These slides are the second part of the Clinical Occupational Medicine 3 lecture, which follows the pulmonary section. These represent slides on infectious disease and occupational hearing loss. Most important to the practice of occupational medicine are the blood-borne pathogens. We covered tuberculosis in the respiratory section and the occupational zoonoses, which we'll touch on in turn. Principal blood-borne pathogens of interest in the occupational setting are Hepatitis B and Hepatitis C, along with HIV. The OSHA blood-borne pathogen standard was established in 1991 and has had a major effect on the control of blood-borne pathogen exposures in the occupational setting. The blood-borne pathogen standard in 1991 codified a variety of procedures that are required now to be used within hospitals and health care settings. This codified the idea and use of universal precautions for all medical procedures and any instance where blood or body fluids were likely to come in contact with the health care worker. It established annual training and mandated that hospitals and health care settings have exposure reduction plans. Importantly, it also mandates engineering controls. This, for example, is why you see the puncture-proof buckets in procedure rooms and in most health care and clinic settings. It offered Hepatitis B vaccine to potentially exposed workers and was one of the major factors in reducing the incidence of Hepatitis B in health care workers. Nine years after the OSHA blood-borne pathogen standard was implemented, Congress passed the Needle, Stick, Safety, and Prevention Act of 2000. This required OSHA to amend the blood-borne pathogen standard to require employers to document that they were implementing and using safer medical devices. Fundamentally, after the implementation of the blood-borne pathogen standard, workers were still being stuck and injured by unsafe medical devices. So, the Needle, Stick, Safety, and Prevention Act is what mandates things like the snap-on protective caps you see on phlebotomy needles and other ways to make sharp instruments safer for health care workers and those handling blood and body fluids. Who's at risk for transmission of viral blood-borne disorders in the occupational setting? Fundamentally, most health care workers, anyone who's involved with handling of blood and body fluids, and those individuals and workers who will come into contact with those materials. So, police, firefighters, correctional officers and personnel, emergency response personnel, and anyone working in laboratories where these materials are handled. Prior to the OSHA blood-borne pathogen standard, the risks for Hepatitis B transmission were quite horrendous in health care workers. The risk after a Needle, Stick ranged from 1% to 40% after a Needle, Stick, particularly if there was an infectious antigen-positive source patient. The risk could range up to 20 to 40% from a percutaneous stick. So, in those days, essentially in the 1980s, there were estimates that about 6,500 to almost 10,000 health care workers were infected with Hepatitis B every year before implementation of the standard. Since 1991, implementation of the standard with a mandate for vaccination, as well as increased vaccination of infants, children, other individuals growing up, and other high-risk individuals, and as well with the use of universal precautions, there's been an enormous decline in the occupational risk for contracting Hepatitis B. Risk factors in the occupational setting for transmission of Hepatitis B are fundamentally the same as the other viral disorders, Hep C and HIV, and that contact with blood or serum is much a greater risk than is that from semen, saliva, and other body fluids. Transmission is increased in a stick from a large-bore hollow needle or trocar, in other words, something that contains blood or body fluids within the hollow part of the needle. If it's been freshly used, that way there's a high viable viral load, and a deep percutaneous stick which injects the material underneath the skin versus a scratch or a splash. Again, these are similar risks for Hepatitis B as for Hep C and HIV, and we'll see these repeatedly in this lecture. A few figures on Hepatitis B vaccination. This is now universal, and as the groups who obtain vaccination as infants and children grow up, the need for vaccination in health care workers at the start of work becomes less and less. The response rates to Hep B vaccination are about 90 to 95% in healthy adults. Non-responders are generally the obese, older workers, those with diabetes or renal disease, other chronic disorders, or immune suppression. If you re-vaccinate individuals, the non-responders, that 5 to 10 percent, will have about a 30 to 50 percent response after a second set of three doses, or in other words, six doses total. The recommended protocol for individuals who don't respond to the first set of three vaccinations is to give a second set of three, and then retest them for antibodies and immunity. Now, I like to preface some of these slides by saying that there's a lot of different practices throughout the country, and different employee health services, for example, will have different policies and protocols on Hepatitis B vaccination. What I'm going to do is quote you chapter and verse, principally from the CDC, because that's what the boards are going to take, and individual variation amongst other health centers is not something that the boards can manage to track. So, with that caveat in mind, I'll remind you of a couple of facts. After Hepatitis B vaccination, detectable antibodies are lost over time. So, if you were to redraw Hep B antibody titer in someone who was vaccinated 5 or 10 years ago, you might not necessarily get a detectable IgG from that testing there. However, an anamnestic response, meaning that B cells respond to antigens and start to elaborate IgG, will still occur after a challenge. So, you could test someone