In this presentation, we will review potential occupational reproductive hazards as well as the impact of psychiatric disorders in our employee population. So we'll begin our discussion with a case. We have a 35-year-old female art professor who notifies her employer that she begins to become pregnant soon via in vitro fertilization. Which of the options should be the next action by her employer? Should her employer, A, insist that she take all of her family medical leave act time immediately after giving birth, B, educate her regarding her potential exposure to lead in the soldering and ceramics classes, C, prevent her from working in the soldering room due to potential lead exposure, or D, provide vocational rehabilitation so that she may become a music professor? So we'll discuss why response B is the correct answer to this question as we move through our discussion in this section. The terms teratogen and fetotoxin both refer to agents that are capable of causing damage to the reproductive and or endocrine system and or damage to a developing fetus. These agents include those in the usual categories, physical agents such as ionizing radiation, drugs such as diethylsilvastrol, which harmed the children, the female children of the women who were treated with this drug during pregnancy and put these female children at a higher risk of developing cancers of the female organs later in life, as well as antineoplastic agents. And this makes sense because chemotherapeutic or antineoplastic agents are targeted to destroy or harm rapidly replicating cells. And we know that the developing embryo is basically a ball of rapidly dividing and developing cells. Metals such as lead or methylmercury can also be teratogenic and fetotoxic. Alcohol, we'll talk about fetal alcohol syndrome, and tobacco smoke. This slide should be familiar to you from medical school courses in embryology and human development. And if you take a look at the center of the slide, you'll note that the individual bars for each developing body organ system all overlap for the most part the period between three to eight weeks of development, with some extending all the way through and in fact beyond full term at 38 to 40 weeks. So what we can learn from this slide is that most of the developing body systems are most vulnerable during the period of three to eight weeks after conception. And it's important to realize that many women may not be aware that they are pregnant. And furthermore, some women may not be sharing that they are pregnant prior to the end of their first trimester. However, it is very important for them to be aware of the potential effects of occupational reproductive hazards on anticipation of a pregnancy, as well as early pregnancy and fetal development. Furthermore, it's important to note that some body systems, including the central nervous system, are still developing even after birth. And so the effects of certain agents, including the heavy metals, are particularly important on younger children's neurological development. This slide illustrates the average frequency of adverse reproductive outcomes per 100 known pregnancies, and can be useful in counseling parents who are concerned regarding the cause of the loss of a pregnancy. Now, certainly, each parent would be very concerned about the loss of their pregnancy. But again, it is important to understand that there are average and expected background rates for these adverse reproductive outcomes. We'll now discuss some regulations that impact reproductive health policy for those exposed to potential reproductive hazards in the workplace. The Pregnancy Discrimination Act of 1978 amended the Civil Rights Act to prohibit sex discrimination on the basis of pregnancy. The Americans with Disabilities Act specifically excluded pregnancy when initially promulgated in the year 2000, but did not exclude infertility. Furthermore, the Americans with Disabilities Act, as amended in 2008, included reproduction as a major life activity, supporting that those with problems related to their reproductive capacity might be qualified persons with a disability. The Family Medical Leave Act, or FMLA, provides up to 12 weeks of unpaid leave that can be used for a disability or disease occurring during pregnancy. It can be used to care for an adopted or newborn infant, and may not apply if the employee only needs to avoid specific exposures. EE in this bullet is shorthand for employee, if you're not familiar with that abbreviation. So this is part of the answer to our review question in that we do not need to place an employee on family medical leave if that employee can be accommodated with restrictions. In the example in our case, if our art professor could function without having to perform duties that would put her at risk of occupational lead exposure, such as operating soldering or the kiln. The Johnson Controls decision was a ruling by the U.S. Supreme Court in 1991. Johnson Controls operated a lead battery factory, and had a policy limiting women of childbearing age who were not sterile from working in certain procedures due to the potential occupational exposure to lead. The Supreme Court ruled that this fetal protection policy violated the Pregnancy Discrimination Act, and further ruled that the company can't exclude only female workers from the known hazard. The court ruled that employees need to make their own decision after they have been informed of potential risks. And this then forms the basis for the correct answer to our review question at the beginning of this presentation. The art professor should be educated on the potential reproductive risks associated with her occupational exposures. Breastfeeding is a possible mechanism through which an infant can be exposed to toxicants. Toxicants can be transported into breast milk via passive diffusion, and characteristics of chemicals that contaminate the breast milk include those that would facilitate