Speaker 1 (00:01): Hello, I'm Dr. Rabeea Khan, Assistant Professor of Environmental Medicine and Public Health at the Icahn School of Medicine at Mount Sinai in New York. Welcome to this podcast series on occupational and environmental medicine. Today's episode is focused on occupational asthma. Asthma is characterized by reversible airway obstruction, airway inflammation and increased airway responsiveness. Occupational asthma refers to asthma that is directly caused by exposures in the workplace. It typically occurs in individuals who previously did not have symptoms of asthma. In this review, we will not be addressing work exacerbated asthma, which is defined as an exacerbation of preexisting asthma due to workplace exposure. The prevalence of occupational asthma varies across industries and countries. It is estimated that occupational factors contribute to approximately 10% to 15% of adult asthma cases. However, the two prevalence is challenging to determine accurately due to under-reporting and misdiagnosis. (01:09): There are two subtypes of occupational asthma, sensitizer-induced asthma and irritant=induced asthma. Sensitizer-induced asthma is caused by exposure to respiratory sensitizers, which are substances that induce an immune response in the airways. Sensitizing agents can be further divided into high molecular weight agents and low molecular weight agents. High molecular weight agents are usually proteins or glycopeptides, examples include animal allergens, for example, pigeon droppings, plant and plant products like natural rubber, latex, cereals and grains like flour and gluten, enzymes, antibiotics and even fish and insects. High molecular weight compounds cause asthma via a type-1 IgE mediated response and an immediate asthmatic response is more commonly seen. Examples of low molecular weight agents include industrial chemicals such as diisocyanates which is the most common cause of occupational asthma in many industrialized areas, acrylic, monomers, wood dust, platinum and other metal salts and acid and hydrides. Delayed asthmatic responses more commonly occur with low molecular weight agents. Low molecular weight compounds are incomplete antigens that form complexes in the plasma with proteins. Some also cause occupational asthma through non IgE mediated pathways. However, the mechanisms through which these low molecular weight agents cause asthma is not as well understood. (02:45): Sensitizer-induced asthma is characterized by a variable amount of time during which sensitization to the agent takes place, and this latency period can range from weeks to years. It varies with the type of agent and the level of exposure does impact the rate of sensitization. For instance, the latency period is short, shorter with exposure to low molecular rate agents such as diisocyanates than with higher molecular rate agents. It varies between different types of high molecular rate agents as well, sensitization to laboratory animals occurrs more commonly and rapidly than sensitization to flower. However, once a person is sensitized, even very low exposures to the agent can induce an asthmatic response. (03:33): Irritant-induced occupational asthma is non-immunologic so no sensitization occurs, and it is caused by exposure to agents that directly irritate the airways leading to asthma symptoms without a latency period. These irritants tends can include chemicals like sulfur dioxide or chlorine gas, or substances like dust or fire smoke. It can result from a single high dose exposure, which is called reactive airways dysfunction syndrome or RADS, where symptoms begin 24 hours to several days after exposure or lower dose repeated exposures. (04:12): Occupational asthma should be suspected in every adult with new onset asthma. Diagnosis of occupational asthma is made by confirming the diagnosis of asthma and by establishing a relationship between asthma and the work environment. Symptoms of occupational asthma the same as of non-occupational asthma, patients may complain of wheezing, dyspnea, chest tightness and cough, concurrent eye and upper respiratory tract symptoms like conjunctivitis and rhinitis might also occur, especially with high molecular weight compounds. As previously mentioned, onset of symptoms occurs faster with high molecular weight agents than low molecular weight agents as immediate reactions are more common with high molecular weight agents. Classically, we think of patients with occupational asthma as being symptomatic at work and improving during weekends and vacations, but patients don't always fit this pattern. Symptoms may increase progressively over the work week or they may improve in different work environments in the same job. (05:16): It is also possible that the sensitizer causes a late phase reaction, so symptoms occur after work in the evening, or the patient may also be reactive to other non-specific irritants outside of work in addition to occupational trigger, which will hide the work-related pattern. With persistent long-term exposure, the symptoms may become chronic and lose the relationship to work. Finally, workers may not be exposed to the ideologic agent every day, and intermittent exposures make it difficult to relate the symptoms to work. Evaluation of occupational asthma requires a detailed work history of past and current jobs to assess the likelihood that the asthma is work related. Attention should be given to agents that the worker has been exposed to, levels of exposure, ventilation in the work environment and whether or not respiratory personal protective equipment is used. Certain occupations such as metal workers, automobile painters, welders, electronics assemblers, laboratory technicians, healthcare workers are known to have a higher incidence of occupational asthma. (06:31): Helpful clues that the problem is in the workplace is presence of other workers with intermittent respiratory symptoms, and onset of symptoms after changes in the work such as the start of a new job assignment or the use of a new chemical. A visit to the patient's workplace can provide invaluable information. This may involve industrial hygiene assessments, air sampling and analysis of workplace materials or substances to determine the presence of known respiratory sensitizers or irritants. The Occupational Safety and Health Administration requires that material safety data