Hi, I'm Denise Kessler, the Preventive Medicine Section Chief from the University of New Mexico. I'm talking about the fundamentals of occupational medicine. An overview of the topics include an occupational medicine principles discussion and then looking at occupationally related illnesses and injuries. This includes the respiratory system, the musculoskeletal system, the neurological system, as well as special topics to include metal toxicity, hearing loss, and cancer. And finally, it'll be looking at understanding OSHA regulations. The American Board of Preventive Medicine examination content outline indicates that for the occupational medicine specialty examination, clinical occupational medicine is 48% of the exam. For the public health general preventive medicine specialty examination, occupational and environmental health is approximately 10%. In the aerospace medicine specialty exam, occupational medicine is not specifically listed. However, much of what is done does include occupational medicine. So what is occupational medicine? From the American Board of Preventive Medicine, occupational and environmental medicine focuses on the health of workers, including the ability to perform work, the physical, chemical, biological, and social environments of the workplace, and the health outcomes of environmental exposures. Practitioners in this field address the promotion of health in the workplace and the prevention and management of occupational and environmental injury, illness, and disabilities. The Bureau of Labor Statistics keeps record of injuries in private industry. This data is from 2022. There were 2.8 million reported injuries per year that year. There were 460,700 million reported illnesses that year. And there were over 5,000 fatalities that were reported in that year. Industry rates vary by different sectors. In the goods producing sector, manufacturing has a high industry rate. And in the service sector, transportation and public utilities are high in injuries and illnesses. It can be difficult to determine which industry is the most dangerous because they use different varying measurements of injuries and hazards. In the National Safety Council, construction has the most workplace deaths. Education and health services has the most non-fatal injuries and illnesses involving days away from work. Agricultural, forestry, fishing, and hunting has the highest death rate for 100,000 workers. And transportation and warehousing has the highest injury and illness rate involving days away from work for 10,000 workers. So as you can see, it would be difficult to compare these different measurements. Also from the National Safety Council is the cause of work-related injuries. The leading causes that involve days away from work include exposure to harmful substances or environments such as electricity, radiation, temperature extremes, or infectious diseases. This particular area was increased after the COVID pandemic. Also leading causes include overexertion and bodily reaction. Examples would be lifting, pushing, carrying, and repetitive motion activities. Slip, trips, and falls also are a cause of problems, as is contact with objects and equipment. Examples of this would be hit by a moving object, a vibration injury, and crush injuries. There are other categories which are not quite as leading in causes of injuries, such as violence injury from either a person or animal, transportation injuries, and fire and explosives. A basic fact is what a disease might be, and that would be an injury, illness, or physiological or anatomic dysfunction, an alteration in general state of health. When it's an occupational disease, it's caused or made worse by work or by exposures in the workplace. An environmental disease would be caused or made worse by exposures in our ambient media, such as air, water, and soil. Of course, an occupational disease could also be attributed to the environment. An occupational disease is produced in the work environment. Generally, it's over a period longer than one work day or shift. The impact can be from various hazards to include physical, biological, and chemical, and it may result from exposures to toxins, poisons, fumes, or other continuing conditions of the work environment. It could be from repeated stresses or strains or systemic infections. It's important to remember that occupational diseases have the same clinical and pathologic expressions of disease of those that are non-occupational, and it's really the causation of the disease rather than the pathology that distinguishes illnesses as an occupational disorder. So obtaining the occupational information and the medical history is absolutely critical. Remember that an occupational and environmental condition can impact any organ system, but it commonly is seen to impact the musculoskeletal system, the pulmonary system, or dermatological system such as allergic or irritant contact or acne. Also, there can be hematologic effects such as from benzene and arsine. Those who practice clinical occupational medicine most often are involved with worker compensation cases. They must determine diagnosis, whether or not there is a work-related causation, and then treat the worker. Each state has its own regulations governing occupational medicine in workers' compensation, so knowing the regulations that impacts one's practice is critical. Achieving the diagnosis in occupational medicine is very reliant upon taking an excellent history. Looking at the patient history, it should include an evaluation of the mechanism of injury, the symptoms, the past medical history and review of systems, which may provide additional information as to the causation, the social history, the occupational history, and the non-occupational activity history. Each of these areas will result in multiple questions to fully understand the case and make determinations of diagnosis and work-relatedness. The timing of symptoms is very important. Generally, they begin after work with a particular agent or process. There may be a lead-in time from first working with the material to the start of symptoms, and then it may be worse on working days, so restart on Monday or whatever the first day of the work week might be. It usually increases through the working week and gets better on weekends, holidays, and vacation time. Of course, there is some variability with that, but it is important to realize some basic concepts. Again, the timing of symptoms is important. You may see characteristic patterns in relation to work. For example, with latex urticaria, it would be minutes to one to two hours after contact. In asthma, it's usually between one and two hours after contact, but there could also be late reactions that may occur, such as in bed at night. In vicinosis, which involves cotton dust, there's chest tightness on Monday morning and then better as the week progresses in early stages, and then as the disease worsens, it goes further into the work week. Nitroglycerin workers have angina symptoms that develop after withdrawal, so over the weekend, resulting in rare historical cases of Monday morning deaths. This might be in the explosive industry where people would be working with the nitroglycerin. Also important in taking the occupational history is the non-work exposures. So consider their housing. Is it an area of their house that has lead paint that might be exposed? Are there plumbing issues? What's the water source? What's the location? Are they next to a waste dump? Hobbies are really important because oftentimes people are exposed to different chemicals or even physical hazards when they're doing different hobbies. So jewelry, stained glass, casting lead sinkers, woodworking, gardening, and farming all are important to discover. What are other habits such as alcohol and tobacco? What about the household members? What's the jobs and exposures of other members? Is there illness going on in their house and do they have pets that might be causing issues for them? And of course, if they have a second job, what are they being exposed to at that job? It's also important to consider if other workers are affected. An initial worker with a problem may be a sentinel case involving overexposure to other workers and if many workers are exposed, you can expect more than one will be ill. You also need to consider the environmental history. Are others in the area affected? Remember the most vulnerable are usually the elderly or children. And while we think of sentinel cases with chemical exposures, it could also be a physical exposure such as new equipment in a manufacturing setting that is causing back pain in everybody who uses the equipment. The environmental exposure history may be important depending upon what the person is presenting with. So delving into that would be critical. Do they live near a source of environmental exposures? Consider the air, groundwater sources. What's the community environmental factors? Again, do they live near a freeway, a dump site, industrial plants? Is sun exposure important to look at? And what is the type of dwelling? Do they live in an apartment, a house, a mobile home? Is there a concern for asbestos, radon if there's a basement present, formaldehyde? What's the age and condition of the dwelling? Are there others again in the dwelling such as smokers? And what's the heating source? Are they using wood stoves and fireplaces or gas stoves? So that's an overview of the important aspects of history that should be obtained. Let's look at some of the respiratory system issues that occur in the occupational setting. And it should be noted that this presentation would not be able to cover every single possible illness or disease that might be impacted occupationally or might be on the examination. But this gives you some guidance for your studying. And of course, make sure that you're expanding your studies to include other areas that I am not covering in this evaluation or assessment. Upper airway conditions can happen in the workplace. The upper airway is from the nares to the larynx. One of them would be allergic rhinitis, which causes rhinorrhea, sneezing, itching, congestion. The cause is aero allergens, so pollen, animals, and diisocyanates are examples. Allergic rhinitis is caused by the same allergens that can cause occupational asthma. So that's important to keep in mind. Irritant rhinitis is usually dose dependent, not sensitization. It is appearing with nasal symptoms, facial pressure, mucosal erythema. Irritants include smoke, nitrogen oxides, ammonia, and formaldehyde as examples. And then vocal cord dysfunction can also be seen as an occupationally related condition. This is acute irritant exposure that causes paradoxical vocal fold