with Hepatitis B surface antigen and provoke an anamnestic response. So, therefore, because the fact that this anamnestic response still occurs, and therefore it's considered that Hepatitis B vaccination still remains active, the CDC does not recommend periodic serologic testing of individuals from time to time who have had Hepatitis B vaccination, and they don't recommend giving those individuals booster doses of vaccine if they have lost detectable antibodies. So, here's chapter and verse again from the CDC that recommends that serologic testing is not recommended to assess antibody concentrations in any age group except in certain circumstances. And as we'll see in some of the next slides, those certain circumstances are right after a needle stick, for example. Another slide from the CDC. I'll just mention back in the bad old days when I was a medical student and they were first offering Hepatitis B vaccine, there was little post-vaccination testing so that I didn't get mine, for example. But now, if health care workers are vaccinated for Hepatitis B, there is a recommendation for post-vaccination testing for a response in health care workers who are going to have blood or body fluid contact or other patient contact. And the main reason for this, as we'll see when we get to treatment of Hepatitis B needle sticks, is that knowledge of that antibody response is going to help you determine what the appropriate post-exposure prophylaxis will be. Ideally, you test within one to two months, but within about a one to six month window, after the completion of the vaccine for an antibody check. And of course, consider revaccination if this person is a non-responder. This slide outlines the current MMWR recommendations for prophylaxis after Hep B exposure. In other words, a needle stick from a positive or a higher risk source. So if they're not positive or they test negative, then you need not go through this protocol. Just want to fundamentally illustrate a few points rather than going through this slide completely. If the exposed worker has been previously vaccinated and is a known responder, then there's no action needed. If the response was unknown to the previous vaccine, an antibody level should be checked. If it's found to be above 10 millius per ml, then there's no action needed. If it's less than that, and this is a high risk source, then a suggestion is made to give hepatitis B immune globulin and begin revaccination. The other points concern non-responders. If there's a non-responder after one series of three, giving H big and revaccinating. And if there's non-response after two series of three injections, that person is considered a complete non-responder and should be given hep B immune globulin twice one month apart. There are, of course, concerns around work with all blood borne pathogens. If a worker is injured, in other words, sustains a needle stick from a positive patient and they're following the prophylaxis regimen, whether that be revaccination or hepatitis B immune globulin, they're highly unlikely to infect patients. And as long as they continue obeying universal precautions, they're unlikely to present a hazard in the health care setting. The CDC notes that hospitals may restrict infectious workers, in other words, those who are hepatitis B antigen positive from performing exposure prone procedures. This generally consists of surgery or related types of work. And it's not clear whether restricting other carriers who don't do procedure type work is supported at all. Most states have specific individual regulations. The CDC doesn't give much more guidance than this. And so most often you have to attend to what your state public health department may say about whether or not and how individuals who are potentially infectious can work in health care settings. Moving on to post exposure prophylaxis from HIV exposure. The main thing to note is that the risk from exposure to an HIV positive source patient is much less than hepatitis B was back in the days prior to vaccination. The risk of transmission and seroconversion from a needle stick from a positive source patient is about 0.3 percent or three in a thousand. And the risk goes down with non-percutaneous exposure to mucous membranes. And it's not clear if there's any transmission through a splash on intact skin. The transmission risks are essentially much the same as we saw in the case of hepatitis B, that is to say a deep percutaneous injury, i.e. a needle stick, the large bore hollow needle that contains fresh blood, visible blood on the device and exposure from an end stage AIDS patient AIDS patient or someone with a high viral titer. HIV post exposure prophylaxis was based on two axes. First was on exposure, the highest risk, of course, being percutaneous exposure and the lowest risk of splash on intact skin. And again, we list the high risks for seroconversion after a needle stick. The second axis is the source HIV status running from HIV negative to unknown through a low viral load up to the most infectious, the patient with a high viral HIV load. Previous guidance for HIV post exposure prophylaxis would take into account those two axes and then would recommend combinations of two, three or greater than three antiviral drugs. This was all much more simplified and streamlined when the U.S. Public Health Service initiated its 2013 guidelines for prophylaxis when health care providers had been exposed. And it replaced those guidelines that differentiated the unknown low and high viral load, which were oftentimes very difficult to figure out and figure out in a timely way so that you could treat the source, the worker patient who had been stuck. So these U.S. Public Health Service guidelines represent the current guidance for HIV post exposure prophylaxis. A couple of important points on these. They recommend the initiation of post exposure prophylaxis within a golden window two hours after a needle stick or other exposure has