sheets are made available to workers in many industries in the United States. These information sheets list names and chemical ingredients of products that are used by the worker and may be helpful in identifying the causative agent. (07:27): The diagnosis of asthma can be confirmed by conventional means, barometry with the measurement of forced expiratory volume in one second, FEV-1, and forced vital capacity, FVC, is the most reliable way to assess for airway obstruction. A 12% improvement in FEV-1 of at least 200 milliliters after inhaled bronchodilator is defined as a significant bronchodilator response indicating hyper responsive airways. A greater than 10% decline in FEV-1 across a work shift is suggestive of occupational asthma. Non-specific broncho provocation testing with methacholine or histamine challenge may be useful, especially if barometry is normal. If the patient is still working, testing may be performed on a workday and then repeated after time away from work, at least two weeks away. An improvement in airway hyper-responsiveness after time away from work is suggestive of occupational asthma. Specific broncho provocation testing which involves an inhalation challenge with the suspected agent is a gold standard for the diagnosis of occupational asthma. However, it is rarely used as it requires specialized testing centers, it is costly, time-consuming and potentially dangerous for the patient. (08:46): Serial peak expiratory flow monitoring can also be used to assess if asthma is work related. The workers ask to record peak expiratory flow at least four times during the day or at least two weeks, which measurements are made both while the patient is at work and after work. Respiratory symptoms and medication use are also recorded. Normal peak expiratory variation is less than 15%. A decrease in peak flow by 20% or greater at work compared with values at home suggests occupational asthma. Challenges with the use of those technique include reproducibility of readings, patient compliance and effort, presence of other irritants in the environment during testing and interpretation of results. One advantage is that it can detect late responses that occur after the workday ends. Immunologic testing may also be performed to assess the patient's sensitivity to particular allergens or substances encountered in the workplace. (09:47): Skin tests with appropriate extracts may help identify the causative agent, particularly if it is a high molecular weight compound. For example, extract substances such as animal proteins will result in a positive skin test in an individual who is sensitized. A negative skin prick test with high molecular weight allergens is a good indication that the particular allergen is not responsible for occupational asthma. Skin prick testing may also be helpful for certain low molecular rate compounds such as platinum salt, but sensitivity with low molecular rate agents is lower and tests are not as readily available. IgE antibodies measured by RAST or ELIZA may also confirm exposure to a specific allergen. However, testing is available only for a limited number of agents and it's also not readily available. It's imperative to note that a positive skin or antibody tests only confirm sensitization to that agent, it does not confirm that the agent is responsible for asthma. (10:51): Pharmacologic management for occupational asthma is the same as non-occupational asthma, including systemic and inhaled corticosteroids and bronchodilator medications. The primary intervention with sensitizer-induced asthma is to eliminate the worker's exposure to the causative agent altogether. Recall that once the worker is sensitized, further exposure to even very small quantities can induce bronchospasm. The use of respiratory protection is inadequate and should not be considered an option in this case, so it's possible that the worker has to be taken out of work completely. Early recognition and removal is the best prognostic factor. This continued exposure after the onset of symptoms can lead to more severe asthma, which can persist even when the exposure is eventually discontinued. In contrast, patients with irritant-induced asthma may be able to remain in their jobs if changes are made to reduce further exposure. Options include modifications in the work environment, substituting the causative agent, improving ventilation or the use of respiratory personal protective equipment. (12:06): When the diagnosis of asthma is confirmed, the healthcare provider should advise the patient that because it is a work-related illness, the patient is entitled to file for worker's compensation. This will help cover medical expenses and lost wages. Unfortunately, the majority of patients with occupational asthma are left with some degree of impairment. For this reason, early diagnosis, removal from exposure and appropriate treatment is critical to improve outcomes for these patients. (12:38): As a recap, here are some key takeaways. Occupational asthma should be suspected in every adult with new onset asthma. Diagnosis of occupational asthma is made by confirming the diagnosis of asthma, for example via spirometry with the bronchodilator response, and then by establishing a relationship between asthma and the work environment. There are two subtypes of occupational asthma, immune mediated sensitizer-induced asthma which is characterized by a variable latency period, and irritant-induced asthma which results from exposure to agents considered to be airway irritants in the absence of sensitization. A pattern of increased symptoms while the patient is at work or within several hours of completion of a shift, and a definite improvement on weekends or vacation is common in occupational asthma. However, patients may not always have the symptom pattern. (13:36): Evaluation of occupational asthma requires a detailed work history of past and current jobs to assess for potential exposure such as unidentified vapors, gases, fumes, dust or other allergens. Early recognition and elimination of the allergen is the best prognostic factor as continued exposure after onset of symptoms can lead to more severe asthma, which can persists even after the exposure is eventually discontinued. (14:04): Thank you for participating in this activity. Please continue on to answer the questions that follow and complete the evaluation.