motion. It's important to differentiate vocal cord dysfunction from asthma as they may present with similar symptoms. And this is the vocal cords responding to hypersensitivity to an irritant such as ammonia, cleaning chemicals, or dust. Other important occupational lung diseases include the pneumoconiosis. Today we'll talk about asbestosis, silicosis, and co-workers' pneumoconiosis. And then airway diseases to include occupational asthma and inhalation fevers. For the board exam, be able to differentiate these respiratory diseases. Remember that dust-related diseases, the pneumoconiosis, are restrictive and airway diseases are obstructive lung disease. So how do we know if they're obstructive or restrictive? An important part of that would be interpretation of spirometry and pulmonary function tests. This is a spirometric testing volume recording that you would see if you ordered a pulmonary function test. It's the cumulative volume of air measured over time of a single forced expiration. One of the important measurements is the forced vital capacity or the FVC. This is the total volume of air expelled in the maneuver. Also important is the forced expiratory volume in one second or the FEV1. This is the volume of air expelled in the first second of expiration. And finally, also important is the ratio of the FEV1 to the FVC. These indices are interpreted comparing to normative population standards. So it's matched for age, sex, height, weight, race, ethnicity, and a percent of the predicted values for those factors are included. Because of that, it's important to recognize that there's a lot of room for error because of the population comparisons. A normal FEV1 and FVC usually would be both over or equal to 80% of the predicted value. A normal FEV1 over FVC ratio would be equal to or greater than 70% predicted. So this chart just shows that again. So if everything is normal, the interpretation would be normal. If the FVC is normal, but the FEV1 is low, the ratio would then be low, and it would be interpreted as an obstructive finding. If the FVC is low and the FEV1 is low, it may look like the ratio is normal, but it's pseudonormal, and it's restrictive finding. So let's look at the pneumoconiosis. These are broadly considered dusty lungs, and they result with lung inflammation from inhaled dust that cause fibrotic changes in the parenchyma. There's usually 10 to 20 years of exposure required for the onset of the disease, and the damage is permanent. Again, it shows a restrictive lung physiology with progressive hypoxia. Silicosis is a finding that is the most prevalent chronic occupational disease in the world. Silica is a major component of rock and sand. Granite countertops are commonly installed in kitchens and could be a cause of exposure in manufacturing. There are safety processes used to keep the worker safe, such as the use of water when cutting the stones, respirator use, and dust collection systems. Any activity with crystalline silica could result in disease formation, depending upon whether or not the precautions are in place, so mining, milling, and stonework, quarrying, and tunnel operations, foundry and boiler work, and sandblasting and drilling. It also is found that this increases susceptibility to tuberculosis and anaerobic infections. The silica nodule is the characteristic lesion. There's an orderly progression through increasingly severe disease stages, so it starts out as small rounded opacities, which become confluent, and then lead to progressive massive fibrosis in the lung. Again, the spirometry shows a restrictive pattern, and silicosis is a carcinogenic, causing lung cancer. This chest x-ray shows the small round opacities. They look like rice scattered throughout. Silica and coal have a tendency to be found in the upper lung fields. As the opacities start to coalesce, the findings are more obvious. As the lungs become more fibrotic, there may be tenting as the lower lungs get pulled upward. Severe cases may result in larger fibrotic masses with progressive massive fibrosis, PMF, that result in respiratory failure. Coal worker's pneumoconiosis, or black lung disease. This is usually not seen unless a worker has spent over 20 years in the mining industry. It's very similar to silicosis in appearance. While coal is less fibrogenic than silica, in mining coal, there are other things that are being cut through besides the coal, and it may include silica as well. This is a microscopic view of the abnormal alveoli from coal's impact. Coal miners also often may have a chronic bronchitis in addition to the pneumoconiosis. Spirometry is primarily obstructive initially and then restrictive in later phases. This chest x-ray demonstrates fibrotic diseases in the upper zones from coal dust. Patient history is really key to be able to tell if it's coal or silica that may be the findings in a chest x-ray. Asbestos is another important consideration in pneumoconiosis. There are several different types, and they are all carcinogenic. The fibers get deep into the lungs. Occupations at risk include asbestos mining, manufacturing and installation of insulation for ships and buildings, brake linings, asbestos tiles, and other industries. The serpentine are considered curly fibers versus the amphiboles are needle-like. Ninety-five percent of the asbestos in place is chrysotile, and again, the ability to penetrate the lung is usually deep, and it depends on the fiber diameter, which are usually less than five microns, and the latency is at least 20 years for most diseases. And looking more specifically at the time of disease to exposure, there is some variability. Benign pleural effusions are usually seen approximately 10 years of latency. Pleural plaques are seen at 10 to 20 years of latency after the onset of the first exposure. Asbestosis, which is the pneumoconiosis that we're talking about, not cancer, it's usually 10 to 20 years of latency. And lung cancer is usually over 25 years of latency. Finally, mesothelioma can be 35 to 50 years latency. An ABPM board question may be, what is the first to be seen, which would be the benign pleural effusions, and then the pleural plaques. In asbestosis, the findings show fibrosis on the chest x-ray, especially at the lung bases. There are small irregular or linear opacities. Again, the spirometry shows a restrictive pattern. And in pathological evaluations, there are asbestos bodies, which are protein-covered fibers that contain iron. It's the only pathologic feature that's unique to asbestosis. The linear streaking is not to be confused with the coal or silica dust findings on x-ray. And the asbestos bodies are usually not seen except for postmortem. This is an x-ray with asbestosis. The lower lungs show streaking, linear opacities that are classic for asbestos. The pleural plaques are visible on the lateral sides here. And again, the difference between asbestos and silica and coal on x-ray could be a board question. Asbestos and tobacco are not a good combination. Cigarette smoking increases the risk for bronchogenic lung cancer. It does not, however, increase the risk for mesothelioma. And it does increase the susceptibility for asbestosis. Asbestos increases the risk also for cancers of the esophagus, the oropharynx, and the larynx among smokers. Next, we'll be looking at obstructive disease to include asthma and RADS. Asthma is a reversible inflammatory disorder of the small airways. It's intermittent and, again, reversible compared to COPD, which would not be reversible. It's increased bronchoreactivity to a variety of stimuli. With asthma, the FEV1 is improved after giving a bronchodilator. Occupational asthma is important to first have the diagnosis of asthma before considering whether or not it's occupational. And once the diagnosis of asthma is established, then it can be considered whether or not it's occupational. That gets back, again, to the importance of taking the history. Again, with the asthma, it's reversible or variable airway obstruction. The airways are hyper-responsive, and it would be in specific occupational situations. It's the most common compensable occupational respiratory disease in the United States. And as I noted before, the most common occupational respiratory disease worldwide is silicosis. In occupational asthma, there could be an immediate or a delayed reaction. It could be early in a worker's career or after years of exposures. It may cease when exposure stops or, unfortunately, it may persist with a reaction to a variety of irritants as well as allergens after the exposure stops. Reactive airways dysfunction syndrome, or RADS, is an irritant-induced asthma secondary to a high-intensity and short-duration exposure. Factors include a history of ATOP. Occupational agents may act as nonspecific irritants or allergens. Again, so developing asthma at the workplace may result in difficulties with exposure to other things, such as smoke or dust. And smoking increases the sensitivity to many allergens, such as the platinum salts or anhydrides. It's also an irritant or nonspecific trigger for people who already have asthma. There are two types of work-related allergens. Large molecular-weight antigens are usually biologic, such as those listed here. Examples would be in a research animal handler. Manufacturing setting for drugs may also be the site of development of asthma. IgE responses to the biologics are the cause and result in rapid-onset immediate allergic responses. So, again, as examples, includes vegetable dust, such as flour and wood dust. Animal dust, such as cockroaches, rodents, or enzymes, or drugs, such as penicillin. More complicated are the small molecular-weight antigens. They're very small, and they're probably not IgE-mediated. The mechanism of action is not known. These result in delayed reactions, so this is when a person may have symptoms in the middle of the night. The testing is not really available for small molecular-weight antigens, as they are for the large molecular-weight. Isocyanates are used in many settings, such as auto-painting, to include the epoxy resins and metals, such as chromium, cobalt, and nickel. There are diagnostic tests for asthma. It's primarily spirometry, which would show an obstructive response, so reduced FEV1 with a normal FBC. It's also reversible with the use of a bronchodilator. Another important tool is doing peak flow meter readings throughout the day. So this would be checking how much their flow is at work, at home, on weekends, in different locations and scenarios, so they can determine if there's an impact to a specific exposure. There's also available a methylcholine challenge test, which is nonspecific provocation of the airways, but this is not usually needed with the spirometry