occurred, but occurring no later than 36 hours. They recommend that if you're at all suspicious of transmission for HIV, in other words, a source patient who is suspicious for HIV transmission or high viral load, post exposure prophylaxis should be initiated without regard to the source or the health care worker's baseline status and then reevaluate the situation, both the source patient and the health care worker within the next two to three days after exposure. Once you start to get appropriate data, particularly on the status of the source patient, you can always withdraw post exposure prophylaxis at that point, but you don't want to be in the position where you would have to start it at a later time, say after 36 hours from the needle stick. And then they recommend repeat HIV testing in the injured worker at six weeks and 12 weeks and six months after exposure. The recommendations have also simplified the PEP regimen from a three drug or four drug regimen, depending upon the circumstances. And now the preferred PEP regimen is essentially a two pill, three drug regimen that consists of Raltegravir twice a day plus Truvada, which is a combination of Tenofovir and Emtreeva once daily for a period of four weeks or 28 days. If the injured worker can tolerate that and its side effects. There's some potential problems that the Public Health Service notes with post exposure prophylaxis have listed some of them here. And just to briefly go through them, what you do in a delayed exposure report and generally you should contact infectious disease experts in your area. What do you do with an unknown source? For example, a worker has been injured by a needle in the laundry, and this should be done on a case by case basis. They recommend against testing needles or other sharps for HIV because these can give you false negatives, false positives and otherwise complicate the management. Don't delay post exposure prophylaxis while waiting for consultation in an exposed pregnant person. You can always withdraw the PEP, but you can't restart it later. If there's no known or suspected resistance of the source patient's virus, you want to select drugs to which ideally the source patient's virus is known or consult ID for the profile in your area. The toxicity of PEP regimens is oftentimes a reason why people won't complete it. They note that symptoms are often manageable with anti-diarrheals and anti-emetic medicines. And if there's serious medical illness in the exposed person, you want to obtain some consultation also. I think most people are familiar with the extent of hepatitis C right now in that it essentially accounts for a tip of the iceberg sort of problem. This goes back to my generation and the sex, drugs, rock and roll lifestyle. And now it's recommended that individuals of my generation be tested for hepatitis C because in many cases it's been a latent or subclinical infection. It's drawing to the fore, as I mentioned, because of that tip of the iceberg point, which is to say now that it's accounting for a plurality of chronic liver disease and a number of deaths annually per year from liver disease, as well as for indications for liver transplantation. So it's become a serious infectious risk that goes back many decades. The prevalence of hepatitis C infection and hepatitis C carriage in health care workers has been found to be no greater than in the general population. And that's a prevalence of about one to two percent. There was an article some years back that claimed that first responders had a much higher prevalence, which suggested that they may have been getting infected at a greater rate. That's not proven out very well. And so it's clear that they're getting infected at a much higher rate that they probably have about the same prevalence as most other health care workers. Seroconversion rates for hepatitis C lie somewhere in between HIV and hepatitis B. The numbers are a little less reliable, but it appears that seroconversion after a needle stick occurs at a rate of about 1.5 to 2 percent. And again, Holobor needles are the most likely transmission agent, with some evidence that corneal splashes can transmit it, or at least have been reported. The problems with hepatitis C prophylaxis have been a little more intractable than hepatitis B. This is changing now because the treatment is much better and as well the tests are much better than they used to be. But up until now, tests for level of source infectivity have been very difficult, whereas very simply you could get a hep B E antigen. Here you have to do PCR and looking at viral RNA. There's of course no vaccine currently available and there's been no described good post-exposure prophylaxis. So for post-exposure evaluation of the injured hepatitis C worker, first off the source patient needs to be tested. And this generally consists of an initial hepatitis C antibody. And if that's positive or suspicious positive, it should be followed up with a PCR for hepatitis C RNA. In the injured worker, generally recommended hep C antibody to document a negative antibody response and generally recommended a set of LFTs at baseline, although of course it's not clear how useful that is. If you've got a high risk injury and the source patient has a positive hep C RNA, you wanna follow hep C RNA in the injured worker. If the hepatitis has a high sensitivity and is very quick to detect infection, it can be positive within two weeks. We're left with some question marks in the post-exposure evaluation of hepatitis C. There's no evidence that giving immune globulin for post-exposure hepatitis C does any good. And there really aren't any good studies on antiviral drugs or the use of interferon for post-exposure prophylaxis. There seems to be possibly an improvement in infection resolution with early initiation of antivirals if you have a positive RNA response in the injured worker. But of course, in many cases, those individuals will spontaneously