transport across membranes. And those include low molecular weight, nonpolar, and lipophilic agents. Some examples of those agents include polychlorinated biphenyls, as well as DDT, or dichlorodiphenyl trichlorethane, as well as solvents. And you'll recall that during our presentation on solvents, we discussed the various characteristics of solvents that make them more likely to cross membranes. An example would include ethyl alcohol, as well as industrial solvents, such as trichlorethane. The cartoon on this slide illustrates the classic scenario of toddler exposure to paint chips leading to lead poisoning. Maternal occupational exposure to lead or environmental exposure to lead can also result in an increased risk of spontaneous abortion, increased stillbirths, increased preterm delivery, and delayed cognitive development, as well as low birth weight. It's important to note that lead levels might increase during pregnancy, even when we have removed an employee from occupational and other exposures. In order to understand this, we need to remember that lead follows the same route as calcium. Remembering our inorganic chemistry, both lead and calcium carry a plus two valence. So lead can be stored in bone, and when a pregnant woman is using her bone calcium to form the baby's skeleton, this process can result in mobilization of lead that had been stored in the mother's bone stores. This explains why lead levels might increase, even though exposure has stopped. It's important to educate both potential parents regarding any potential reproductive hazards in advance of pregnancy planning. This is called anticipatory guidance, and is specifically included in the OSHA lead standard. It's important to note that the OSHA lead standard is quite outdated with respect to its recommendations for recommended exposure levels for pregnant women or any worker who wishes to bear children. The ones in the standard are less than 30 micrograms per deciliter of blood lead. Again, this is outdated, especially with the knowledge of current very low average lead exposures and community lead levels. So please remember that lead levels should be below 5 to 10 micrograms per deciliter. Other heavy metals, including mercury and cadmium, can also be toxic to a developing fetus. In our discussion of neurotoxic agents, we talked about the Minimata May environmental disaster where ingestion of contaminated fish, fish contaminated with methyl or organic mercury, resulted in children who were born with a cerebral hemorrhage and in children who were born with a cerebral palsy-like syndrome. In addition, cadmium through ingestion of contaminated water in Japan was also recognized as the cause of a unique syndrome of osteoporosis, kidney disease, and osteopenia called Itai-Itai or ouch-ouch disease. Cadmium has also been recognized as a teratogen resulting in decreased skeletal development in animal studies and in low birth weight. Exposure to solvents has been associated with low birth weight and preterm delivery in the infants of those who were exposed, as well as with the risk of increased spontaneous abortions in those exposed to solvents, including toluene, xylene, and perchlorethylene. Exposure to solvents has also been associated with decreased fertility, and when we were talking about solvents in our discussion of neurotoxic agents, remember we talked about properties of solvents that make it more likely for them to cross barriers, including the placenta. So it makes sense that solvents like ethyl alcohol can cross the placenta as they are lipid-soluble and often cross membranes. A fetal solvent syndrome, much like the fetal alcohol syndrome, has been proposed, and the photo on this slide is a photo of an infant born with fetal alcohol syndrome to illustrate some of those characteristics. That's what FAS stands for in the legend on that photo. It's important to remember that infants who are described to have a fetal solvent syndrome exhibit more of a developmental delay and do not necessarily have the facial abnormalities found in infants with fetal alcohol syndrome. Studies of the relationship between occupational exposure to anesthetic gases and risk of adverse reproductive outcomes, including spontaneous abortion or miscarriage, and rates of congenital malformations have shown conflicting results. One review of occupational exposure to inhalational agents published in 2003 revealed no association between occupational exposure to anesthetic agents and reproductive health effects with the exception of occupational exposure to nitrous oxide in an unscavenged operating room. This would be a situation that might occur in a dental procedure operating room, for example, where administration of nitrous oxide via mask was used as an anesthetic agent as opposed to use of a closed anesthetic agent administration system such as that used with an intubated patient. Occupational or environmental exposure to carbon monoxide in the mother has been associated with both spontaneous abortion or miscarriage and low birth weight in the fetus. As with many other toxicants, the lower the exposure and resulting health effects in the mother, the more likely a better fetal outcome. So with respect to carbon monoxide, there's a better expected fetal outcome if the mother is not exposed to such concentrations of carbon monoxide that would lead to loss of consciousness or disorientation in the mother. This slide contains other chemicals in different categories that have also been associated with adverse fetal outcomes. These include pesticides, including chlordecone or 2,4-D, which have been associated with decreased fertility. Chemotherapy agents, which have been associated with increased spontaneous abortions or miscarriages as well as birth defects. Ethylene glycol ethers, which are a broad category of frequently used solvents in applications such as paint thinners and surface cleaners, which have been associated with increased risk