testing. Amylologic testing can also be available if needed. Amplified airways dysfunction syndrome, or RADS, again, is bronchial hyperactivity after acute exposure to an irritant. The asthma symptoms persist. They usually have had no prior respiratory disease, and an example would be emergency response workers or firefighters who are exposed to a sudden huge amount of pollutants, smoke, and particulate matter. Respiratory related illnesses are several different varieties of possible causes. This is associated with exposure to indoor air, and it can be, again, very nonspecific or it can be very specific. It's primarily upper respiratory symptoms, such as cough, eye irritation, fatigue, headache, nausea, and skin rashes. It's important to note that there's no regulations governing indoor air specifically. The most common cause for building-related illnesses would be poor ventilation, with dust, carbon dioxide, environmental tobacco smoke, humidity, or possibly combustion byproducts being the source of the illness. Examples of building-related illnesses include infectious agents, such as Legionnaire's disease. Legionnaire's disease is pneumonia caused by the Legionella bacteria. It's exposure by aerosolization, such as from cooling towers of a building's air conditioning system, hot tubs, or fountains. There's increased risk in those who have medical conditions, which would increase their susceptibility. A building-related illness could also be secondary to specific contaminants, so if the building materials are releasing formaldehyde, that could be the cause, or if there's allergens present, that could be the cause. It shouldn't be confused with mass psychogenic illness, which is a socially mediated illness among many, or sick building syndrome, where the symptoms are dissimilar, but there's no finding in the building that caused the actual illness. When evaluating a building-related illness, it's important to have a careful walkthrough with an industrial hygienist or a building scientist so that the possible sources can be discovered, such as the poor ventilation or perhaps water damage. Any sampling done should be considered carefully because of the lack of knowing what normal values should be in some of the tests that might be available. Looking at carbon dioxide in humidity, and then if there's a specific source to that building that might not be traditionally seen in all buildings, testing for that might be something that would be helpful. Well, let's look at inhalational fevers. These are syndromes with flu-like symptoms and short duration, but they may be incapacitating. Symptoms include things such as fever, myalgias, cough, chest discomfort, headache, and malaise. There's usually a high level of exposure that results in illnesses for most people, so it's not sensitivity dependent. Examples include metal film fever, organic dust toxic syndrome, and polymer film fever. In metal film fever, this is exposure to freshly generated metal films during welding. Primarily, it's the zinc in the galvanized steel, but it also may be impacted by the cadmium, copper, iron, lead, magnesium, manganese, and tin that would be a part of the welding. The person looks very sick, but it's not long lasting. They would have a fever, chest tightness, dyspnea, and myalgias 3-10 hours after exposures. Again, thankfully, it's self-limited. There's no leukocytosis, there's few pulmonary findings, and no apparent sequela. Workup again would be an essential normal findings, and it's usually in newer workers or someone who was on a break from work and is getting re-acclimated. Polymer film fever is very similar. They may get plural polymers on their hands, and then if they do something such as light up a cigarette, they would get exposure because the agent would be vaporized. You can also see a similar reaction in farmers that are exposed to biologics. Irritant injuries can occur. The metal film fever results from the metal vapors that condensed into fine particles, but welding can also release gases. This is looking at irritant gases or fumes rather than particulates. The more water soluble they are, the more upper airway injury will happen. Water soluble phosgene is not water soluble and goes deep into the airways to cause pulmonary injury, but sulfur dioxide would give upper airway injury. Looking at that a little more closely, again, the water solubility is what causes the irritation. Ammonia and bleach mixed results in chlorine gas, which is very irritating. Water insoluble gases are more dangerous and causing lung damage. Again, phosgene is not a good thing. It hydrolyzes the lungs to hydrochloric acid. It was a poisonous gas used in the World War I era, and it's now used as intermediate in chemical reactions in the manufacturing of other chemicals, pesticides, and pharmaceuticals. Again, water soluble is usually upper respiratory irritation and includes sulfur dioxide as well as chlorine, formaldehyde, ammonia, and acid mists. Water insoluble, again, would be more prone to lung damage, and along with the phosgene would include the nitrogen oxides. Along with the water solubility, the particulate size is also important. The less than 10 micron particle would deposit in the upper airways, such as dust. If it's 2.5 to 6 microns, it would deposit in the lower airways, such as fire smoke particles, and less than 2.5 microns would deposit in the lung tissue, such as the asbestos fibers. And again, the water solubility also will determine the site of injury. So the highly soluble will be in the upper airways, the moderately soluble will be in the lower airways, such as chlorine, and the low solubility will deposit in the lung tissue, such as the phosgene. One final consideration in the respiratory system exposures would be asphyxiants. With asphyxiants, oxygen is displaced and replaced with gases that are asphyxiant. So it might be seen in coal mines with CO2 and methane pockets, it could be seen in fires, and sewage workers may also be exposed to asphyxiants, as well as any confined space. So simple asphyxiants would be those that reduce the oxygen content by displacing the oxygen. The symptoms would be headache, confusion, nausea, and may result in loss of consciousness and even brain injury. Again, it can be seen with CO2, methane, nitrogen, ethane, and propane as some examples. All asphyxiants interfere with the cellular metabolism and includes carbon monoxide, hydrogen cyanide, and hydrogen sulfide. They each vary in the symptoms that they would present with. So carbon monoxide may result in a headache, confusion, nausea, and brain injury. Hydrogen cyanide would cause headache, dizziness, dyspnea, and potentially brain injury. And hydrogen sulfide, which is where you have the complaint of a sewer gas odor, there would be respiratory tract irritation and brain injury. Well this ends our discussion of respiratory system, and we're going to be moving on from here. Next we're moving on to musculoskeletal system. The musculoskeletal disorders that might occur in the occupational medical setting are very important. Of course, there are multiple body areas that could be impacted in the musculoskeletal system, but I'm going to focus on two important areas of commonly seen injuries. Much of the information provided today is from the ACOM guidelines, which is part of the MD guidelines. The MD guidelines originated by Dr. Presley Reed, so you may have heard of the prior Reed publication, Medical Disability Advisor. The ACOM guidelines and the MD guidelines are evidence-based clinical practice guidelines. Low back pain is very common. 80 plus percent of adults across their lifetime will have low back pain, both work and non-work related. Over 90 percent of the cases will resolve within six weeks. Most episodes will respond to symptomatic and physical measures and to time. Low back pain ranks second to URIs among the symptomatic reasons for office visits. There are some risk factors to developing low back pain at the workplace especially. This includes lifting heavy weights incorrectly or posture or torque on the trunk, smoking, vibration, and work dissatisfaction or little control at work. Psychosocial impacts at the workplace are seen to result in both injuries and in delayed recovery. We're not going to look at those closely in this presentation, but it's an area of importance in the practice of occupational medicine. Acute low back pain has important elements with the first visit in the clinic. A comprehensive occupational medical history and back examination really needs to be completed. Also important is checking for red flags such as neural impingement or compromise. There's usually an excellent prognosis and uncomplicated low back pain will have a return to work within four weeks in 82 percent of the cases. Ninety-three percent of the cases will return to work within three to six months. Again, it's important to assess for psychosocial factors and fear avoidance is very important to evaluate because it might cause delayed recovery. Maintaining ordinary activities as tolerated leads to the most rapid recovery. There are red flags to look for when evaluating for back pain. These are uncommon but critical to identify. These would include things such as infections like tuberculosis, brucellosis, or vertebral osteomyelitis. The reactive spondyloarthropathies such as ankylosing spondylitis or reactive arthritis are also important red flags. And of course tumors are important to evaluate if the possibility exists. This could include metastases from the breast, prostate, or lung, multiple myeloma, vertebral hemangiomas, or osteoid osteomas. Once the patient history is collected, which includes such things as the mechanism of injury, the prior history, the location and intensity of the pain, sensory and weakness changes, and other things as discussed previously, the corresponding physical examination is critical. Testing of the suspected involved nerve roots would be completed as indicated in this figure. So considering the location of the pain, the location of any numbness, and then if there's any motor weakness, especially when considering L4, L5, and S1. Then making sure that reflexes are completed as well as the screening examination tests such as squatting, heel walking, and walking on the toes. Other elements that are important would include looking at the range of motion and the general appearance. To image or not to image, hopefully you are aware that this is something that's really important to consider in an occupational medicine setting in regard to low back pain. It's really important, unless there are red flags present, to avoid routine x-rays or imaging in the first four to six weeks. Again, the red flags are such things as signs of cancer