clear a hepatitis C infection as well. So a lot of mystery involved with how to evaluate these individuals post-exposure. So in broad brush general terms for post-exposure evaluation of the injured worker is that a high risk exposure should be watched for evidence of chronic liver disease. Using PCR to detect early hep C RNA across a period, and I say six weeks, but you can even get it at two weeks if there's a high exposure scenario. And to refer to hepatology, infectious disease, anyone who might be involved with appropriate treatment of these patients, and to consider treating them sooner. Again, depending on the circumstances of the exposure and the injured worker's own health. One problem that occasionally rears its head in the healthcare setting are cases of varicilla because it's quite communicable. There may be cases or clusters in the hospital. This has dropped quite a bit since the introduction of varicella vaccine, but you may see individuals who did not have the vaccine. They may be foreign born or may have missed their vaccinations as children. So cases in the hospital need to be isolated and put under negative pressure. Airflow is in tuberculosis. Antibody testing for varicella or some assessment of vaccination should be done at the pre-placement examination. And if there's evidence that they're not immune to varicella they should be offered the vaccine. There are rapid serologic tests for susceptibility if there's a case that breaks out and the healthcare worker's status is not known, and they may need to be furloughed during periods of active communicability if they haven't been able or haven't been vaccinated. Daily screening or temporary reassignment so that they don't infect other workers or other patients in the hospital. These slides were initially put in by Peter Rabinowitz in about January or February of this year when we were preparing to do in-person occupational medicine board review. And of course, since this has moved on quite a bit, Peter was showing slides of the settings in which COVID-19 had its origin. So we'll just look at these slides very briefly. These were slides that he obtained of the wildlife trade and the situations which made the origin of COVID-19 possible. And of course, he's provided the question that we've all been asking ourselves after the emergence into a worldwide pandemic. And of course, as I mentioned before, these slides were inserted in January or February of this year. And certainly the answer to this question is yes, and it has fundamentally altered what we know and practice in occupational medicine. Peter Rabinowitz is, of course, interested in animals as sentinels of human disease and of emerging infections that cross-transmit from animals. Here he's given us a slide with an incomplete but noteworthy list of infections that are demonstrably transmitted from animals to humans. Next few slides, we'll look at a couple of other occupational zoonoses. These are quite traditional zoonoses, as distinct from what we saw on the previous slide, and are worth looking at because transmission in the occupational setting is very demonstrable and susceptible to preventive efforts also. Brucellosis is transmitted by a set of gram-negative coxobacilli, and these are present in livestock and cattle. Therefore, slaughterhouse workers, farmers, dairy workers, and of course, veterinarians may be susceptible to the brucellosis. Brucella species can also grow and be present in cattle and animal byproducts, and this includes both beef and dairy materials, and it's one reason why unpasteurized cheeses are regulated and very markedly not recommended for use in infants, children, and pregnant women that can cause miscarriage and other illnesses. The symptoms are rather gradual in onset, or can be acute, but can be somewhat confusing and nonspecific. They can consist of headaches, myalgias, lymphadenopathy, hepatitis, a variety of other symptoms. It's often termed undulant fever because it will progress up and down in a waxing and waning quality rather than causing a fever that stays high. Leptospirosis is another bacterial infection. This is spread by contamination of water or tissue, generally by urine or feces of an infected animal contaminating water. And field workers, slaughterhouse workers, people who work in sewers, and along with human and animal wastes, people who work in the fishing industry, and once again, veterinarians may be susceptible to leptospirosis. Oftentimes, it may just cause a fever, in general, malaise with myalgias. In some severe cases, it can affect the liver and the kidney and hepatic necrosis or acute renal failure can occur. As a consequence, it can also affect the brain in very few instances. Entity is known as Wiles disease, particularly when it involves the liver and conjunctival suffusion can be a hallmark of some of the more severe cases of leptospirosis. Psittacosis is the last of the three zoonoses we'll discuss here. It's sometimes maybe termed ornithosis or parrot fever, giving you one idea where it comes from, those who handle and keep exotic birds such as parrots and parakeets. It might be more widespread or more seen in poultry farmers and poultry processors, those processing turkey, goose, and duck. It's a chlamydial infection and causes an atypical pneumonitis similar to that of other chlamydia or mycoplasma infections. The X-ray can look worse than the symptoms and it can have the kind of hazy look of an atypical pneumonia or pneumonitis. It can be accompanied by fever, headaches, myalgia, and rash and it's oftentimes underdiagnosed, oftentimes put down to a typical community-acquired pneumonia such as most other mycoplasma or chlamydial infections might be. So you have to be thinking of it and thinking of a potential source or cause for it. Next from occupational infections is a segue into travel medicine because many of these can be a hazard for the traveler and particularly those traveling for work. We tend to think