of spontaneous abortions and tobacco, which has been associated with decreased fertility. Up until this point, we've mainly focused our discussion on the effects of potential occupational reproductive toxicants on the mother or the female. Now we're going to turn our attention to the father or the male. In contrast with females, whose eggs or ova are formed before birth and then are released periodically during a woman's reproductive years, sperm are formed continuously through a male's reproductive years. Agents have been noted that result in decreased sperm count or motility, and these include physical agents, such as exposure to extreme heat or exposure to ionizing radiation, as well as chemical agents, such as heavy alcohol drinking or heavy use of marijuana. Heavy metals, including lead, have resulted in low sperm count, known as oligospermia, absent sperm or azospermia, as well as decreased libido, which, as you can imagine, would result in decreased reproductive capacity. One pesticide, dibromochloropropane, or DBCP, was noted as one of the first agents that uniquely affected the male reproductive system. This agent was a nematicide that was used in agricultural applications, and the workers who were exposed to it noted that they had not only an absence of sperm or low sperm counts, but that these health effects in some workers were irreversible after exposure had ceased. We mentioned chlordecone on the previous slide. It is also seen here with its brand name, Kepone, as a toxicant that affects the male reproductive system, specifically resulting in oligospermia or low sperm count. We'll now switch gears a bit into the second part of this presentation, and again, we'll begin with a case. We have a 35-year-old carpenter presenting with complaints of heart palpitations and difficulty focusing on his work duties, worsening over the past three months. The most likely explanation for his symptoms, remembering that we are now transitioning into a discussion of the impact of psychiatric conditions in the workplace, would be A, solvent exposure, B, lead exposure, C, tertiary syphilis, or D, an anxiety disorder. Again, although solvent exposure could explain his palpitations, as well as headaches or difficulty focusing, we are now transitioning into a discussion of mental health in the workplace. Likewise, lead exposure could result in headaches and potentially difficulty focusing, as well as fatigue, and tertiary syphilis, as you know, could certainly have cardiac complications. However, the correct answer to this question is an anxiety disorder, which could certainly cause irregular heartbeat perceptions by an employee and difficulty with focusing over work duties. We'll now move into our discussion of mental health conditions in the workplace. As a reminder, the Diagnostic and Statistical Manual of Mental Disorders, fifth edition, was published in 2013. So some of these categories and information might be slightly different from the last time that you reviewed these in preparation for board exams. Psychiatric disorders are just as prevalent in our working population as they are in the general population with the exception of those that might interfere with employability such as severe mood disorders or the schizophrenic psychotic disorders. This slide illustrates the general spectrum of psychiatric disorders as categorized and organized in the DSM-5. It's important to recognize the impact of psychiatric diagnoses on the work environment, particularly their impact on health and productivity. There's a well-documented association between psychiatric conditions and lost work days. And again, the largest impact is in lost productivity or presenteeism rather than frank absenteeism. And what that means is that workers may be present, but they are not focused on their work, which as you can imagine with safety-sensitive workers would be particularly harmful. Almost 10% of US adults may be affected by major depression and major depression is responsible for 200 million lost work days per year. An additional 3% of US adults, suffer from generalized anxiety disorder and women have twice the incidence of men suffering from this condition. Although some of the listed risk factors for workplace violence may seem intuitive, there is actually an evidence basis in the epidemiology to determine these risk factors. And they include working alone, contact with the public, exchanging money, and certainly working with high risk individuals. So this could, for example, include psychiatric patients and or prisoners. Regarding the epidemiology of workplace homicides, 85% of these incidents are related to robbery. And this makes sense given the information we reviewed regarding occupations at risk and situations of risk on the prior slide. Cab drivers experience the highest rate of workplace homicide, whereas those in retail sales experience the highest number of these incidents. When thinking about education and prevention initiatives, it's important to note that worker on coworker violence accounts for only 7% of homicides. And so through this, we can understand that the majority of these incidents are assaults on employees by people who are external to the work environment. Job related stress, like any other stress, is a harmful of physical or emotional response when an employee's job requirements don't match the employee's capabilities, resources, or needs. There are many risk factors for job related stress, some of which are listed on this slide, including work overload, lack of control over the job, a non-supportive work environment, unclear role or conflict in your role, and the presence of a rotating shift work schedule. You likely studied stress models in behavior and social sciences classes in medical school. And one that is commonly applied to work stress is the one in the center of this slide, the job demand control model, also called the Karasik model. This model is based on the premise