Modern Occupational Diseases Diagnosis, Epidemiology, Management and Prevention

The beginning of the 21st century is experiencing tremendous social, political, and technological changes, combined with unprecedented climate change. Recent trends towards non-standard employment, growing economic and health disparities, and the decline of unions have served to undercut worker health and safety protections. Traditional workplace hazards remain important and preventable contributors to injuries and illness while new and/or newly recognized work factors are also becoming apparent. To meet the needs of the changing times, the traditional focus of occupational safety and health on industrial hazards is shifting toward a more holistic framework that incorporates other work stressors, underlying disparities, and the interactions with non-work factors. In this chapter, the major issues affecting workers today are examined through the two defining public health crises of our time, the COVID-19 pandemic and climate change. Initial lessons and observations from these global challenges inform the direction occupational safety and health will take to protect workers and prepare for an uncertain future. 

The development of occupational epidemiology has been steadily accelerating, regardingmethodology and the number of studies being conducted. This chapter reviews the general application of occupational epidemiology and illustrates some of the various studies reported in the literature to assist in the practical application of the epidemiologic approach. The epidemiologist uses analytic tools such as the case-control method to examine the complexity of variables to understand workplace exposures to disease. The analytic methods used to examine epidemiologic data have become more sophisticated over the past several decades as the focus of occupational epidemiology has shifted to the detection of early health effects associated with low-level exposures. In the future, epidemiologists need to collaborate more effectively with toxicologists, environmental scientists and biostatisticians to improve the collection of exposure data and develop more precise methods for estimating exposure that account for metabolism and excretion of toxic materials. Continuous improvement of epidemiologic analytic methods and prevention of occupational disease and surveillance are needed.

Asbestos, due to its unique physical properties and abundance, was widely used in commercial applications at the beginning of the 20th century. By the 1930s, reports of respiratory illnesses in workers with occupational exposure to asbestos began to surface. Inhalation of asbestos leads to a localized inflammatory response that attempts to clear inhaled asbestos fibers. This inflammatory response and retained asbestos fibers are central to the pathogenesis of asbestosis-related pulmonary disease. Asbestos causes a range of pulmonary diseases ranging from benign, incidental pleural abnormalities to progressive, fatal pulmonary fibrosis to malignant neoplasms of the lung and pleura. The benign manifestations of asbestos exposure, the focus of this chapter, can be grouped into pleural and parenchymal diseases. Asbestosis is a fibrotic, parenchymal disease caused by asbestos exposure. After several decades from initial asbestos exposure, patients develop dyspnea, exercise intolerance, and hypoxia with restrictive physiology on pulmonary function testing similar to other interstitial lung diseases. The most common pleural manifestation is pleural plaques, which are localized areas of pleural fibrosis that are often found incidentally. While normally asymptomatic, they are a marker of asbestos exposure. Other pleural manifestations tend to be symptomatic and include diffuse pleural thickening and acute benign pleural effusion. This chapter discusses pathogenesis, clinical presentation, radiographic and physiologic manifestations, and management of benign asbestos lung diseases.

Silica refers to the compound SiO2, which can be found as amorphous or in a variety of crystalline forms. The most common crystalline form is quartz, one of the most abundant minerals in the Earth’s crust. Other less common forms found in nature include cristobalite and tridymite. Small particle aerosols, including crystalline silica, can be generated by many activities carried out in industries such as construction, manufacturing, and mining. Respirable crystalline silica (RCS) refers to particles small enough to remain suspended in air and be inhaled into the deep lung. Inhaling sufficient amounts of RCS causes a fibrosing interstitial lung disease called silicosis. It also causes or is a risk factor for a spectrum of diseases, including lung cancer, chronic obstructive pulmonary disease, chronic renal disease, increased susceptibility to tuberculosis, and various autoimmune diseases. These adverse outcomes can be prevented by recognizing potentially hazardous conditions and taking steps to control RCS exposures. Unfortunately, despite being preventable, silicosis continues to occur in many settings, including recent outbreaks in emerging settings. In the USA, recently-promulgated regulations by the Occupational Safety and Health Administration (OSHA) provide a comprehensive set of interventions to control RCS exposures and provide RCS-exposed workers with health surveillance for early detection of silicosis. Current treatment options for those with silicosis are limited and primarily consist of avoiding further exposure and symptomatic management, so primary prevention is extremely important.