of travel medicine as focusing on vaccinations, but that's only one of the three components of the travel medicine consultation. First really starts with education because most of the hazards of overseas travel are related to safety and injury prevention. Briefly ask yourself, what's the most common cause of injury or death and amongst travelers? And the answer to that is traffic accidents, particularly in places where there's poor traffic control. Education about water and food safety is essential in preventing gastrointestinal infections in particular as are precautions and education about insects because those also represent a fair number of the means by which travel diseases, particularly infections are spread. We'll talk a little bit later about vaccinations. They should be destination specific and they can be required versus recommended. As well, you wanna attend to routine vaccinations, make sure that individuals have their hepatitis B vaccine, make sure they have their tetanus vaccine updated. And lastly is prescription of medications, particularly for self-care of things like travelers diarrhea and antimalarials to take regularly while they're away, particularly in malaria prone areas. The only absolutely required vaccination for travel to some specific locations, principally in Central and South America is that for yellow fever. Immigration and border patrol may demand that travelers have a certificate indicating vaccination to yellow fever. And this has to be dated at least 10 days prior to travel. There can be a medical waiver for those ineligible and there's cautions for those over 60 for receiving the yellow fever vaccine. This is essential and part of the initial travel medicine consultation because some travelers may travel to spot A, then landing or be in transit to a country that requires yellow fever vaccine, particularly from travelers coming from the first country and they may not be permitted entry if they don't have yellow fever vaccine certificate. Two major vaccines should be recommended as destination specific for travelers going where these disorders might be endemic. Hepatitis A is recommended for travelers who are going to consume shellfish and related foods. This has now been on the pediatric schedule for nearly 25 years and many younger travelers will have been vaccinated against it in youth. It's two doses, six months apart, and is oftentimes now given as a combination with a hepatitis B vaccine. Again, anyone traveling where water might be contaminated with hepatitis A as well as the food should be considered for a hep A vaccine if they haven't had it. Typhoid similarly should be given in areas where disinfection of the water can't be guaranteed or assured. This comes in two forms, the oral pill typhoid vaccine, which is a live bacterial vaccine taken over about the course of a little more than a week versus the intramuscular inactive vaccine. Neither one of them is completely efficacious and care should be taken with water sources even if travelers have had the typhoid vaccine. Two other destination specific vaccinations are Japanese encephalitis, which should be given to travelers in Asia, particularly those traveling to rural areas or if mosquito control is poor or suboptimal. This can be checked in the CDC yellow book and the two-dose vaccine is approved for all ages. The second is meningococcal vaccination for meningitis. This is given or highly recommended for travelers to Sub-Saharan Africa in the meningitis belt, particularly if there's evidence that they'll be staying in crowded quarters, hostels, or having contact with a lot of people. It's also recommended for travelers for the Hodge and should nearly essentially be a requirement for that given the large number of people with potential exposure. Other vaccines are not destination specific but can be termed risk-based vaccines, rabies is amongst these, and education may suffice for many travelers. The vaccine should be given to fewer travelers and these should be travelers who are known to have or will have animal contact, particularly cave explorers because bats may aerosolize the rabies virus and this can be transmitted via inhalation. Campers in very remote areas or for people with prolonged stays in endemic countries where they may come across this may also be considered for rabies vaccination. Hepatitis B, again, is nearly ubiquitous, at least for travelers coming from the United States because of vaccination in childhood, but this should be considered particularly in, say, the older traveler who may not have obtained it in youth or for individuals who might experience bloodborne pathogen exposures, handling blood or body fluids, or going off, for example, on medical care expeditions. Individuals who might have sexual contact with infected people, particularly in endemic areas, or getting tattoos should also be considered for a hep B vaccine if they've not yet had it. Inquiries should be made in the travel medicine consultation as to whether individuals are up to date on their routine vaccinations. An annual vaccination for flu, particularly in the winter months, is essential. The tetanus booster should have been obtained within 10 years after travel, and the acellular pertussis vaccine should have been given at some point in late adolescence or adulthood. MMR, varicella vaccine, and pneumococcal vaccine for those over 65 and with chronic conditions should also be recalled, and polio vaccine should be given for travelers going to areas of concern. These may change from time to time, so it's best to look up the areas where polio may be endemic or have become a recent or current problem. Baseline PPD testing, or more recently, quantiferon testing, may be useful as a baseline for people traveling to endemic areas and a test after return. For healthcare workers, this is probably something to keep in mind, particularly if they're traveling to endemic areas or engaged in medical work while abroad. A