that an imbalance between the demands made on a worker and the worker's ability to control or modify those demands in the work environment can lead to increased risk of job related stress. And one example of this might be back to our example of workers like Lucy and Ethel on an assembly line where you have very little control of the chocolates in that instance coming down the assembly line and you just don't have a way to address that stress. Another exhibited on this slide might be someone whose inbox as you can see is overflowing and they are pressed for time to accomplish all the tasks of their day. People who have more ability to control and more discretion over the order or the amount of work that they do may have a reduced risk of occupational stress. Most if not all of us experience the health effects of shift work during our medical training and internship and perhaps during our residencies. Shift work health effects include disruption of sleep patterns, which leads to disruption of our natural thermoregulation and circadian rhythms. The symptoms associated with trouble adjusting to shifts are listed here. And again, most of us have experienced these from time to time. Recently shift work that involves circadian disruption has been associated with development of breast cancers and has been classified by the International Association for Research on Cancer or IARC as a group 2A or probable human carcinogen. Shift work also leads to increased use of caffeine, alcohol and even prescription or non-prescription sedatives as employees try to cope with the fatigue and or trouble sleeping related to trying to acclimate to shift work. Certainly not all employees who work shifts will develop health problems or a shift work sleep disorder. Based on studies of law enforcement employees, the following measures are recommended to reduce the risk of developing shift work sleep disorder. These include rotating shifts forward from day shifts to afternoon to night because circadian rhythms tend to adjust better when moving forward in time as opposed to when moving back in time. Employees should be educated in good sleep hygiene including using room darkening shades if necessary and avoiding stimulating activities before rest and setting set sleep hours whether they are sleeping during the daytime or during traditional nighttime sleep hours. Employees should be educated to use stimulants and sedatives whether prescription or non-prescription carefully. These are often used again to cope with the fatigue and or to become more relaxed to get to sleep when adjusting to rotating shifts. Post-traumatic stress disorder as described in the DSM-5 is a reaction that goes beyond the expected natural reaction after a traumatic event. Features of post-traumatic stress include intense fear, helplessness and horror as well as the recurrent presence of intrusive thoughts or dreams, revisiting, re-experiencing or recollection of the trauma and employees self-protective urges to avoid stimuli that remind them of the trauma. For example, an employee who experienced or witnessed a violent act in the workplace might be reticent to return to the workplace after that event. Critical incident stress debriefings are one part of a critical incident management and response program that is aimed at reducing the adverse effects of a traumatic incident on employees. A critical incident stress debriefing can be led by a behavioral health professional, a chaplain or any other person who is skilled and trained in leading this educational intervention for employees. As part of the critical incident stress debriefing, affected workers, including supervisors are gathered. They are given a opportunity to discuss what happened facilitated by the leader of the critical incident stress debriefing. Their concerns should be addressed and as occupational medicine professionals, we would also include addressing concerns related any exposures included in the incident. Screening for workers who needed individual assistance would be included and that could lead to referral for those workers onto mental health services, for example, or medical services if needed. As part of a critical incident stress debriefing, the incident response is reviewed, lessons learned are gathered and this information can inform additional interventions for employees as well as inform a disaster response plan to prepare and respond to future events in the workplace. Employee assistance programs support the health and productivity of the people whom they serve. Use of these programs began in the 1940s and their purpose is to help organizations resolve productivity issues by identifying employees who have problems that could be impacting their focus in productivity and health in the workplace. These could include drug and alcohol, substance use disorders, relationship challenges, anger management issues, financial stressors, other family stressors and other mental health or psychological conditions. These programs generally include features of screening employees who are referred or who self-refer for assistance, offering a variety of levels of care which can range from peer counseling to social work to formal mental health or psychiatric referral and treatment. That concludes the section on psychiatric disorders as you may have understood from this slide. This is also no longer Dr. Liddell with a head cold but we tag team this section so I take over from here. So the next set of slides deal with occupational health and the heart and they're basically two facets to cardiac disorders in the workplace. The first and probably less important is of workplace exposures and their effect on the heart. In other words, primary causes of disease from toxicants. The issue there is that these are somewhat few and far between as we'll see and many of them have been controlled across the past couple of decades. So there are very few real heavy exposures that are causes of