or infection, cauda equina, trauma, or ruptured abdominal aortic aneurysm. Why is it important not to image? Because of studies showing that there's a lot of false positive findings. In those with no symptoms or over the age of 60, 90% had degenerative or bulging discs, 36% had herniated discs, and 21% had spinal stenosis. So if imaging was done in those situations, it might lead to unnecessary surgery. It's important to consider activity and work restrictions with low back pain. Bed rest is not recommended. It's really important to consider staying at normal activities or a gradual return to normal activities, depending upon the severity of the condition. In the Cochrane Review, they noted that there was a small benefit to stay active alone in acute nonspecific low back pain. And there's no evidence that advice to stay active is harmful. There are many medicines available for low back pain, but there are a few that are known to be a benefit. The primary one would be the NSAIDs. For acute low back pain, there's good evidence that this is beneficial. In subacute, chronic, or post-op low back pain, there's modest evidence that this is useful. And it has been noted that acetamethophen is inferior to NSAIDs, but if someone has risk factors for coronary artery disease, excuse me, cardiovascular disease, they may need to take acetamethophen instead of the NSAIDs. Muscle relaxants may be used as a second line agent after the NSAIDs for moderate or severe low back pain. Opioids are not recommended. However, they may be used with severe pain for short duration, depending upon the actual case. Corticosteroids has modest evidence that they may be beneficial for acute radicular pain. Lidocaine patches have been used for low back pain, but there's no recommendation that it should be used for acute low back pain. Capsaicin topical agent can be considered for short-term use in acute low back pain or for temporary flares in chronic low back pain. There are other medications that are widely used. However, they should be considered with the evidence in mind when determining whether or not to use those in the clinic. Physical modalities are often used and there are some benefit. Low stress aerobic exercise, such as a graded walking program, is of the most benefit. Manipulation or mobilization can selectively be used after NSAIDs and exercise for chronic low back pain if there's not a significant improvement. There's insufficient evidence to make other recommendations. Traction is not recommended. Myofascial release has no recommendations because few studies have been done and so there's insufficient evidence. PT or OT is recommended, but there's insufficient evidence. This is often because studies that have been completed were weak in their evidence because there were usually multiple modalities that were used so concluding about a particular modality was not really able to be done. PT and OT may be useful for four to six visits, although mostly in those who would otherwise have resolved their symptoms on their own. So in conclusion on low back pain treatment, over 70% of back pain will be nonspecific low back pain or lumbar strain. It's important to look for red flags during the evaluation as well as to complete a comprehensive history and physical evaluation. Avoid imaging unless there's red flags or if the radicular signs and symptoms have not improved over four to six weeks. Patient education is very important. Continuing normal activities as tolerated is key to recovering from low back pain. Surgical consultation can be considered if a radiculopathy is not improving and this would be specifically for discectomy considerations. Moving on, looking at upper extremity cumulative trauma disorders. Tendon disorders, nerve disorders and neurovascular disorders. These are often seen in occupational medicine. Generally considered to be degenerative rather than inflammatory would be the tenosynovitis, the tendonitis, lateral and medial epicondylitis, rotator cuff tendonitis and ganglion cysts. It's important to separate out by location and try to narrow down the diagnosis and what is going on. So again, the history and physical examination will be essential. In general treatment would include NSAIDs and physical therapy. Corticosteroid injections may potentially be of use and work modifications will be important to prevent repetition of forceful and awkward postures that might be impacting the presence of the disorder. Some of the nerve and neurovascular disorders include carpal tunnel syndrome, which impacts the median nerve. Cubital tunnel syndrome, which impacts the ulnar nerve. Thoracic outlet syndrome, which is a group of conditions that's caused by pressure on the nerves or blood vessels by the ribs, neck muscles or clavicle. And vibration syndrome, which is also known as hand arm vibration syndrome. This can manifest with vascular symptoms such as Reynolds disease, with tingling, numbness and pain in the fingers. Looking a little bit more closely at carpal tunnel syndrome, this is median nerve entrapment in an anatomic compartment. It's where the carpal tunnel is created in the wrist. So the median nerve and the flexor tendons are in a very small space and anything that results in a decrease in that size of that space can result in the carpal tunnel syndrome development. There are non-occupational causes to include diabetes, hypothyroidism, obesity, rheumatoid arthritis and pregnancy. It's more common in females. There's clear occupational associations with repetition plus force and awkward posture. Common work includes hand tool use such as in carpentry, meat packers and boning, manufacturing and assembly line. The median nerves by sensation to the digits as illustrated in the picture. So the thumb, ring finger, half of the ring finger, middle finger and the index finger on the palmar aspect as well as the back of those same digits. It also does some muscular innervation in the thumb area, which is why it can be seen with senior atrophy in severe cases. Again, clinically, there may be intermittent hand paresthesias in the median nerve distributions. It can interrupt sleep and cause morning awakening. It isn't unusual for people to say that they woke up in the middle of the night and shook their hands to make the symptoms go away. It can be precipitated by things such as driving, smoking, drinking, smoking, drinking, smoking, drinking, it can be precipitated by things such as driving, use of the phone or gripping, dependent upon the posture and the force that's used in those activities. If there's motor weakness, it's a late sign because the median nerve is 90% sensory. People suffering from carpal tunnel syndrome may drop small things like pencils because of the sensory issue rather than the motor issues initially. Carpal tunnel syndrome is very common and it's associated with both non-occupational and occupational reasons. It can even be seen due to age, so good history is very critical. Factors that aggravate it include highly repetitive flexion, extension of the wrist, high force gripping and grasping with pinch, vibration, vibration, such as with a jackhammer, prolonged static flexion, extension, although there's less data on this activity. Occupations at risk include meat, fish and poultry workers, garment workers, assemblers and electricians. Nerve conduction studies may be abnormal in the general population with no symptoms may be abnormal in the general population with no symptoms being present. So it's really important to make sure that if electrodiagnostic studies are done, that it is quality tests that are completed. The median nerve which has increased motor sensory latency across the wrist and EMG could show de-innervation of the thinner muscle, specifically the abductor pollicis brevis. It's not recommended for initial assessment to confirm the diagnosis because usually the diagnosis can be made from the history and physical examination. Splinting is often done primarily at night, but also in other non-work times and work restrictions would be important to avoid high force combined with repetitive hand gripping or pinching and avoid use of high acceleration vibrating handheld tools. Exercise is not recommended for acute or subacute. Corticosteroid injections can be completed in carpal tunnel for primarily subacute and chronic carpal tunnel syndrome. It may result in improved symptoms that only last for up to six weeks, but it is a good indication that surgical intervention may be useful in that particular case. Physical therapy is not recommended unless there is coexisting wrist or flexor tendonitis. And again, surgery might be useful, especially if there's positive EMG findings and or clear weakness in the thumb. And if there's persistent symptomatic sensory complaints. There's no recommendations for or against ultrasound or MRI to use for diagnosis in carpal tunnel syndrome. Cubital tunnel syndrome is the second most common nerve entrapment condition after carpal tunnel syndrome. It is entrapment of the ulnar nerve often in the cubital tunnel or the condylar groove. The pain is in the medial forearm with numbness and tingling of the fourth and fifth finger, such as demonstrated on the picture of the hand and the elbow. It may worsen with elbow flexion or pressing the elbow against the surface. There's weakness in the intrinsic muscles of the hand when it's a very severe case. This would include decreased fifth finger abduction. There may be tenderness over the ulnar groove and the tunnels may be positive at the elbow. Risk factors for cubital tunnel syndrome have not been clearly defined, but it's felt to be that it's due to hyperflexed elbow position, repetitive and forceful torque of the hand and arms, such as use of screwdrivers or power tools. It can be diagnosed with nerve conduction studies showing a slowed conduction velocity across the elbow, though its norms are not as reliable as those for carpal tunnel syndrome. Ultrasound or MRI may be helpful if it shows swelling of the ulnar nerve across the elbow. Treatment of cubital tunnel syndrome would include activity modifications to avoid the hyperflexion, the use of the elbow pad, especially in situations where someone may be resting their elbow against the surface, and NSAIDs. Night splints may also be of use. If there's no improvement, the person may need surgery, which would be an ulnar nerve transposition. Radial styloid or de Quervain's tenosynovitis can be frequently misdiagnosed, at least initially, with carpal tunnel syndrome due to the location. It's similar to trigger finger in that the tendon is entrapped and motion becomes difficult with a thickening tendon. It occurs when the tendons that move the thumb up or down in the middle of the thumb and