brief look at antimalarials from this slide. Chloroquine is taken weekly. The problem with chloroquine is that there are few areas in which malarial parasites are still sensitive to chloroquine, which leaves some of the other alternatives on this slide more useful for the chloroquine-resistant areas. Doxycycline is useful and, of course, inexpensive. This has to be taken daily, and the downsides are related to pregnancy and young children, particularly with problems that can develop around skeletal malformations and the bones. You should also avoid sun exposure, which may be a particular problem in tropical areas or areas where malaria is active because sun exposure may be unavoidable in many of those places. Other options are malarone, also taken daily, not intended for pregnant women and at a high cost, and mefloquine, which can be taken weekly, similar to chloroquine. The problem with mefloquine is sort of a series of well-publicized psychiatric problems and should be avoided in individual psychiatric histories. However, mefloquine has the alternative positive aspect of being useful for taking in pregnancy. The global burden of dengue fever has widened in recent decades. This may be a result of several factors, including climate change as well as encroachment into areas where humans and mosquitoes may be coexisting. It's spread by the Aedes mosquito, which also may transmit yellow fever, and a very large number of the world's population is at risk for it. Dengue can have a variety of symptoms and can range anywhere from a mild and barely symptomatic infection to high fever, headache, rashes, pains, bleeding, and can lead, therefore, onto hemorrhagic fever with vomiting, respiratory distress, and bleeding, so a wide spectrum of severity in dengue infection. There's no treatment as a viral infection, and the prevention is to avoid mosquito bites with appropriate insecticides, pesticides, mosquito repellents, and netting. A travel medical kit should be put together for anyone traveling overseas, and the first and foremost point of a travel medical kit is to remember and recall to refill the traveler's prescriptions that they would normally take and the over-the-counter medicines that they use regularly because many may not be obtainable overseas. Comfort medications should be next and include nonsteroidals, cold meds, antacids or anything else that people normally use from over-the-counter and some just-in-case medicines including bandages, antibiotics, things like Pepto-Bismol and Benadryl. Antidiarrheals should always be included in such a kit as well. Most individuals traveling to endemic areas can receive a supply of self-treatment medicines for traveler's diarrhea. These should be taken along with loperamide and oftentimes, particularly for toxigenic infections like E. coli can prove very helpful in stopping the diarrhea rather quickly. So, ciprofloxacin has oftentimes been the mainstay but there is resistance among them to some of the quinolones. Azithromycin or riframaxine may also be useful as self-treatment medicines for traveler's diarrhea. The main resources for travel medicine are the CDC and its yellow book, now essentially a virtual book. The International Society of Travel Medicine can give additional references and assistance and provide certification for providers in travel medicine. There's some online tools that travel medicine clinics will use and other travel information, not necessarily specific to vaccinations or disease, can be obtained from the U.S. State Department. All right, the last section of this lecture is going to deal with occupational hearing loss. Really, when we're talking about work-related hearing loss, we're talking about progressive longstanding chronic noise-induced hearing loss. We'll speak very briefly about acoustic trauma which is usually a single episode such as exposure to a blast. And along with these, we should always remember that noise may also induce tinnitus in individuals, particularly if there's accompanying hearing loss. Noise-induced hearing loss is hallmarked by two main factors. One is that it's a sensorineural hearing loss. Almost always, this means that it starts in the inner ear, in the cochlea and the nerve transmission cells rather than in the middle ear. For example, disruption of the ossicles or the tympanic membrane. And it's usually bilateral because exposure usually occurs surrounding. There are some cases in which workers may have unilateral hearing loss or one ear worse than the other. For example, workers who have to shoot rifles or do hunting, for example, may have worse loss in their opposite-handed ear because of the way that the firearm is held. Some ambulance drivers and truck drivers may have, at least in the United States, left-sided hearing loss worse than the right side. And this is because of noise exposure out the window from a siren, for example, that may affect the left-sided ear, the side closest to the car window, more so than the right side. Noise is measured in the workplace by means of sound level meters. And then this is transformed into what's known as the A-weighted scale, which is a scale that incorporates human hearing range. Two numbers that we'll see constantly throughout this are the OSHA action level, which is 85 decibels on the A scale, and 90 decibels, which is the permissible exposure level for hearing loss, according to OSHA. This slide gives you an idea of sound levels for common activities. Normal conversation might occur at 65 decibels, and a busy office might be well within that range. When you get into the industrial and manufacturing setting, drill presses and power saws are going to be up at and over the OSHA permissible exposure level. Grinders and jackhammers will be above that. Recall that the decibel scale is logarithmic, so that an increase of 10 decibels represents a tenfold increase in sound. So to go from 80 to 90 decibels is 10 times the sound pressure. One point I didn't