen, and in this case results in a delayed rash if one has already been sensitized. This delayed rash comes after exposure and develops across the course of about 12 to 48 hours. It can be localized, it can be diffused, as I mentioned in a previous slide, this may not just be localized to the area where the worker has gotten materials on the hand, for example, or limb, but it may spread up limbs and be present in other parts of the body. Because it's idiosyncratic, meaning that sensitization occurs first, only a small percent of people may be exposed, and typical of ACD are these grouped linear vesicles or blisters, a lot of edema, a lot of erythema, and a lot of itching. So if I told you to go out and get allergic contact dermatitis, and as you probably suspected from the previous slide in the pictures, the easiest way to do it for most of you would be to go out and pull out poison ivy in your garden or backyard, and so these are really classic examples of ACD. The actual sensitizer within these plants is called urushiol resin, and it's a highly prevalent sensitizer. Over 70% of people who are exposed become sensitized to it. There has to be a run in incubation, but that's very quick, and after you're sensitized and become exposed again, your reaction time after exposure can be anywhere from about half a day to two to three days, and as you probably remember, it can spread on up the arms or legs also. These next couple of slides indicate most of the frequent causes of allergic contact dermatitis, particularly in the workplace, and of which there are many. Nickel is the primary metal that sensitizes workers. There's a huge variety of workers involved in nickel plating, the use of nickel alloys, metal work, and the like. Chromium is also very frequent, cobalt a little bit less. Epoxy resins and other formaldehyde- based resins are used in a lot of gluing or adhesive activities, as well as castings and moldings are frequent causes. Natural products, including colophony, which has its origin in pine resin or pine sap, and at the bottom, other plants, including ruse, which is the allergen that we saw with poison ivy. Alstroemeria are lilies, and this can put an end to many florists' career. There are a number of products that go into the making of rubber, and natural rubber latex itself doesn't normally cause allergic contact dermatitis. ACD is usually caused when people are allergic to rubber products. It's usually caused by some of the materials that go into give rubber its particular qualities, the hardeners, the accelerants, and the crosslinkers, the antioxidants that keep rubber from breaking down. So there's a variety of these materials that go into rubber, and from which many people develop an allergy. Second slide with more causes of ACD is here. Organic dyes, paraffinil and diamine, or PPDA, is used in hairdressing, and many hairdressers can find their careers ended by severe ACD, even at a younger age. Paraffinil and diamine is also one of the rubber products that I mentioned on the previous slide, and that goes into rubber, so allergies can occur in varieties of workers. Some preservatives, naturally occurring lanolin or thimerosal, which has mainly been taken out of many materials, including medicines. There's a big variety of fragrances, and in the hospital setting and health care setting, again, some, a lot of biocides and germicides, such as those that release formaldehyde on contact with surfaces, or the quaternary ammonium compounds, can be allergic sensitizers also. So, patch testing is the main diagnostic method for allergic contact dermatitis. What this entails is filling up stainless steel wells with samples of known or suspected allergens, placing them on the patient's back, giving them a good sedative for 24 or 48 hours, and then bringing them back to see, look for reactions in the, after about two to three days. Remember that allergic contact dermatitis is a type 4 or delayed type hypersensitivity reaction, and therefore, what you're looking for is exactly what you look for in a PPD or skin TB test. You're looking for induration accompanied by erythema, and as you see in the lower right-hand corner, vesiculation also, all indicative of a positive reaction. Dermatologists have some standard ACD patch testing kits. This generally has some of the more common allergens. We mentioned some like nickel and chromium, and some of the fragrances and the like. Most of those oftentimes don't apply very well to workers who may be working with really specialized and specific allergens that aren't found in the world outside of work. Some specialized dermatologists will have complex kits of antigens available. They'll have shoe materials, which include rubber and chromium, and also some of those rubber components, the accelerants, antioxidants, and hardeners we mentioned in the earlier slide. They have kits that have some specific resin components, such as those in epoxies, and some natural products like colophony. And they may have concentrations that reflect work exposures and would be very different from that seen in patch testing outside of the work setting. So for diagnosis of ACD, a couple of points to remember, what you want to initially have with your patient is a history of exposure to a known allergen or one that you suspect strongly. Compatible clinical