heart disorders in the workplace. Now, the other facet is of cardiovascular disease and its effects on work because cardiovascular disease itself is very, very prevalent and it may affect the ability of workers to continue on particularly in highly physical jobs or otherwise reduce their capacity for work and the workplace can be a focus for both diagnostic and preventive efforts. Moving first to the identification and diagnosis of occupational causes of cardiovascular disease, we find that there are great difficulties in identifying them. For starters, cardiovascular disease is very common in Western society. So to identify specific work-related risks, you see them superimposed on a high baseline of risk. Along with that, there's multifactorial etiology. So workers are obese, they have family histories, they may smoke, they may have a variety of other causes of cardiac disease and work contributions are difficult to tease out of several risk factors in an individual worker or even in a group. They're long latency disorders, they tend not to come on rapidly and until things like calcium scoring have come along, there aren't particularly very good, accurate, non-invasive tests for early disease. And lastly, as you'll see with most of the symptomatology we look at and with every other in the main occupational disease, the clinical expressions are similar whether the disease is occupational or non-occupational. So angina will look and act the same whether it's due to smoking and obesity or whether it has an occupational cause. The means by which we'll approach occupational agents and their effects on the heart is mainly by their main or major effects that can cause angina or similarly atherogenesis that can contribute or cause dysrhythmias, cardiomyopathy or hypertension. So a good way of organizing them is by the main effects and disorders they create. We'll only just touch on carbon monoxide briefly here. This is elaborated further in the toxicology lecture. So just to briefly remind you here, formation of carboxyhemoglobin from carbon monoxide will shift the oxyhemoglobin dissociation curve to the left. What that means is there's relative anoxia in the presence of carboxyhemoglobin because the hemoglobin is less likely to give up its oxygen and dissociate oxygen into the tissues. This can lead to decreased exercise threshold and if individuals have subclinical cardiac disease, they may in this case be prone to angina and related disorders. It's also of note that carbon monoxide may be directly atherogenic or accelerate atherogenesis. Workers who have been exposed to carbon monoxide in the long-term even below the OSHA PELs have developed evidence of atherosclerotic cardiovascular disease after 10 to 20 years and have an increased mortality from cardiac disease than do comparable workers without that exposure. This is an occupational exposure of historic interest in cardiovascular disease. Workers who handled organic nitrates used in TNT, trinitrotoluene and related other explosives were noted to have an increased risk of sudden death from about the 1950s into the 1960s. This seemed to be arising from abrupt withdrawal from organic nitrates. And just like in clinical medicine, these nitrates, which are essentially the same or very much the same, had vasodilatory effects in these explosive workers. Just as in clinical medicine, nitrates are readily absorbed through the skin, same rationale as putting nitroglycerin on the skin for absorption, and as well through the respiratory route. Acute exposure has the same effects. Workers develop rather severe headaches along with lower blood pressure. And since they're not being treated or generally had it, they may even develop hypotension and tachycardia along with flushing. When these exposures went on chronically, the workers began to develop what you might call Monday morning angina, which is two to three days after their last nitrate exposure. On Friday, the last day of the work shift, they began to start to have chest pain when their nitrates wore off. And so the blood vessels, which were originally dilated, appeared to vasoconstrict, and that vasoconstriction was unopposed. If they went back to work on Monday morning, they started to feel better, which is different from the usual occupational exposures where you feel better over the weekend and start to feel badly again when you come back to work on Monday. Here, the nitrates tended to relieve those angina symptoms that they were getting by vasodilatation. So many of these workers were developing angina, and some of them went on to develop MIs or sudden deaths from arrhythmias. So just to reiterate the material, in the previous slides, these acute effects started being noticed in workers in the 1950s and the early 60s, and many of them had sudden death occurrences occurring again a day, two days after exposure ceased, so over the weekends or the holidays because of the wearing off of the nitrates. They'd be relieved by return to work, so Monday morning, they might feel terrible, and after return to work and the nitrates getting back on board, they used to feel better. Autopsies would show coronary spasm in the absence of overt coronary artery disease. So these were young workers, and overall, the epidemiology showed about a threefold increase in acute deaths in these younger men from ischemic cardiovascular disease without having several lot of atherosclerosis. Most of these have been very well controlled. They're now isolated from the worker or in other cases, personal protective equipment is used, so it's unlikely that you may see this. It's of note for historical interest, particularly with respect to the physiology, which is the same as treatment of cardiovascular disease. Carbon disulfide is of interest as one of the unique compounds that causes atherogenesis, directly causing it by itself. Its use is as a variety of solvents, but in particular of interest is that it's the main