mention on the last slide, but is a useful rule of thumb, is a ballpark estimate of noise levels on the workshop floor. And says that if you can't carry on a conversation with somebody next to you without shouting, then that pegs the estimated sound level of the shop at about 90 decibels. So that is at or about the OSHA PEL. Chronic noise-induced hearing loss across a lifetime is significant. Individuals exposed at 85 decibels across a working lifetime have a small risk of impairment, even at those lesser noise levels. And when the mean exposure increases to 90 decibels, about 25% or a quarter of workers exposed at that level will have hearing impairment or a hearing handicap towards the end of their working life. Noise-induced hearing loss often doesn't develop until after about 10 years of exposure to noise at those levels has occurred. And as a result, it's also insidious. It's usually not the worker themselves who notices it, but family or coworkers who point something out to the worker that they're not hearing or seem to be misunderstanding what's said to them. And interestingly, the initial problems, because these are usually high-frequency noise losses before the low frequencies are affected, is that clarity of speech seems to be affected rather than the loudness or intensity. So these are people who might mistake some of those higher-pitched consonant sounds at the ends of words. Fish versus fist, for example, or hat versus has those end high-pitched consonant sounds. And so speech sounds mushy and unclear rather than seeming softer. And understanding speech in a noisy room where there's some sort of interference makes this more problematic. So pure tone audiometry is the mainstay of testing for noise-induced hearing loss and is mandated under the OSHA noise standard surveillance requirements. Here, the individual's in a booth, which should be soundproofed, and is presented with a single tone at pure frequencies, and they signal whether they hear. The signal is the threshold or the lowest volume in which they hear that single tone. Here's the typical result of audiometry, for example, in somebody with early to moderate noise-induced hearing loss. And what's characteristic of noise-induced hearing loss in the workplace is a notch at 4,000 hertz, in other words, loss of acuity, such that the hearing threshold is much higher for noises at 4,000 hertz than it is for the lower and for the higher-pitched frequencies above 4,000 hertz. Remember that the speech range is generally about 500 to 3,000 hertz, and so this person may have only very mild symptoms with this loss at 4,000 hertz, which is somewhat higher than speech. This is also differentiated from presbycusis, or hearing loss of increasing age, which is the dashed line, which shows a progressive downward slope past 4,000 hertz and is worse at 6,000 and 8,000 hertz. So again, for noise-induced hearing loss, one sees on the audiogram early impairment at 4,000 hertz, and the higher and lower frequencies are relatively spared, and that contrasts with presbycusis, where it deepens the higher frequency you go, and it becomes clinically noticeable when you get an average loss at thresholds of about 25 decibels in the speech range, which I mentioned, again, is at 500 to 3,000 hertz. So audiometry can actually pick up these impairments at 4,000 hertz before workers realize that they may be clinically impaired. And here's another set of audiograms showing the initial audiogram, which is at thresholds between zero and five hertz loss, which is essentially nothing at all, with a deepening notch, the subclinical loss after about 10 years, and the deepening notch that occurs at 4,000 hertz after 20 years, at which this individual might start to be noticing impairment in hearing. And at 40 years, there's a combined effect of age and noise such that the 4,000 hertz notch has deepened with additional deepening at the higher frequencies. So again, to reiterate, speech is becoming less intelligible as this loss progresses downward into the speech frequencies below 4,000 hertz into two and 3,000. Acuity is affected because this is knocking out nerve cells at those frequencies and not the volume. So standard hearing aids, which amplify the noise, aren't very much help. Newer technologies, such as cochlear implants, may be helpful instead. And removal from exposure is really the treatment because once hearing is gone, it's gone, and there's no restoring it through specific treatments. We'll see some definitions and distinctions about measurement of noise-induced hearing loss in the next couple of slides. This has to do with the concept of a threshold shift, which is a temporary or a permanent decrease in hearing acuity as measured by audiograms. Most everyone's going to be familiar with the temporary threshold shift. This occurs following acute overexposure to noise. This can happen if you leave your headphones on too long for a prolonged period of time. You sit next to the speakers at the Black Sabbath concert, and it gives you that kind of fuzzy, cotton-in-your-ear feeling where your hearing is diminished. And in general, that persists for hours to a day or so. And after a period of quiet and no further exposure, if you were to put people on an audiogram, they will show a return back to their normal baseline. The permanent threshold shift occurs when there's damage to hair cells that has become irreversible, as opposed to the temporary threshold shift where they can come back. So the permanent threshold shift is diminished acuity that won't resolve on retesting. And this is an indication that there have been prolonged noise levels that are not adequately controlled. These are going to be in and around the area of 85 decibels or greater at the workplace. And again, that they are not particularly well or adequately controlled. These become reportable on the OSHA log, the OSHA 300 log, if on an audiogram there is a 10-decibel average shift from baseline