findings, which include the rash, vesiculations, and other findings fairly common to allergic contact dermatitis. And ideally, to get them patch tested and have a positive patch test that's consistent with their exposures and put all that together. And that generally will make your diagnosis of ACD. A few pitfalls in the diagnosis. The main one is generally sending them to a patch tester or dermatologist who doesn't have the materials. So they may try a lot of the standard materials. But as we mentioned, many of these things can be unique to the patient's work setting. And so they may not have the material and the patient is not tested for that material. There's also some problems with not exactly false positives, but positive patch test when there's not been significant use or exposure. Nickel is a frequent culprit. In this instance, oftentimes patients are told that they're allergic to nickel, which may be correct, but it may not have a workplace origin. Remember that nickel allergy is common. It's prevalent in about 6%, 8%, 10% of the population. More prevalent in women, in which the prevalence is probably about 10% to 12%. And this is a consequence of generally jewelry wearing in early youth and adolescence. And many people become sensitized at that time. Treatment of allergic contact dermatitis is a bit more complex than irritant contact dermatitis. Remember that it's an allergic disease and it's going to worsen if you don't get people out and away from exposure. So the key here is to really prevent further allergen exposure. And if you can remove the worker from the source, if you can enclose it, ideally if you can substitute a new material that's non-allergenic or as a last result, give them gloves or personal protective equipment. Those are all really important. You can use topical or systemic steroids depending on the extent and severity of the case. Many of you who've treated poison ivy realize that you need to oftentimes give people a big whack of Meddrol or prednisone and not just depend on treatment with topical steroids. And you want to minimize irritant exposure because if irritants are on skin that's already damaged by allergic contact dermatitis, you can have an ongoing persistent dermatitis with a much poorer recovery. As with most allergic diseases, allergic contact dermatitis and asthma, for example, the more you remain in a job or work in which the sensitizer is present, the worse your prognosis is going to be. It will continue to progress and become worse. And so if you can recognize the disorder early and remove the patient from the allergen, and that can range anywhere from enclosure substitution to getting the worker out of that workplace, you're going to have much better prognosis and be able to treat it much more effectively. So the main take-home points for contact dermatitis in general, it's, as I mentioned, the most common occupational dermatosis or skin disease. The majority of it, 70% to 80%, is going to be irritant. A lesser proportion is going to be allergic contact dermatitis. And remember that little trivial factoid about atopics being at higher risk for irritant contact dermatitis rather than allergic. Distinguishing allergic versus irritant contact dermatitis can be very difficult when you're first evaluating a patient. A couple of underlying points to suspect ACD in the workplace is understanding when there's a known allergen that's in frequent use within the workplace and when involvement extends beyond the contact site. So if workers are getting it on their hands and there's erythema, blistering vesicles, and the like, going on up the arm where it doesn't come into contact, you might suspect that you've got an allergen. You don't or shouldn't be doing pre-placement patch testing to sort out people. It's really demonstrably of little use. A history of allergy to certain materials may be useful at pre-placement time, but not patch testing. And you improve the prognosis, as I mentioned, with early recognition and removal from exposure, particularly in allergic contact dermatitis. All right, so we're going to move on to all the other occupational dermatoses. And remember that contact dermatitis is far and away the most prevalent, so these are going to be much less frequent altogether. So contact urticaria, people know what a wheel and flare hives look like. Here, this picture off to the right generally is reported as erythema with pruritus or burning. And unlike allergic contact dermatitis, this is starting within minutes to several hours, up to about 24 hours after exposure, although most of them are much earlier than that. So the opposite from allergic contact dermatitis, contact urticaria is an immediate hypersensitivity or a type 1 reaction. And it shares a lot of characteristics with allergic rhinitis, with asthma, and even anaphylaxis. This is all IgE-mediated hypersensitivity. Big variety of materials that can cause it. And in general, what you want to do is the patient's report of what they were doing immediately preceding the onset of urticarial lesions. So this is the wheel and flare that we saw in the last picture. We have tended to put a great emphasis on natural rubber latex, particularly because it's used so much in the health care setting. In the bad old days when I was a resident, universal precautions had really ramped up. And