the tendons that move the thumb up or outward become painful and swollen. Symptoms are most commonly reported with repetitive gripping and twisting motions of the wrist. It can be seen in jobs that have a lot of thumb action. When there used to be manual pipetting, that was an issue. Blunt trauma or direct pressure may also be involved. And the pain is over the radial styloid in the first dorsal compartment. Most commonly, the abductor pollicis longus and the extensor pollicis brevis are involved. The Finkelstein's test, which is grabbing a flexed thumb and doing ulnar deviation of the wrist can result in pain and would be positive then for de Corbin's tenosynovitis. Usually the pain is quite severe. Treatment would include thumb spica splint and possibly corticosteroid injections. Lateral epicondylitis is also frequently seen. This is a gripping and extension of extensive repetitive use of the forearm muscles. It includes hammering, gripping and twisting. So the hand is flexed and extended using the elbow with the wrist is held stable. There also could be sustained extension of the wrist. The extensor carpi radialis brevis stabilizes the wrist when the elbow is straightened. And it may result from a tendinopathy rather than inflammation with micro tears in that muscle. The pain is in the lateral elbow and the wrist is extended against force and in supination. It is seen occupationally in laborers, plumbers and electricians. It's also seen in those doing ultrasound in the obstetrics area because of the posture and the high number of repetitions that's often seen in that career. Non-occupationally, of course, it's also known as tennis elbow. There's also increased risk in those that have obesity or who are smokers. Recommended treatment include NSAIDs, restrictions to include no high force gripping or pinching or use of vibrating handheld tools. An elbow band is also usually very important in treating lateral epicondylitis. This takes the force off of the epicondyle as it compresses the soft tissue. Iatrophoresis may be useful. This is ultrasound with the use of corticosteroids. It would not be the first line of treatment, however. All right, that was a very short look at musculoskeletal disorders, but it will give you an idea of some of the things you might need to consider as you study for the examination. Looking at another very important topic which is metal toxicity. There's lots of metals that are used in the occupational setting that can cause potential diseases. It's a very critical topic for occupational medicine. It includes lead, chromium, arsenic, mercury, cadmium, phosphorus, beryllium, and nickel. Things to consider in exposures would be the root of exposures, the length of time of the exposed, the quality, quantity of the exposure. All of those things are important to consider when looking at whether or not symptoms that a person reports could be due to an exposure to a metal. Another consideration is coexisting exposures. Oftentimes, it's not just one metal involved, or if it is one metal, there might be solvents or other agents in use, so it's important to consider that. There's also individual factors to include age, gender, genetics, coexisting pathology, and the nutritional state of the individual. There's some difference between acute and chronic exposures. Acute is usually due to the physiologic or biochemical changes in the nervous system and do not involve degeneration of the neurocellular elements. It's often after a single high-level exposure, and it's fortunately usually reversible. Chronic exposures may result in symptoms from repeated lower-level exposures. They may not be reversible. The pathophysiologic alterations occur of the structural elements of the nervous system. Lead is an important source of exposure to be considered in both the workplace and outside the workplace. Lead is used and seen in demolition and construction, such as with bridge workers, housing renovation, such as with paint removal or plumbing alterations, in mechanics, at the auto shop, with smelting and refinery workers, with rubber and plastic manufacturing, and with battery manufacturing. The primary source of lead exposure for children also include the deteriorating lead-contaminated paint dust, lead-contaminated soil, and, as we've seen in the more recent past, the important consideration is the water pipes. Lead was taken out of gasoline in the 1970s and it was taken out of paint at the same time. It was very obvious that there was improvement in the lead-lead level seen, as this graph indicates. Lead is usually seen with lung exposures because of the generated dust that's inhaled at the workplace. Leading can also cause exposures in both children as well as workers. It's distributed in different tissues in the body, so the blood and red cells do have the presence for approximately a 30-day half-life. The soft tissue, it can be seen a half-life of one to two months. Bone is an important area of collection of the lead, as the half-life can be 10 or more years. Lead unfortunately also crosses the placenta. It's primarily excreted in the urine, approximately 70% is excreted in the urine, but it also goes through bile, skin, hair, nails, sweat, and breast milk, and what isn't excreted is absorbed in the bone. The mechanism of injury of lead exposure shows that there's both CNS and PNS involvement, disruption of neurotransmitters, axon degeneration and segmental demyelination, and degeneration of neurons. Acute encephalopathy can be seen with high blood levels, such as over 150 micrograms per deciliter. More commonly see a subacute or chronic encephalopathy with cognitive, functioning, and mood impact. The peripheral neuropathy scene is primarily motor. The symptoms of lead toxicity are, as noted, acute exposure is unusual, but can happen. It would be seen with headache, nausea, abdominal pain, constipation, possibly ataxia or encephalopathy. If the exposure level is really high, such as 90 micrograms per deciliter, encephalopathy and seizures can result. Subacute or chronic exposure is what is more often seen. It's dose dependent and it impacts multiple systems. Commonly it might be seen with headache, irritability, fatigue, myalgias, decreased concentration and abdominal colic and constipation. The neuropathy is more motor than sensory, so both wrist and foot drop can be seen. The reproductive impact of lead could include spontaneous abortion and reduced sperm production. The nephropathy scene is very prominent in lead toxicity. It causes gout and hyperuricemia with reduced urate and uric acid excretion. Hypertension will ultimately result with long-term renal damage. Lead gum lines occur with lead exposure to the gums in reaction to the sulfur that's produced from the oral bacteria. This is rarely seen in the U.S., but has been seen in other countries in the recent past. Surveillance is important for lead exposures. Russia does have a standard, although it's felt in general that it is not up to date on the allowable levels and should be much lower than what it is. Currently medical surveillance is required if there's over 30 days of exposure to the action level. There's removal from the workplace required if the blood lead is over 60 micrograms per 100 grams. The action level is 30 micrograms per cubic meter of air averaged over 8 hours. There should be no exposure to levels greater than 50 micrograms per cubic meter. Lead surveillance testing includes whole blood lead levels, which indicates the soft tissue levels. The zinc protoporphyrin, or ZPP, which is elevated when the Hame synthesis is impacted by lead. CBC and peripheral smear, BUN, creatinine, and urinalysis also provide important information. The blood lead is an indication of recent exposure from days to weeks, and it's recommended to maintain workers at less than 10 or 5 micrograms per deciliter. Chromium is the next metal. It's used in electroplating, metal smelting industry, textile and paints, and medical devices. The toxicity is according to the valence state, so chromium-6 is associated with lung cancer. It's absorbed by the GI system, by the respiratory system, and thermal. Chromium is an immune sensitizer. It causes skin allergy and irritation. It can cause painless skin ulcers, such as the chromium holes with the nasal septal perforation that was seen especially in electroplaters who inhaled the chromium chronically. It's a pulmonary irritant and can result in lung cancer. It can cause renal tubular acidosis and hepatic necrosis. The presence of lung cancer was what resulted in the OSHA standard in the recent past, so that we would see limited hexavalent chromium exposure. Arsenic is a very important agent of exposure. This is seen both in the workplace and outside of the workplace. Sources are air, food, and water. It can be picked up in things such as rice and has even been found in apple juice. It's in many water supplies. The toxicity depends on the chemical type, the valence, the solubility, and the physical form. Chemical exposures can be seen in metal smeltering, such as with lead, copper, and gold, the coal industry, and potentially in the semiconductor and glass industry. It's absorbed through the GI tract as well as the lungs and is excreted in the urine. It's usually excreted quite rapidly, so it's often hard to diagnose exposure. Arsenic can cross the placenta as well. There is an OSHA standard to regulate the exposure level. Acute exposures of arsenic result in GI symptoms, hypotension, tachycardia, and can progress to seizures, followed by cardiac arrhythmias and pulmonary edema, along with a peripheral neuropathy. Acute and chronic exposure results in fatigue, GI symptoms, peripheral neuropathy, ventricular arrhythmias. Chronic congestion can cause skin hyperpigmentation and hyperkeratosis. There's a gradation of skin impact from the hyperpigmentation to the hyperkeratosis to squamous cell carcinoma. Exposure that can result as well includes lung when it's inhaled or skin, lung, and bladder when it's ingested. The peripheral neuropathy is painful sensory rather than the motor impact that is seen with lead. Arsenic can combine with acids and create arsenic gas. This is used in the electronics industry. It can also be used in smelting and cleaning up arsenic pesticides. It causes massive intravascular hemolysis. Acutely it causes jaundice and abdominal pain and acute renal failure. Treatment would be supportive with exchange transfusion. The next metal would be mercury. It comes in different forms. There's elemental mercury, which is a metallic quicksilver. It's most commonly found in the industrial setting. It has been used sometimes only historically in electrical switches, thermometers, dentistry, barometers, batteries, silver and