Coal Worker’s Pneumoconiosis (CWP) was thought to be an archaic disease, but after an initial decline because of the Coal Mine Health and Safety Act in 1969, there has been a resurgence of this disease in the 21st century. For centuries, miners have been exposed to varied types and degrees of coal mine dust. Lung diseases in coal miners are caused by the inhalation, retention, and tissue reaction to the mixed constituents of this dust, which include carbon, silica, and silicates. Respirable dust particles of less than 5 microns are deposited in the proximal and distal airways and the smaller particles are deposited in the alveoli. The tissue reaction to these particles results in a variety of pathologic lesions, including coal macules, silicotic nodules, mixed dust pneumoconiosis, interstitial fibrosis, progressive massive fibrosis, bronchitis, and emphysema. These disorders are recognized primarily through occupational exposure history and characteristic radiographic imaging. With a latency of approximately 20 years, cumulative lifetime exposures appear to be most predictive of the disease severity. Prevention of these diseases should be the primary focus of the industry, the workforce, and the public health agencies. In the US, federal programs of screening and surveillance are in place and active. The treatment of these disorders as with other chronic respiratory conditions, is focused on vaccinations against respiratory infection, bronchodilator therapy when indicated, supplemental oxygen therapy when required, pulmonary rehabilitation programs, smoking cessation, vigilant observation for chronic respiratory infections, and if necessary, lung transplantation should be considered as the last resort.

Chronic Obstructive Pulmonary Disease (COPD) is a clinical syndrome defined as non- or incompletely reversible airflow obstruction associated with persistent lower respiratory symptoms such as dyspnea, cough, and excessive sputum production. The present definition probably includes more than one disease. Despite being largely preventable, COPD is often a disabling disease with accelerated longitudinal lung function loss and systemic comorbidities and is presently the third leading cause of death and one of the most important health care expenditures worldwide. While most cases are unquestionably related to tobacco smoking, it has long been suspected and is also now fairly well established that occupational and environmental exposures, as well as a variety of other factors, contribute to its causation. Most recent estimates place the fraction of COPD causation by occupational exposures at ~15% and ~30% overall and among nonsmokers, respectively. The disease occurs in workers exposed to vapors, gases, dust, and fumes at their longestheld job, and in several occupations that include miners, agricultural, cotton/textile, and construction workers, food, drink, and tobacco processors, and bus drivers, among others. There is evidence of an additive effect of occupational exposures and cigarette smoking. There is presently no evidence that treatments differ from those in widely accepted guidelines, except for the occupational interventions for primary, secondary, and tertiary prevention discussed throughout this book. This is in large part due to treatment trials having required a fairly heavy smoking history and disregarded patients’ occupations. Improved appraisal of the etiological contribution of occupational exposures should lead to progress towards disease elimination.

 Work-related asthma is a common condition that affects men and women who work in a wide range of industries. Adults can develop new-onset asthma after a latency period of months to years of exposure where they become immunologically sensitized or after an acute exposure that causes bronchial wall damage. Adults can also experience the aggravation of pre-existing asthma that may have developed in childhood but becomes worse after exposure at work to respiratory irritants. Exposure to over 300 substances., including chemicals, metals, insects, animals, plants, or fungi, have been identified that cause new-onset asthma. There are thousands of substances, as well as cold air or stress, that can aggravate pre-existing asthma. Guidelines have been developed for prompt recognition and diagnosis of work-related asthma because ongoing exposure after the onset of asthma symptoms is associated with a poorer prognosis. Both primary and secondary prevention have a role in reducing the occurrence and morbidity of the condition. The field has continued to advance with the recognition of an increased number of etiological agents, an understanding of the pathophysiology, an understanding of the prognosis and factors associated with a better prognosis, and the initiation of work on the interaction with genetic variability. Awareness of the disease by clinicians and the promulgation of allowable air standards by regulatory agencies that protect against the development of asthma at work will be essential to reduce the burden of this disease. 