solvent used for dissolving and making materials derived from cellulose. This includes the production of viscose rayon, the rayon fibers that are used to make clothing, and cellophane, which is fundamentally the same thing, except it's sort of flat and sheet-like. There are many other things it's used for. It's a solvent for making rubber, and it gets used as a fumigant, and as with many other things, it's often used in the microelectronics industry. Basically, what happens in the manufacture of viscose rayon is that cellulose from wood pulp is dissolved in carbon disulfide, so you have a very big vat of it initially, and then this mixture is then run through a spinneret, which you see in the lower right-hand side, and when that gives off, this changes from a kind of a liquidy glop form into a solid form with the giving off of carbon disulfide gas, so this is how workers can be exposed, again is from the off-gassing which needs to take place as this material turns from a liquid into a solid. As I mentioned on the last slide carbon disulfide is directly atherogenic so the viscose rayon workers were going on to develop coronary artery disease and in this case a little bit different from the workers with nitrates is that these people were found to have occluded coronaries and atherogenic plaques and in workers who had worked with the viscose rayon industry for a long period of time 10 years or more they had a greatly elevated risk of coronary artery disease death from about two to five fold and briefly although I listed here it's probably not important in terms of the boards but there's a direct role in atherogenesis in blood vessels from carbon disulfide it can chelate trace metals interfere with elastase activity and disrupt blood vessel walls and decrease fibrinolinic activity such that the risk of a clot and thrombosis is increased. This slide shows some direct evidence of atherogenesis in carbon disulfide workers these pointing to the arrow and you can see in other places our retinal microaneurysms were visible on fundoscopic exam in Japanese carbon disulfide workers. Hydrocarbons particularly halogenated hydrocarbons used as either solvents in degreasing or as refrigerants are noteworthy in causing cardiac arrhythmias and sudden death. Similarly you want to think of the same along the same lines and as in clinical medicine with anesthesia induction which is that induction is the most dangerous time for producing an arrhythmia and of course most inhalation anesthetics now are some type of halogenated hydrocarbon like halothane. Chlorofluorocarbons like freon which is now mainly banned as a refrigerant because of the destruction of the ozone layer and some other halogenated hydrocarbons like TCE are responsible for this. Aside from evidence of arrhythmias and anesthesia induction probably the best known production of dysrhythmias from the halogenated hydrocarbons are those from the chlorofluorocarbons used as refrigerants because individuals may get some inhalation exposure to these again less likely now since they've been phased out as refrigerants. What these do is sensitize the myocardium to catechol effects so if there's high or heavy exertion while a worker has inhaled CFCs or other of these hydrocarbons, sudden activity will lead to an arrhythmia because of the increased epinephrine release. There's other solvents like trichloroethylene I mentioned they're implicated in sudden death and findings at autopsy are usually unremarkable. They're clean coronaries and they're consistent with sudden death from arrhythmias. There was a scenario way way back when I took the boards of a sailor who went down to the hold of a ship to repair a refrigeration leak and was found dead by the refrigerator and so the surmise about what had happened was that there was a Freon leak, CFC leak of the refrigerant. The sailor tried to move the refrigerator that was heavy exertion, sent a catechol surge as he might require for moving that and the myocardium being sensitized. The sailor then dropped dead of an arrhythmia. This is one of the sadder episodes in toxicology and occupational health. In the 1960s it was found that the addition of cobalt stabilized beer foam so that when you poured it into a glass from the tap or bottle that nice foamy inviting looking head remained in the glass for some time. So a number of breweries started adding it to their beer mainly in Canada and Belgium. The unfortunate news was that later on cardiomyopathy was reported in many beer drinkers several months after this began. So the question is why it was seen in this population because cobalt therapy is used for anemia without any adverse effects on the heart and a couple of points to that. One is that the effect was dose related and seen in heavy drinkers. Apparently one of the perks of working in a brewery is that you get all the beer you can drink so some of these individuals were drinking up to 10 liters a day which would make me float away. But anyway they were probably getting a heavy dose of cobalt along with the alcohol. Sadly mortality was quite high in these series from a quarter to a third of the affected drinkers in some series. There's another noteworthy point. This is a case report from the Lancet of a couple of years ago in which a resident or doctor had remembered an episode of House because they were questioning why an individual who had just gotten an artificial hip started to develop a cardiomyopathy and having remembered seeing this scenario which was apparently on an episode of House, the doctor got a cobalt level which was really sky-high and made the diagnosis from there. I don't think there's any information there about the cardiomyopathy from drinking. I think they mainly referenced House alone. Moving on to hypertension we see a number of occupational toxicants that may cause or contribute to it. Lead is probably the main bad actor in causing hypertension and it probably has two mechanisms. One