at the levels of 2, 3, and 4 kilohertz. And that's a definition by OSHA of a standard threshold shift. So it's fundamentally the average of the audiogram thresholds at those three levels. And the second part of the recordability is that the overall mean hearing level at those three levels is greater than 25 decibels. So, for example, and we'll see some more working this out in the next slides, but, for example, if somebody came in with a purely pristine 0-decibel average and they develop on a subsequent audiogram shift from baseline of average of 10 decibels at those three levels, that would not be OSHA recordable because the overall mean hearing level in that case is still only 10 decibels loss instead of 25 decibels. So just to kind of repeat the essential points of that, the standard threshold shift is this 10-decibel average shift from the individual worker's baseline at those three frequencies. The company can retest this within 30 days to see if it persists. In other words, to see if they didn't just catch a temporary threshold shift. And if it persists, in addition to recording on the OSHA log, which is this threshold shift plus the overall mean hearing level at an average of 25 decibels, written notification has to be made to the worker. There has to be counseling and assessment of protective measures such as PPE. And this then also revises the worker's baseline. So they're now working from a new baseline at this new threshold shift. And any further reduction from their baseline may get reported as an additional threshold shift. So this slide presents us with a series of data on a sequence of annual audiograms going from the reference or baseline to the 11th annual audiogram. And as you can see just by eyeballing the numbers, there's already evidence of noise-induced hearing loss occurring in the early years and very much deepening across time and deepening downward into the speech frequencies from 4,000 hertz down through 321 and into 500. So the question here, and you take a little brief look at this right now, is where is there a recordable threshold shift? So take a look at this or pause for a moment. In the next couple of slides, we'll show you some calculations. The first point that there is a significant, i.e. average of 10 decibel shift from baseline occurs at the 5th annual audiometry. And the math is outlined here below. And at those three frequencies, 2, 3, and 4,000 hertz, there's a 16 decibel average shift amongst the three values. But the overall mean of those three values is 23 decibels. And so therefore, while this would be medically a threshold shift, this is not an OSHA recordable threshold shift because even though there is a drop of more than 10 decibels on the average across the three, the overall mean has not yet reached 25. For the OSHA recordable threshold shift, we had to wait until the 7th annual audiometry, which shows a 15 decibel average change from that 5th annual baseline because remember, that became the new baseline because of the 10 decibel shift. So there's an average 15 decibel change. And the overall mean here has finally And the overall mean here has finally gone up to above 25 in addition to that greater than 10 decibel change. So now the overall mean hearing loss in those three frequencies is 41 decibels. In most cases, computerized audiometry programs will do this for you and record it. This is a little bit extra just showing you how these are calculated and how the OSHA recordability standard affects how these are reported. So the diagnosis of noise-induced hearing loss takes several components. Again, the mainstay is pure tone audiometry with the high frequency notch beginning at 4,000 Hertz and progressing downward from there with increasing noise exposure and the relative sparing of the higher frequencies until noise exposure has, again, become more prolonged. There should be exclusion of conductive hearing loss. This, again, is from the ossicles in the tympanic membrane. So bone conduction testing is useful to try and distinguish between sensory neural and conductive hearing loss. Unilateral hearing loss should be looked at critically because noise-induced hearing loss is unlikely to be seen as single or unilateral. And so other concerns such as the possibility of an acoustic neuroma or some other condition that might cause unilateral hearing loss should be considered. And this may lead you to do additional testing such as ABRs or an MRI. And there may be other entities in the differential diagnosis such as Meniere's disease. Acute acoustic trauma arises from a sudden massive overexposure to noise and results in immediate loss of hearing. This is oftentimes the result of a single exposure to a blast or explosion, sometimes a artillery or something of that sort that goes off, but oftentimes from an exposure such as an explosion. And this generally results in disruption of the ossicles, rupture of the tympanic membrane, and fundamentally a lot of middle ear damage as well as also provoking sensory neural hearing loss within the inner ear. So it may have those two components. And the extent to which this resolves is dependent upon how severe the original injury is plus whether or not there was other pre-existing sensory neural hearing loss, for example. Tinnitus is a common complaint in those with noise-induced hearing loss, both from long-term chronic noise exposure and from acute acoustic trauma. But it oftentimes accompanies noise-induced hearing loss. And it's not really clear what the origin of this is. And more frustratingly, it's not really clear how to treat it. But it can be very disruptive to individuals' lives and may be a component of the complaint and the disability that workers who have sustained noise-induced hearing loss may feel. So this concludes the occupational medicine part 4 section. And we'll move on to the next lecture when you're ready.

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noise-induced hearing loss