glove manufacturers were trying to pump out gloves with a lot of problems and very little quality control. So that was what caused the latex epidemic mercifully. With substitution and better manufacturing methods, this has really decreased in the health care setting. You may see a lot of this occurring in food workers processing shellfish and other types of crustaceans. Some workers with nuts, eggs, and other animal and plant products may develop contact urticaria. And again, your history is going to be most important in what they're working with. Of the metals, nickel, and I don't have it on the slide, but platinum is also a bad actor in causing contact urticaria. And then a big variety of frequencies and flavorings as well. Some materials and foods, tomatoes come to mind, may stimulate local histamine release so that these people are not having an allergic reaction and you can't get demonstrable IgE from them. But it's localized rather than being more widespread or systemic. Diagnosis, usually suspicion, is relatively easy because they will remember coming in to contact with something fairly readily following which the lesions appeared. And ideally, if you see the demonstrable wheel and flare of the urticarial lesions, that's great. It helps you very much for that. Oftentimes, people will come into the clinic or the employee health service after sustaining a wheel and flare type reaction. And by the time they get there, which may be an hour or two later, these will have died down. So you're left scratching your head as to whether or not you can genuinely see these. There is a number of confirmatory tests, particularly the allergists will do scratch or skin prick testing, which is reproduction of wheel and flare reactions by scratching small amounts of antigen or allergen on the skin and causing a wheel and flare locally. Nowadays, there's a lot of specific IgE blood tests, RAS testing and the like. For most of the common allergens, you can get false negatives and false positives if they were previously exposed. Or if there's a not well-defined antigen enough to raise IgE to, then you may be scratching your head a little bit more with trying to figure out what exactly the cause might be. Again, sort of a little bit of history when latex allergy came to the fore in the 1980s and 1990s, there really were not good IgE tests for latex. Now they're much, much better across the past decade or so. And so we can demonstrably and reliably count on IgE blood testing for latex allergen as indicative of latex urticaria and allergy. This is a slide that pulls together the variety of reactions that people may have to gloves, particularly in the health care setting. And I put this up because it brings out the fact that in many cases, people may have been mistakenly diagnosed with latex allergy, and that in quotes, when the cause might be a little bit more benign and maybe much more treatable. And you want to remember that latex allergy, particularly if people develop very bad urticarial lesions, or if they were to develop asthma and the like, could be career-ending for people in the healthcare field. So the most common reaction to latex gloves is not going to be latex urticaria, what we typically think of as a hospital-based glove allergy. It's going to be just plain old garden variety, irritant contact dermatitis. And why is this? It's because you get your hands in it, they sweat, it macerates, the glove material rubs. Individuals in healthcare setting are doing a lot, their hands are wet and being washed all the time. They come into contact with disinfectants and soaps and a variety of other irritants. So all of those things together may make the glove one of several culprits in the development of a rash. Also think again about what the rash looks like. Urticarial rashes don't persist, that wheel and flares goes up and goes away. If you see a persistent rash, it's going to be more likely ICD. You also may want to consider, although this is going to be a lot rarer, allergic contact dermatitis. And instead of irritant dermatitis, they may have an allergy. And if you remember back a few slides ago, I had indicated that there are a variety of materials that get put into rubber that improve its properties, in this case for gloves, antioxidants so they don't break down, accelerants so they cross-link, et cetera, et cetera. So many of those are going to be the usual culprits in allergic contact dermatitis. One very interesting point here is that if people do have an allergic reaction and ACD to latex gloves, meaning to some of these materials that go into rubber, is that some of those materials might be in other gloves too so you could see them in nitrile or vinyl gloves, which oftentimes get substituted for latex gloves and the reaction may still go on if someone is switched to non-rubber latex gloves. And lastly is latex contact urticaria. And before you call someone latex allergic, particularly with skin disorders, you want to have the compatible physical findings. Ideally, you have seen urticarial lesions and not ICD-type rash, plus supportive testing, which would be IGE, RAS testing, or skin prick test latex. So all of those just go into kind of a differential or a ability to kind of think through what might be causing allergy, particularly in healthcare workers where this is going to be