is via direct renal injury. It causes proximal tubule disease and eventually chronic renal failure. So this is probably the main mechanism by which it causes hypertension. Remember also that it follows calcium in physiology so because of that it may increase vascular tone and vascular resistance by its mechanism of action on smooth muscle of arterioles. If you chelate individuals it's probably only going to work in acute lead intoxication if they're hypertensive but the hypertension again probably mostly from renal damage and chelation of course won't reverse that long-standing renal damage. Cadmium also remember is nephrotoxic. There are some slides we have in the renal section of this lecture of these lectures and also associated with hypertension probably because of nephrotoxicity although it may, hypertension may occur at levels below a overtly nephrotoxic dose. A couple of other lesser-known causes of hypertension in the occupational setting. Carbon disulfide, remember causing direct atherogenesis, may cause a vascular nephropathy in the same way that it's causing atherosclerotic disease around the cardiovascular system and so this is likely the mechanism once again renally determined. Noise and shift work have been associated with hypertension not quite as readily or reliably as some of these other factors but the postulate is that there's a stress-mediated response hormonal mediator release such as cortisol and increased sympathetic release such as norepinephrine and epinephrine may be implicated in chronic hypertension from long-term noise exposure as well as shift work. Job strain as you might remember from Francesca's lecture earlier is the coupling of high psychological demands at work with low control or in other words low ability to meet the demands that are placed on you at work. There's results in stress and stressors and proceeds probably by the same mechanism as we mentioned with noise which is increased catechol release, increased release of stress hormones such as cortisol and development of hypertension, subsequent cardiovascular mortality. It's been well studied in professional drivers. If you look at this person in the picture, he's got a schedule to meet but he's not in control of traffic conditions, weather conditions, angry or irritable passengers and yet has to kind of meet the demands without just leaving or walking off the job or being able to take a break and so those that is a good example of the high demand low control type of work and they have been shown to develop hypertension as a result. Moving a little bit off occupation directly, this is the work of Michael Marmot in the UK, the so-called Whitehall studies and Marmot has showed that increased coronary artery disease and mortality relates to social status difference between jobs and so when his research group compared unskilled manual workers with professional workers who are in class one, you can see the difference in mortality. The class one workers had the lowest mortality, class three having about an average and class five a greatly increased mortality and what's interesting about this is you can say well these may be workers who smoke more, exercise less, eat more, have less medical care etc and this relationship still held when you control for all of those known covariates such as smoking and diet so there's something about continuing on in low status jobs which may have to do partly with the demand control hypothesis but may also be a function of other attributes of work that results in cardiovascular disease long-term. As I noted at the beginning of this lecture there are two aspects to cardiovascular disease in the workplace there are the effects of work intoxicants on the heart which we just saw and on this side there's the effect of cardiovascular disease on work so just to give you some figures on heart disease in the United States there's about 3 quarters of a million MIs every year and of that about 80% of workers are generally able to return to work after their initial MI if they've had an MI inadequately treated more often now they're getting angioplasty and stenting or if they go to bypass grafting. Many workers who suffer MIs or with cardiovascular disease are older they're greater than 50 or even 60 and they moved into more sedentary roles pre-infarction so the sort of the natural progression of jobs is to take them from very strenuous work into less strenuous work maybe they become a supervisor where before they used to do the hand heavy manual lifting and infarction and death are not more frequent at work than at home we sometimes have a picture of someone who's been asked to do a heavy lifting job and they have an MI on the spot but that actually doesn't occur any more than at rest or in bed or at home in a chair a longshoreman study from about 20 years or so ago showed lower rates of cardiovascular mortality that were linked to the heaviest jobs so longshoremen loading and unloading ships if their activity level was very high if they did a lot of on-the-job physical activity their cardiovascular mortality was lower and risk of sudden death lower as well than those who were sitting around and doing less strenuous jobs judging the ability to return to work after an MI or cardiovascular event can be fraught there are a few medical factors that predict return to work and also as we outlined in the back pain lecture many of the same non-medical factors that inhibit people or disable people from coming back to work are also operating with cardiovascular disease so of the medical factors the major predictors of return to work are sort of few and far between if individuals have persistent left ventricular dysfunction in other words fundamentally it's not pumping as well as it could or should be particularly if they have an element of failure along with it that will inhibit or keep people from returning to work as well if they're having persistent angina symptoms indicative