gold extraction. Inorganic mercury is the chlorides and oxides found in disinfectants, explosives, wood, preserves, and folk remedies. And organic, which would be the methyl or dimethylmercury, is mostly found in marine life from contaminated ocean and fresh water. The mechanism of injury depends upon the form of mercury. The methylmercury is very lipid soluble and readily crosses a blood-brain barrier. So the primary target organ is the CNS with atrophy and edema. Elemental mercury primarily also affects the CNS in chronic exposure to mercury vapors and also can see a peripheral neuropathy. Elemental mercury is liquid at room temperature. The inhalation exposures result in 80% absorbed, so quite high. Typically, it can cause cough, a metallic taste, stomatitis, chest tightness, bronchitis, chills, fever, and weakness. Chronic exposure causes a triad of tremor, gingivitis, and neuropsychiatric symptoms. The Mad Hatter's term came from hat makers in the 18th to the 20th century who used mercury to treat fur that was used to make felt hats. They would have a constellation of neuropsychological findings, including restlessness, irritability, and irrational behavior. They would go from very talkative to very depressed and morose with explosive anger. They would have a tremor that would start as a fine finger intention tremor, but could progress. Elemental mercury also causes sensory, neuropathy, and renal disease. Inorganic mercury isn't usually seen, but it can be a GI and upper airway irritant. It comes from cinnabar, which is a stone from which mercury ore is extracted. Inorganic mercury is chlorides and oxides of mercury. Again, it can cause GI mucosal irritation, causing necrosis, so they might present with bloody emesis and diarrhea. It also causes stomatitis and can result in renal damage. Organic mercury is methylmercury and other short-chain alkyl groups. The algae and bacteria take up the mercury in the water and bioconvert it to organic forms, which then bioaccumulates upward in the food chain. It's absorbed very well in the GI tract. It's lipid-soluble, so it crosses the blood-brain barrier, placenta, and is excreted in breast milk. CNS symptoms include numbness, ataxia, tremor, constriction of the visual fields, hearing loss, rigidity, and spasticity. Unfortunately, there have been several well-known cases of organic mercury toxicity. In Minamata Bay in Japan in the 1930s to the 1960s, a vinyl chloride manufacturer discharged organic mercury into the bay. The microbes converted it to the methylmercury with fish bioaccumulation, and pregnant women ate the fish, which resulted in CNS effects in their children. This included cerebral palsy-like symptoms, microencephaly, intellectual impairment, seizures, and nephrotic syndrome. In the 1950s to the 1970s in Iraq, seed grain that was used to make bread was treated with a fungicide that included mercury. It caused psychomotor disabilities and seizures in over 50,000 individuals. In just 1971 to 72 alone, there were 6,500 poisonings and 450 deaths due to this seed grain. Cadmium is used very often for the coloring of plastics and other items. Exposure happens through fumes and dust inhalation. It can be seen in mining, smelting, and manufacturing. Again, it is used in the manufacturing of colored pigments for plastics, paints, glasses, and ceramics. It's also used in electroplating in the automotive, aircraft, and marine equipment industries. It's used in fabrication of light or heat stabilizers for PVC and nickel cadmium batteries. Non-occupational exposures can occur with ingestion, although it's rare that there are cases of ingestion because less than 25% of it is absorbed. Chronic cadmium exposure has been seen to occur from cigarette smoke. Cadmium is very bad for the kidneys. Think about that, if nothing else. In acute exposures, it can be fatal with fume inhalation, and both hepatic and renal insult happens. Chronic exposure can cause significant issues. It causes a proteinuria, so excretes low molecular weight proteins. It progresses to renal tubular acidosis and Fanconi's nephropathy. The calcium wasting nephropathy and renal stones occur. It's also carcinogen and causes both lung and prostate cancer. It causes osteoporosis and osteomalacia, which is seen in Japanese women following rice field contaminations. Beryllium is very light, very strong, so it's used in the aerospace and nuclear industries as well as metal reclamation. Exposure occurs by inhalation, ingestion, and the skin, but it's poorly absorbed. It's a risk to household contact of workers as well. Sensitization may be delayed by years. There's an important screening test, the beryllium-specific lymphocyte transformation test. This screens for asymptomatic sensitization, which is very important to detect, because 40 to 60 percent who have sensitization will go on to develop chronic beryllium disease, so it may result in job reassignment and monitoring. Acute exposure can result in an irritant effect. It can also cause lung cancer and interstitial lung disease that looks like sarcoidosis. Skin contact can cause irritant or allergic dermatitis. Chronic beryllium disease, again, is very important to detect sensitization early on to try to avoid the development of this disease. It's a type four reaction. Symptoms include cough and exertional dyspnea. It causes non-caseating granulomas of the lung and the skin. It can have either obstructive or restrictive PFT findings, and the chest x-rays, such as this one here, can have bilateral infiltrates that are either linear or nodular. OSHA does have a regulation and requires medical surveillance, which includes the BLPT test. And our final metal is nickel. This is used very commonly, and it has an important impact because it causes allergy and contact dermatitis. There's approximately 10 percent sensitivity in women due to jewelry contact and 2 percent sensitivity in men in the U.S., so it's really important to determine if it's occupationally related or if it was general population exposure that caused issues with nickel. Again, it's used in jewelry, metal plating. It does cause a dermatitis. It can also cause asthma if their nickel salt fumes are inhaled, and it can also cause cancer of the parent nasal sinuses and lungs. So these are some of the very important metals. Other metals can also be important, and especially in a clinical practice, it might require really investigating what metals a person is exposed to and what are the symptoms and really delving into etiologies, and that's why the history and the physical will be very important in evaluating these exposures as well as any other occupationally related exposure. The next topic within the occupational injury and illness would be the neurological system. There are basic principles in neurotoxicity that we need to consider. First is a basic what the neural nervous system features are. The central nervous system includes the brain, spinal cord, and the optic nerves. The peripheral nervous system is the somatic and the autonomic divisions, with the somatic being the cranial nerves except the optic, the spinal nerves, the dorsal ganglia, and the peripheral nerves, and the autonomic is the parasympathetic, cranial and sacral nerves, and ganglia sympathetic. There's a wide variety of mechanisms of injury in the nervous system with agents working at different sites. Some agents have affinity for specific sites within the nervous system. There's an incomplete understanding of most neurotoxic diseases, but there are basic principles. There are dose thresholds that usually need to be met to have an impact of toxicity. Usually the findings are symmetrical. A temporal relationship is very important. And always remember that one toxin may cause multiple neurologic impacts such as lead. Solvents are widely used in paints, adhesives, glues, plastics, textiles, and many more industries. The solvent is any substance that dissolves another substance resulting in a solution. There are over 30,000 solvents in use for cleaning, degreasing, thinning, and extracting. They're very important in industry and they're very important for assessments within the clinical occupational medicine setting. Organic solvents do have neurotoxicity. Almost all volatile lipid soluble organic chemicals cause a general depression of the central nervous system. Organic solvents can be carcinogenics, they can be reproductive hazards, and they can be neurotoxins. Examples of neurotoxins would be n-hexane or toluene. Industrial exposure or volitional abuse can occur and possess acute narcotizing effects. Using glue can cause a reversible encephalopathy. There can be chronic industrial solvent inhalation syndromes such as painter's syndromes with exposures that occur for 10 plus years and result in headaches, dizziness, mood, and personality changes, inattentiveness, forgetfulness, and depression. The sensory motor polyneuropathy may also occur with organic solvent exposures. Here are a few examples of some classic solvent-induced disorders. N-hexane and methyl N-butyl ketone can cause peripheral neuropathies. N-hexane is used in the production of glues and adhesives, shoe and furniture manufacturing, and precision industrial grinding with diamond dust. Chronic exposure can result in the sensory motor polyneuropathy. Benzene can cause aplastic anemia and leukemias. Benzene is naturally occurring in volcanoes and forest fires, but it's used in many industries such as to make plastics, resins, lubricants, and dyes. Methylene chloride can cause acute MIs because carbon monoxide is formed in the bloodstream. Methylene chloride is used in such things as paint stripping, metal cleaning, degreasing, and other processes. It's also considered a potential carcinogen. N-tetrachloride is a myocardial sensitizationer and can cause sudden death. It's used as refrigerants, fumigants, and fire extinguishers, and it is also likely a carcinogen. There are central neurotoxicants, and we have mentioned some of these when we discussed the metals. So lead can cause encephalopathy, seizures, and cognitive problems. Manganese can cause Parkinson's. Mercury can cause ataxia and a tremor. Solvents can also be central neurotoxicants, including carbon disulfide, which causes Parkinson's, and carbon monoxide, which can have neurological sequela when there's carbon monoxide poisoning. There's also peripheral neuropathies that can be seen. The cause can be metals. Again, lead can cause a neuropathy, motor, more than sensory. Arsenic causes more the sensory neuropathy that is very painful. Mercury also causes a sensory and can cause a tremor and ataxia. Thallium can cause a neuropathy. It's not used in the United States, however, it used to be used in rat poison. Organophosphate pesticides cause a delayed dying back peripheral neuropathy. With the peripheral neuropathies, the findings are really dependent upon the toxin of the exposure. So again, it can be sensory, such as a symmetrical numbness and tingling from the acrylamide or thallium, or it could be a motor and result in weakness, such as from the N-hexane or the organophosphates. There are four big agents that can cause Parkinsonism. Carbon disulfide, which is a solvent used in rayon manufacturing. Carbon monoxide, again, sequela of a high exposure. Manganese, which has been known to cause Parkinson's in metals production and more recently was also recognized in welding. MPTP is not seen in the occupational setting. This was seen in an incident with people trying to make their own Demerol. Moving on, we're going to talk about hearing loss. Before we talk about hearing loss, we have to talk about sound. Decibel is a measurement of intensity of sound. It's weighted on the A scale to correspond to the human ear's response to sound. Personal speech occurs at sounds of intensity of 50 to 60 decibels. If the sound is over 85 decibels, it may be harmful to the hearing. Hertz is a measurement of the frequency or pitch, so it's in waves per second. The hearing threshold is from 250 to 5,000 hertz. And remember that the area for understanding speech is from 500 to 3,000 hertz. And the duration of exposure to sound is very important. Noise is any unwanted or undesirable sound. So 25% of the U.S. workers that are exposed to 90 decibels over a working lifetime will develop hearing problems. 