 Acute respiratory infections (ARI) are infectious diseases of the respiratory tract caused by viruses, bacteria, and atypical bacteria. They range in severity and even mild cases may cause a significant reduction in workplace productivity. ARIs commonly occur in outbreaks and disproportionally impact workers in occupations where workers are in close proximity to co-workers, members of the public, or where they reside in densely populated housing. High-risk workers include those in the healthcare sector, protective service, food and meat processing, service, and education industries. A person can become infected by inhaling virus-laden aerosols, having virus-contaminated sprayborne drops impinge on exposed mucous membranes, and touching contaminated surfaces followed by self-inoculation. More than one transfer process may be involved in the transmission, and the dominant route may differ for different causative agents, environments, and activity patterns. Preventing ARI transmission in the workplace must be holistic in approach and begin with anticipation and recognition of potential risks, reinforced by the continuous evaluation and implementation of control strategies. Control measures should be layered and multiple routes of transmission should be addressed. Controls should be adapted to the specific workplace and the ARI to prevent pathogen introduction, rapidly detect cases, and promptly eliminate exposure. Prevention and control can be accomplished by promoting vaccination, improving ventilation and air cleaning, providing paid sick leave, flexible working conditions, and work-from-home options. Promoting hand sanitation and providing appropriate personal protective equipment are important but never sufficient in isolation. Occupational health professionals should partner with workplace engineers and human resource departments to design effective programs.

Malignant mesothelioma often develops because of exposure to asbestos. The global incidence and mortality of mesothelioma remain unclear because many developing countries do not report it or the data they report are unreliable. Asbestos usage increased over centuries and reached its peak in 1970s. By the 90s the use of asbestos had been banned or tight regulated in many western countries, including the U.S. Asbestos usage continues to increase exponentially in developing countries. In addition to occupational asbestos exposure, environmental exposure to asbestos and other mineral fibers can cause mesothelioma. Asbestos carcinogenesis is largely caused by the chronic inflammatory process driven by the extracellular release of HMGB1 by mesothelial cells and macrophages. In addition, germline mutations of the BRCAassociated protein 1(BAP1) gene and less frequently of other tumor suppressor genes and DNA repair genes can cause or predispose to mesothelioma. Germline BAP1 mutant carriers develop additional malignancies during their lifetime. Fortunately, several of these malignancies, including mesothelioma, are less aggressive than their sporadic counterparts. BAP1 is also the gene most frequently mutated somatically in sporadic mesothelioma underscoring the critical role of this gene in suppressing mesothelioma growth. The preventive measure aimed at reducing occupational exposure to asbestos and environmental exposure to various carcinogenic fiber effectively reduces the incidence of mesothelioma. Carriers of germline BAP1 mutations benefit from close follow-up for early cancer detection. Because they may be susceptible to asbestos carcinogenesis, they should avoid trades or living in areas where carcinogenic fibers may be present.

This chapter provides an up-to-date review of the occurrence and causes of occupational cancer based on epidemiologic studies and discusses the epidemiology of occupational cancer, the characteristics, research priorities, prevention, and surveillance. Epidemiologic methods have been very successful in documenting cancer risks associated with agents. Epidemiologic data is useful when an exposure-response relationship can be demonstrated. Examples of agents for which epidemiologic studies provide evidence of an exposure-response relationship include benzene and myelogenous leukemia. Vinyl chloride causes liver cancer which is an example of associations between single agents and rare histologic types of cancer. It is more difficult to conduct epidemiologic studies to identify cancer risks associated with complex mixtures. Studies of diesel exhaust, lung cancer, and metal machining oils are cited as having employed advanced industrial hygiene and epidemiologic methods for studies of complex mixtures. At present, less than 20 known occupational carcinogenic agents have been evaluated based on studies in humans and animals by the International Agent for Research on Cancer. Furthermore, exciting developments in epidemiologic and animal studies will contribute to identifying additional carcinogenic agents in the workplace. New biologic markers of exposure and cancer-related outcomes must be identified and integrated into epidemiologic studies. Because epidemiologic data regarding the carcinogenicity of many exposures are not available, research methods to evaluate and improve the predictive value of animal and in vitro systems must be developed. A complete understanding of occupational cancer trends will be required further to research occupational cancer risks and means of prevention.