quite widespread. So moving off the allergic diseases for a few slides, we're going to talk about a real bad actor, at least health-wise, that's hydrogen fluoride or hydrofluoric acid. This is a very useful but very highly corrosive and potentially deadly acid. And it gets used in a lot of occupations. Anyone who does glass etching, printing, or dyeing, wood preservatives and the like, it's used in a lot of metallurgy to help dissolve specific acids. And it gets used in the petrochemical industry and formation of gasoline and other fuels in order to crack the hydrocarbons within it. It also is apparently one of the best rust removers you could ever find. And tire repair shops will swear by it. They oftentimes have a small vial of the stuff and it gets the rust off your tire bolts better than anything known to humankind. And here we see a picture of rust remover that you can get off the internet. You can just find it there and you can't read the label particularly well, but it says contains hydrofluoric acid. So this is gonna be in the mom and pop tire repair shop and can be ordered on the internet. What's noteworthy when you go on the internet is also that when you see this, it will have a little blurb about how dangerous it might be and a little spot or button that says, click here for the antidote. And then this takes you to a second site which sells you calcium gluconate gel so that you can apply this to your hands or fingers if you ever got the HF on your hands. So all joking aside on that because this is really a serious business. Look at the toxicokinetics of hydrogen fluoride. HF is a weak acid. This doesn't mean it doesn't cause damage. It means that the fluoride ion is so powerful that it doesn't give up its proton in the hydrogen very readily or very easily. So it dissociates much, much slower than does nitric acid or sulfuric acid. What this means is that HF can get absorbed through the skin or mucous membranes of a GI tract, particularly through the skin. And then it starts to dissociate rather than like sulfuric acid, which will dissociate right on your skin and burn it. This gets into the tissues then underneath the skin and it starts to dissociate the proton and the fluoride ion leave each other. And the fluoride ion is probably the bad actor amongst the two of them. There are the, obviously the hydrogen ion, the proton is gonna do its own damage as an acid will, but the fluoride ion is going to try and readily complex with any cation it can find. And so what it looks for is calcium and magnesium, both the extracellular and intracellular and causes a lot of tissue damage that way. So because of that slow dissociation underneath the skin and in tissue, you get deep tissue penetration more than stronger acids. When individuals who get this on the hands visit the emergency department, they complain of considerable pain in the fingers or hands, but the burns aren't often visible since they're below the skin. So it looks as though you've got somebody who's complaining of pain that's really out of proportion to the physical findings at least early on in the stage. The picture below here shows some tissue necrosis. This is at a later stage after there's been more deeper tissue damage, but the HF will get into the subcutaneous tissue. It'll get into the muscles and cause injury and cellular necrosis in those areas and can be very painful and also very difficult to treat. You'll get very deeply hypocalcemic and hypomagnesemic from this because the fluoride ion is complexing with calcium and as well because of the cellular damage, individuals become hyperkalemic and may develop ventricular arrhythmias and V-fib. Treatment is really an emergency. One of the manufacturers does a stewardship type video, I believe it's Honeywell, where they go through treatment of hydrofluoric acid burns because it's kept in many companies. So for example, a semiconductor or metallurgic industries. First thing to do if a worker gets it on the skin is to treat it. They oftentimes may have a mix-up batch of benzalkonium chloride or Zephyran, and that can be, that can ice the patient's limb until calcium gluconate's available. Application of calcium gluconate gel or slurry is useful locally. And if there's been a severe splash or injury that you may consider local tissue injection with calcium gluconate or even infusing it intra-arterial if a hand or limb is in danger. Systemic treatment, again, think hypocalcemia and workers who have sustained a heavy accident involving HF should be given calcium gluconate intravenously in addition to treatment locally. EKG monitoring and serum electrolyte testing frequently needs to be done to avoid the hyperkalemia as well as the hypomagnesium and calcium. Last bit is a grab bag of a variety of skin infections. And these can be all kinds of occupations depending on what you do and how these might be transmitted. The top picture shows scabies or mite infestations. Who might have these? These are going to be human service workers, healthcare workers, beauticians, people who work in nursing homes or with children who might be infested. Big variety of anyone who might come into contact with infestations infested skin or hair. Bottom picture shows cutaneous anthrax. This was known as wool sorters disease because the anthrax spores would remain on small hairs that