90 decibels is the OSHA permissible exposure limit. Socioacusis is the nonoccupational noise exposure that can occur from guns, motorbikes, music, or other loud noise sources. It's important to consider both that and presbycuspis, which is hearing loss due to aging, when determining if there was work-related hearing loss or not. And again, engagement in conversational speech requires the ability to hear at the intensity of 50 to 60 decibels. Hearing loss is insidious. It may not show up until 10 plus years after the initial exposure. Combined exposures to noise and physical or chemical agents have synergistic effects on hearing loss. Examples include vibration, organic solvents such as styrene, carbon monoxide, ototoxic drugs, and some metals. So the hearing loss that is seen is resulting from damage that's medial to the ossicles and the staphyl-medial plate. It's in the cochlear, which is the inner ear. The noise causes irreversible damage to the hair cells in the organ of Corti. The initial hearing loss is at the higher frequency. So it usually starts at the 4,000 hertz level. This is important, as you remember, because the area where speech is understood ranges from 500 to 3,000 hertz. So this initial loss is outside of that range, and one of the reasons why it might be a while before it's noted that there's a hearing loss. In the pictures, the normal hair cells on the side showing on your left, showing that there's a full set of hairs running through the cochlea. On the right side, it's showing that there is loss of a lot of the hair cells. So when somebody suffers from sensorineural hearing loss, they may have an inappropriately loud voice. They maybe have a reduced ability to discriminate speech. Consonant sounds are high pitches, so they may have those easily confused. Tinnitus is common to be present. The problems are with the speech acuity more than the volume. So that's why standing hearing aids have little effect. So this is what you would see in an audiogram, which is very important to be able to interpret, both for the examination as well as for clinical practice. Again, classically, the notch is seen at 4,000 hertz as the initial step, and then it's easy to see that it is at least the start, if not the progression of a hearing loss that's related to noise-induced, versus hearing loss that's due to old age would be a continuation of a downward slope rather than the upward notch towards the end. So the higher frequencies, such as at 8,000 hertz, and the lower, from 500 to 2,000 hertz, are frequently, at least initially, spared. And then as the noise exposure continues, unfortunately, the hearing loss can continue and spread. OSHA does mandate a hearing conservation program. It has multiple elements, and these elements are classic for what most of the OSHA standards have as far as topic areas. So in general, for all OSHA standards, be aware of what is often covered throughout each one of the standards, and we'll talk about OSHA standards in a little bit. But it includes the work site surveillance, and this would be the supervisors and other people, safety professionals, doing visual inspections and noise measurements and analysis. It includes the medical surveillance, which would be doing the autometric testing. It includes employee training, engineering controls, hearing protection, and record keeping. The medical surveillance for the noise-induced hearing loss would be reviewing the audiometric testing and looking for a standard threshold shift. This is equal to or higher than 10 decibel shift in either ear, and it's OSHA recordable if it's over or equal to 25 decibel shifts in one ear when averaged among the 2,000, 3,000, and 4,000 hertz findings. And the standard has very clear information under the medical surveillance as far as what to do and the potential for retesting before determining if there's a standard threshold shift. So that would be important for you to be familiar with that. Our next topic under the occupational injuries and illnesses would be cancer. Cancer has been mentioned already, and this will just take a look again at some of the cancers that are associated with the occupational setting. Again, a good compilation of data is incredibly important. The medical history, the physical examination, workplace data, and sometimes even doing a literature review is very important if someone shows up in the clinical setting with the possibility of having a cancer that is work-related. And it's important in this to consider the Bradford Hill criteria, which would include the consistency of observations, the strength of the observations, the specificity, temporal relationship is very important as all these are, the exposure-response relationship, is it biologically plausible, and is there any experimental evidence? As an example, one person came in believing that they had balding, which was due to an exposure at the workplace. However, a review of the medical records showed that the balding was present prior to them being in the, having any exposures. So the first occupational cancer, which was described was squamous cell carcinoma. Percival Potts in the 1770s was the one who identified this, Ruge, Ruge. He identified that chimney sweeps often had scrotal cancer. It was determined that the soot collected in the Ruge, and so remained in skin contact for an extended amount of time. Polycyclic aromatic hydrocarbons, or PAHs, are also important to consider. They're byproducts of fossil fuel combustion. They are associated with lung cancer from inhaling these agents. It's seen in the soot, as well as in products such as asphalt. There are several agents which are known to cause lung cancer that are seen in the workplace, including asbestos, silica, the polycyclic aromatic hydrocarbons, the chromium compounds, nickel, and beryllium. Also important to consider is radon, as well as tobacco, when determining whether or not it is work-related or not. Again, lung cancer would present the same if it's work-related or non-work-related, although the latency is often shorter with more intense exposures, so it may affect younger persons. There are examples of multiplicative risk, such as cigarette smoking and asbestos. And the occupational association may be missed in many cases, especially since many people would go to their primary care physicians or other physicians who would not consider asking occupational history. Basalthelioma is a pleural cancer. It's highly associated with asbestos exposure and relatively rare otherwise. Exposure may be short in duration and low intensity. The mean latency is one of the longer impacts of asbestos exposure, being 30 to 40 years. It presents with pleural effusion in a mass. It has a poor prognosis and poor chemotherapy response. Occupational skin cancers may occur. Non-melanoma would be basal cell carcinoma and squamous cell carcinoma. There's also pre-malignant forms of actinic keratosis and Bowen's disease, and then melanoma. The squamous cell carcinoma is caused from UVB light and sunlight, so outdoor occupations and those that have a tendency to burn. It also is associated with ionizing radiation, pHs, and arsenic. Melanomas also are associated with occupational settings that especially are in the outdoor location, so agriculture, military, maybe need to be considered. In general, melanoma accounts for 75% of the annual skin cancer deaths, and it's seen much less occupationally than squamous cell carcinoma. Melanoma is curable if it's caught early enough. There are hematological cancers such as benzene. Benzene is used in petroleum refining and in the rubber manufacturing. Gasoline contains 1 to 1.5% benzene. The inhaled benzene is excreted by exhalation to approximately 20 to 50%, so it isn't the highest amount of absorption compared to some of the other agents. The metabolites cause marrow toxicity, and benzene results in aplastic anemia and leukemia. Leukemia is primarily the acute non-lymphocytic leukemias, but also the chronic myelogenous leukemia. Multiple myeloma can also be seen environmentally. Prior aplastic anemia and or leukopenia are not required for initiation of leukemia with benzene exposure. Liver cancers can be seen. Hepatic angiosarcoma was seen with the use of vinyl chloride monomers, arsenic, anabolic steroids, and Thorotrast, which is a contrast medium that was used in the 1940s to the 1960s. Hepatocellular carcinoma can be seen, especially following hepatitis B and hepatitis C. It is not seen in the U.S. because of the blood-borne pathogen standard put into place. Urologic cancers also can be work-related. Bladder cancer can result from PAHs, from PAHs, especially if they're smoking. Aniline dyes historically work the cause of bladder cancer. Aromatic amines such as benzidine and beta-naphthalene. Renal cell carcinoma can be seen with exposure to trichloroethylene, which is used as a degreasing solvent and also in paint remover and adhesive production. And asbestos, and there's less evidence, but it is thought to be associated with cadmium and uranium. Renal cell carcinoma is primarily associated with non-occupational causes to include smoking, obesity, and hypertension. Well, that