The importance of causation of occupational diseases and the role of the International Agency for Research on Cancer (IARC) are discussed in this chapter. As a case study, the process by which silica dust was judged a known human carcinogen by IARC is reviewed. Silicosis is a chronic occupational lung disease known to be caused by inhaling crystalline silica, and the pulmonary cancer risk after the diagnosis of silicosis is a part of the IARC review of evidence. Laboratory animal evidence and mechanistic findings supporting IARC evaluation are also described. There remains a need to explore the association between silica exposure and other nonlung tumors, especially gastrointestinal cancers. The Occupational Safety and Health Administration (OSHA) developed a new regulatory standard that lowered the permissible exposure to 50ug/m3 in 2016. OSHA labeled silica as a known human carcinogen because of the IARC assessment. Occupational medicine leaders need to address several current silica dust problems such as silicosis/coal workers pneumoconiosis among coal miners, acute silicosis and auto-immune diseases among countertop workers, and intervention programs to lower silico-tuberculosis among South African miners. Future research studies need good silica dust monitoring estimates and high-quality industrial hygiene samples to evaluate the associations between silica exposure and many diverse diseases.

Arsenic is a naturally occurring element with exposures in various work settings. Arsenic exposure can occur environmentally, particularly through drinking contaminated water and ingestion of some foods. The most toxic forms are inorganic arsenic, iAs (trivalent, pentavalent), and its metabolites, as well as the highly toxic arsine gas, the latter causing hemolysis. There are also organic arsenicals in food, particularly seafood, of little or no known toxicity. Inorganic arsenic is well absorbed through ingestion and respiration and is quickly cleared from the blood, distributed throughout the body (including across the placenta), metabolized in the liver, and excreted in the urine with metabolites monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA). Most of it is excreted with a half-life of days. Inorganic arsenic disrupts numerous enzyme systems, causes oxidative stress and induces alterations in gene expression. Acute severe poisoning, rarely seen in occupational settings, is life-threatening, usually presenting with gastrointestinal symptoms and severe diarrhea that can progress to cardio-pulmonary collapse, requiring treatment in intensive care, with chelating medication. Chronic iAs exposure can lead to characteristic skin lesions, increased cancer risks (particularly skin, lung, bladder), and other cardiovascular, neurological, endocrine and reproductive adverse health effects. Assessment involves history, physical exam and urine arsenic (can be a spot sample corrected for creatinine), speciating the sample for inorganic species. This urine arsenic biomarker assesses current exposures. Treatment and prevention focus on identifying and eliminating or decreasing exposure, both in the workplace and environment. 

This chapter provides general information and educational resources that can explain methods to safely access elevated worksites in the construction industry and develop teaching and training tools from the provided content. Fatality data are presented to emphasize the dangerous nature of construction work at elevations. These data verify that falls from elevations are still the primary cause of fatal injuries in the construction industry. The NIOSH Fatality Assessment and Control Evaluation (FACE) program is highlighted throughout the chapter. The NIOSH FACE database of fatality reports identifies risk factors and recommendations for mitigating future fatal injuries. Additionally, NIOSH research activities are discussed that relate to fall prevention and protection. The activities discussed are a sample of popular fall protection techniques available to construction workers. They emphasize creating a safe working environment using ladders, scaffolds, and lifts through proper training and awareness. Proper planning, training, and practice can reduce the potential of fatal fall-related incidents from occurring. 

 In most industrialized countries, work-related musculoskeletal disorders (WMSDs) are a major occupational health problem resulting in productivity loss, employee absenteeism, and high workers’ compensation and healthcare costs. Understanding the etiology and control of WMSDs and associated risk factors is imperative for reducing the burden of this problem. This chapter is organized by five topics on WMSDs: (1) the problem and surveillance of WMSDs; (2) the etiology of WMSDs and their risk factors; (3) risk assessment methods for job-related physical risk factors; (4) risk intervention effectiveness; and (5) ergonomic guidelines and standards for the prevention of WMSDs. The authors focus on the breadth of the scientific knowledge and literature pertaining to WMSDs for occupational safety and health professionals interested in learning about the field of ergonomics. This chapter also provides anticipated future challenges in the areas of surveillance, risk interactions, risk assessments, and intervention evaluations. The research agenda for WMSDs published by the National Occupational Research Agenda (NORA) Musculoskeletal Health Cross-Sector (MUS) Council in 2018 is recommended as supplementary reading for the future direction of WMSD research.