of continuing or ongoing ischemia and they've been adequately treated that will also very likely inhibit people from returning to work the non-medical factors again are a little softer but really significant in return to work amongst people who have had an MI coping styles suffering an MI can lead to depression and reevaluation of one's job other aspects of one's life and that can really fundamentally affect whether or not people do want or feel they should return to work as well as whether they can progress subsequently in cardiac rehab or other types of therapy along with that goes a perception of work such as work demands or the satisfaction gotten from work and if those if demands are high or satisfaction is low then that will keep people from return the ability or aspects of the job some of these may indicate whether that's a physical job or not such as high education jobs tend to be less physical age may play a role as well and whether or not people return and like with back pain or any other disability system the benefits and incentives of the sick role of the compensation system of disability payments and the like are very much going to affect whether people return to work so these factors are probably playing a very major role in whether people do return or not possibly more so than the medical factors that that might be objectively permitting or keep we do have some objective ways of judging whether or not people can return to work after an MI and that relates to exercise testing putting people on a treadmill and seeing how they perform and some guidance is available here the dictionary of occupational titles and related material tend to list energy demands of a job and depending on what sort of energy demands have been met on a treadmill the average energy demands of that job could be about 40% of the peak workload achieved on a treadmill and of course the peak energy demands of a job should be less than the maximum workload that a post-MI patient achieves on a treadmill or testing so as an example someone who can generate about eight METs metabolic equivalents basically the moving into Bruce stage for past about nine minutes could be reasonably asked to work at a light to medium physical demand level that doesn't mean even sedentary they can be expected to pick up 20 pound things to be able to walk or stand for periods and the like and that average is out to about three or three point five metabolic equivalents and keeping them very safe at those levels so most jobs people could return to particularly the moderately demanding jobs this relates to the previous slides both in the exercise testing and the other predictors of disability a group in Sweden took post cabbage patients and put them on a treadmill half of these patients who were considered quote totally disabled by their cardiologist or by their GP based on the results of these exercise tests could have safely performed their normal job their normal job duties or some type of equivalent work based on what they scored on a treadmill test and so that suggested to them that there were a host of other factors that weren't particularly objective and might be more psychological or psychosocial inhibiting people from returning so when you're looking at the disabled individual disabled by cardiac disease obviously you want to go through the history of their treatment and consider inadequate treatment if they're not able to attain a high level of function you know are they deconditioned have they not had a good exercise program communicate with cardiologists and whoever's treating them but also think about other psychological factors such as depression consider whether accommodating or changing the non essential requirements of the job will allow return these people might be eligible for example for ADA compliant jobs or they may be able to move into accommodated jobs or less strenuous jobs and of course think about socioeconomic explanations which relate to things like the sick role or the disability benefits people might obtain a caveat however about exercise testing this is somewhat the reverse of putting people on a treadmill after they've had cardiovascular events or disease but the exercise testing of asymptomatic workers can be somewhat fraught particularly if your exercise testing younger asymptomatic individuals they might be in their 20s or 30s working in safety sensitive jobs such as firefighting or police work but because the prevalence of cardiac disease in those workers is going to be very low the predictive value of a positive test is going to be low because of that low prevalence you're going to get a lot of false positives and that high false positive rate is going to require additional workup which for the most part in the majority of people will probably go for not so what you want to do is probably be somewhat more judicious about exercise testing workers in those jobs if there's no cardiac history the likelihood that those tests will have a better predictive value will increase if you start the testing at about age 40 in particular if there are other risk factors of positive family history history of smoking overweight or obesity hyperlipidemia or other factors that may increase the risk for development of cardiovascular disease and so because one of the problems here is that you may exclude individuals who are proven healthy if you do it simply on the basis of an exercise test so you want to be careful about who you're testing and who you're saying might be at higher risk for cardiovascular disease because of the low prevalence and therefore the increased false positives this concludes this lecture thank you for listening and we'll move on to the next clinical lecture following

occupational reproductive hazards

psychiatric disorders

teratogens

vulnerability of developing body systems

regulations

anxiety disorders

job demands

hypertension

occupational toxicants

cardiovascular disease