would prick or auto-inject the anthrax spores beneath the skin. So hence the name wool handlers disease because people who handled or worked animal hides tanning, for example, or leather production would develop these. It looks exactly like in the picture. A necrotic ulcer develops at the injection point, spreads out into a black eschar. If you think it's sort of a historical incident, there was an MMWR from about, I believe about 10 years or so ago, about two cases of cutaneous anthrax that had developed in all weird places, Hartford, Connecticut. It turned out that these were individuals who were making traditional African tribal drums and to do so they were importing hides from Africa and working them. And these carried anthrax spores and they auto-inoculated in that way. So it's still something that you might consider and see. Sporotrichosis is one that the boards have loved for years. For some reason, I'm not sure. It's known as Rose Gardner disease. And this gives you a clue as to how it's transmitted. It lives in the soil as a fungus. And for an individual who pricks and inoculates their hand or finger with sporothrix, this may set up a localized infection, initially a kind of a nodule that ulcerates. And then the classic is, as you see in the picture, nodules that extend farther down the lymphatic. So this is somebody who had it in the hand and these secondary nodules develop across the lymphatics. This is plain old garden variety acne. Essentially looks like folliculitis. The picture may not be ideal. A variety of workers could develop this. Anyone who's in contact with oils, greases, cutting agents and the like may develop it. So this picture, again, is a machinist who developed it from frequent splashes. And this clogs up the pores that may become secondarily infected and go on to develop acne vulgaris. A couple of other workers might be at risk for this. One might be the kid who works over the friolator in the fast food restaurant who's also getting splashed with oils. And depending on how clean the area is kept and how clean he can manage to keep his skin, this may also develop into the similar type of acne. And lastly, would be people who have to wear occlusive clothing, things like polyester uniforms, particularly in hotter human climates, in which the same type of thing is likely to happen. In this course, I used to show a picture of chloracne. The picture was of a veteran of the Vietnam era who had sprayed Agent Orange and had developed chloracne as a consequence of dioxin exposure. And I'd tell people that you'd never see a case of this, or it was very unlikely to see. Then along came Viktor Yushchenko, the president of Ukraine, whose enemies tried to kill him. His enemies tried to sabotage his election, apparently by feeding him dioxins. It's a poor way to kill somebody. But of course, he developed this disfiguring cystic acne over the face, and it was clear evidence that he had developed and then ingested dioxins. So chloracne develops from exposure to halogenated aromatic hydrocarbons. And as I mentioned, dioxins, these were contaminants of the herbicides used in Agent Orange. So a variety of Vietnam era service officers and enlisted men were exposed to dioxins in the sprain, as well as individuals exposed to polychlorinated biphenyls or PCBs who worked with their manufacturer, worked with electrical equipment in which it had come, or who work in cleanup of areas that are contaminated may also be at risk for that. These are very disfiguring lesions. They're very hard to treat. Retinoids help a little bit, and sometimes these patients have to go to surgery for relief. Here are the two types of pigment disorders, hyper and hypopigmentation. Hyperpigmentation is most often seen with arsenic and arsenicals. So exposure to arsenic may cause this. Oftentimes, hyperpigmented lesions are on the soles of the feet, as you see here, and on the palms of the hands. These are markers, as I'll mention later on, of systemic ingestion of arsenic. They don't occur with local skin exposure to it. Other compounds that can cause it are coal, tars, and asphalt, as well as creosote. Hypopigmentation or vitiligo can occur from direct toxicity to melanocytes and many phenolic compounds and hydroquinones may cause this. They can be skin lighteners and, in this case, cause a kind of a patchy vitiligo. Particularly in the healthcare setting, germicides and biocides are most responsible for causing these here, although these are relatively rare. Back in the day, photographic chemicals also used to cause a lot of hypopigmentation. These aren't used as much. I think it would be relatively rare to see people using those materials now. Again, this is direct toxicity to melanocytes, and the vitiligo may be permanent or may be very, very slow, if at all, to return. And now moving on to the last set of bad actors. These are the skin cancers, and we start off with squamous cell cancer. Its main risk, as most everyone knows, is going to be chronic sunlight or ultraviolet exposure. And remember that many people may be exposed at work to ultraviolet light or have to be out in the sunshine. And as well, recreationally, they're going to continue to be exposed on weekends or holidays. There's also some chemical carcinogens, which we'll see in the next set of slides. You want to consider a chemical