concludes our look at the occupational injuries and illnesses. We're going to spend a little bit of time just considering OSHA standards themselves. They're very important for compliance for occupational hazard safety. So OSHA sets rules after review of the evidence. They must go through a rule-making process, so they can't make any changes except using the rule-making process. This makes sure that evidence is used, but it also delays the process and at times has resulted in standards not being put forth, such as the ergonomic standard, which was proposed years ago. Standards may require practices, methods, or processes necessary to protect workers. They may require use of personal protective equipment, and employees must comply with the regulations that are applicable to their own actions and conduct. The level of exposure is critical in determining the level of exposure to the disease. The level of exposure is critical in determining if the health of the worker will be impacted. So in determining the level, there are some important criteria that need to be met, and you should be aware of the definitions of both OSHA and NIOSH limits. The OSHA permissible exposure level, PEL, is the regulatory limit on the concentration of a substance in the air. So OSHA uses a time-weighted average, and they usually use eight hours to reflect the eight-hour work period of a 40-hour work week. PELs may also contain a skin notation, which indicates concern for dermal absorption. Many of the PELs were set shortly after the Occupational Safety and Health Act of 1970 created OSHA, so there is often concern that the standard is not set at a regulatory level that would be the most protective of workers. The PELs were based originally upon the American Conference of Governmental Industrial Hygienists 1968 Threshold Limit Values, or TLVs. TLVs are required by the OSHA Hazard Communication Standard to be in safety data sheets when available, and I'll mention safety data sheets again shortly. TLVs are not publicly available without purchasing. NIOSH created the recommended exposure limits based upon evaluation of known data on the hazard. NIOSH provides these exposure limits to OSHA directly for consideration for standard setting. These are available publicly, such as with the NIOSH Pocket Guide to Chemical Hazards, and you should be familiar with this because it covers many of the chemical hazards that are important to know about in practicing occupational medicine. For NIOSH RELs, the TWA that indicates the time-weighted average concentration used was up to a 10-hour work day during a 40-hour work week, so slightly different than what OSHA used. There is a short-term exposure limit, or STEL, that's usually a 15-minute time-weighted average exposure that should not be exceeded at any time during a work day. There's a ceiling REL, which is a value that should not be exceeded at any time. And there's an immediately dangerous to life and health, which is a concentration above which a worker may experience irreversible health effects without proper respiratory protection. Many of NIOSH's recommendations are based upon data sets years ago, such as most of the IDLH values were set in 1994, so some of this data might not be of the best settings currently. Also, it should be noted that not every agent has something such as a ceiling REL. That would be specific to hazardous agents, and you would need to look into the NIOSH information to know whether or not it did have a short-term exposure limit or a ceiling exposure limit or the immediately dangerous to life and health concern. OSHA identifies that their permissible exposure limits may be out of date and advises the use of NIOSH's RELs and the TLBs. OSHA provides information on the Cal-OSHA PELs as an additional resource, but they would not be enforceable outside of California. And it should be noted that OSHA allows states to have their own OSHA standards, as long as they're at least as restrictive as OSHA's standards, and they can be more restrictive than OSHA, federal OSHA. These are the standards that require medical surveillance of some sort, either a medical exam and or possibly testing. Some of these are applicable to agents that aren't in use anymore, but many of them are important for today's practice. So, acrylonitrile, arsenic, asbestos, benzene, blood-borne pathogens, 1,3-butadiene, cadmium, carcinogens, chromium-6, coal-oven emissions, compressed air environments, cotton dust, 1,2-dibromyl-3-chloropropane, ethylene oxide, formaldehyde, ASWAPR, hazardous chemicals and laboratories, lead, methylene chloride, methylenedianine, noise, respiratory protection, silica, and binyl chloride. The importance of any of these standards would really come down to if you are seeing workers in your practice who would be impacted and need to follow the involved regulation. When OSHA does not have a specific standard, they may enforce things under the General Duty Clause. This clause states that employers shall furnish a place of employment which is free from recognized hazards that are causing or are likely to cause death or serious physical harm to employees. An example of the use of the General Duty Clause would be in enforcing TB surveillance in the healthcare setting. There's no TB standard, although OSHA did have one planned, but they do enforce it with using the CDC recommendations for TB programs. Citations have occurred under OSHA's General Duty Clause. For example, with musculoskeletal disorders, if there's poor control of hazardous lifting, repetitive tasks, or awkward postures, OSHA did have a proposed ergonomic standard in the past which was not able to be brought forward. Indoor air quality or workplace violence would also be concerns for citations under the General Duty Clause. Along with the standards which are for specific agents, OSHA also has four very important general standards which are applied to all settings and it doesn't matter what the specific agent is. So, this includes the recording and reporting occupational injuries and illnesses, the personal protective equipment standard for respiratory protection, the access to employee exposure and medical records, and the hazardous communication standard. The recording and reporting occupational injuries and illnesses is where the OSHA recordable information is provided. It is OSHA recordable if it's a new injury or illness and an event or exposure in the work environment is a discernible cause of or contributor to the injury or the illness. OSHA has general recording criteria, especially for events or exposures that cause death which also has a time of expedited reporting required, but it also includes days away from work, restricted work or transfer, medical treatment beyond first aid, loss of consciousness, and significant injury or illness diagnosed by a physician or other licensed health care professional. That's why many employers consider it very important in the medical care of workers to have documentation of whether or not there were, for example, days away from work or what the medical treatment actually was. There are forms within that standard. The Form 300 is a log of the work-related injuries and illnesses. The Form 301 is the injury and illness incident report. These are kept by the company and copies must be provided to the employee or their representative such as the union. And then the OSHA Form 300A is a summary of work-related injuries and illnesses, and this is annually required. It must be certified by the company. It must be publicly posted for a three-month period, which is set to be February 1st to April 30th of the year following the year of the report. This would not contain anything such as names of individuals as it is just a summary, and the names of individuals would be considered very confidential. The next important general standard would be the respiratory protection, personal protective equipment. This has requirements which include a written program and an identified program administrator, assessment of the hazard, the determination of the selection of a respirator, and what was the decision logic behind selecting that particular respirator, how to clean and store the respirator, the medical clearance, which is an important part of it, making sure that the person medically can wear the mask without any harm. Fit testing is also required, training of the respirator operator, and also required training of the employee and replacement options. The other important standard would be access to employee exposure and medical records. So, the employee medical records need to be maintained for the duration of employment, 30 years. It's separate from any insurance records. Access must be provided for designated representatives. There are privacy protections, and the exposure records and analysis must also be kept for 30 years. Extending the time of maintaining medical records past employment makes sense when you consider that there are latency periods that are involved with some exposures. It's also very important to realize this if you're in a clinical setting and assuring that the medical records are maintained for that long of a time period. The final standard is the hazard communication standard. This requires chemical manufacturers to convey hazard information to the employers by labels on the containers and by safety data sheets. Safety data sheets used to be called material safety data sheets, in case you've noticed that terminology used by employers. The employers must keep and maintain access for the employees to all of the safety data sheets, as well as the representatives, such as the union or physicians. There are some challenges when it's a secret ingredient that is maintained as a trade secret, but they still need to provide that information to physicians, unions, and employees when there's exposures. The safety data sheet includes information such as whether or not it's a fire hazard, known medical problems, and how to respond with first aid and other such medical evaluations. So, they're an important piece of information providing data on any exposures that might happen to an employee. The hazard communication program must be in place, which would include training on the safety data sheets and all the information contained within the safety data sheets, as well as assuring access to the safety data sheets for employees. Thank you, and good luck on the board exam.

occupational medicine

OSHA regulations

work-related diseases

low back pain

carpal tunnel syndrome

cubital tunnel syndrome

nerve conduction studies

electrodiagnostic tests

activity modifications

surgical interventions

musculoskeletal disorders

metal toxicities

occupational exposure risks

preventive measures

workplace safety