carcinogen if squamous cell cancer is occurring in a non-exposed area. If you see multiple tumors, particularly exposed to non-exposed areas, or in the younger patient, because remember, it's generally disease of much older individuals. A small historical note. Remember that squamous cell cancer was the first occupational cancer ever described. Percival Pott in the 1770s described scrotal cancer in chimney sweeps, which was fundamentally squamous cell cancer of the skin. These were generally young boys, orphans, individuals who were small enough to shove up the chimney and get the chimneys clean. They got a bath once a year, whether they needed it or not. And the soot would collect mainly in the rugae of the skin, whereas many other areas, it could just be brushed or washed off. So the areas where the soot had collected were the areas in which the cancer had developed. So Pott describing these several hundred years ago without the chemical knowledge, but what we know about these is now this develops as a consequence of polycyclic aromatic hydrocarbons, or PAHs, which are carcinogenic byproducts of fossil fuel combustion, such as oil, and in this case, coal, and also caused lung and bladder cancer. So here again are the major causes of squamous cell cancer of the skin. We mentioned sunlight. And again, we'll mention PAHs. And in the modern day world, many of these oil and coal products, such as asphalt, coal, tars, mineral, and shale oils still contain PAHs, and exposure to them can result in significant exposure and risk for squamous cell cancer, as well as I mentioned lung and bladder cancer. These can be synergistic with sunlight. So the picture here, which is of somebody working on a road crew in what looks like Florida, or at least a very sunny area, has a real double whammy against him there in the development of squamous cell cancer. He's exposed to both sunlight and to the PAHs, which are off-gassing from hot asphalt while laying the road. The other major contributor are inorganic arsenic compounds. Recall that I showed you a picture several slides ago of hyperpigmentation consequent to arsenic. These can then develop into squamous cell carcinoma in situ, and eventually full-blown squamous cell carcinoma, arsenic also causing lung cancer, as mentioned in Francesca's lecture. So these are sort of the three major ones, sunlight, PAHs, and inorganic arsenic compounds. Basal cell carcinoma is the second of the skin cancers. This has no known other occupational risk factor aside from sunlight and UV exposure. There's no chemical or metal exposure risk known. It can usually be differentiated from squamous cell carcinoma. They're better defined and localized, and they're somewhat more indolent. But again, just the take-home point here is that sunlight or UV exposure, rather than any chemical toxicant or metal exposure, is responsible for basal cell. And the last of the three bad actors is malignant melanoma. Again, this has no chemical or metal exposure outside of sunlight and ultraviolet light exposure. Malignant melanoma, the epidemiology tells us that attribution to work can sometimes be difficult. The associations are oftentimes with a younger age of onset along with a long latency. And then in general, it's most often been associated with early damaging sunburns or equivalent long-term high UV or sun exposure in childhood, adolescence, and youth. And so many people aren't working by that time. But some occupational surveillance systems have picked up some younger exposed worker groups in whom you could attribute melanoma to work. And remember that construction workers oftentimes start their jobs early. In many countries, they may actually start at about age 15, 16 after leaving school. People who work on farms are often exposed from a young age, particularly on the family farm. The children are oftentimes involved. And at age five or six, they may begin to work outside in helping with the family farm. And so they may be exposed from a very young age to the sunlight and military personnel, such as Northern Europeans who served in World War II, for example, in North Africa or in the Middle East. And this is our last slide for skin disorder. It's a little bit of an unusual entity. This is a disorder termed acroosteolysis. And this arises from exposure to vinyl chloride monomer, which again, from back in Francesca's lecture, is also a carcinogen, particularly related to the liver. So vinyl chloride monomer, in addition to its cancer, may cause sclerodermatous skin changes, Raynaud's phenomenon, and lytic lesions in bone. So you see these fairly well outlined in the terminal phalanges of those lytic lesions. And those can be quite painful, particularly with the sclerodermatous skin changes in the Raynaud's, along with the lytic lesions. This is sort of a one-off as far as a disorder caused by a specific toxicant. Vinyl chloride monomer, of course, now regulated as a carcinogen. And so the opportunity to see this happen is probably very much reduced if it's seen at all now. So this concludes the skin lecture and the second set of occupational medicine lectures, which you may see in your reader notes.

occupational skin diseases

contact dermatitis

irritant dermatitis

allergic contact dermatitis

prevention

treatment options

skin infections

skin cancers

acroosteolysis