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Diseases arising in occupational environments involve exposure, primarily through inhalation, ingestion, or dermal absorption. In the vast majority of work environments, inhalation of toxicants is a primary concern. Inhalation exposures can occur with gases, vapors, liquid aerosols, particulate aerosols, fumes, and mixtures of these. Dermal exposures are also important and can arise from airborne materials as well as liquids splashed onto the skin, immersion exposures, or from material handling.
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Additional exposure hazards exist for infectious agents. Exposures leading to occupational infections may arise through inhalation or ingestion of microorganisms, but can also arise from needlesticks in health care workers or through insect bites among farmers, natural resource workers, and others employed out of doors. Additionally, poisonings from toxic plants or venomous animals can occur through skin inoculation (eg, zookeepers, horticulturists, or commercial divers).
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Agents Associated With Diseases
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There are a myriad of agents responsible for occupational diseases. While some act on a particular organ such as the liver or kidney, others can affect multiple organ systems. Table 34-2 presents a list of the major occupational diseases and examples of agents that cause them. This is not intended to be all-inclusive. Rather it is meant to highlight what are historically the most prevalent and widely recognized occupational diseases, plus those that continue to be prevalent in the workplace. The toxicants listed are those for which there is a strong association with the disease or the most conclusive data to support causality. Examples are shown for cancer and for diseases of the lung and airways, heart, liver, kidney, skin, nervous system, immune system, and reproductive system. Several examples of occupational infectious diseases are also listed to highlight the fact that, in many work settings, infectious agents may constitute the major hazard and may coexist with chemical hazards. Most of the occupational diseases listed in Table 34-2 are associated with industrial chemicals. These are discussed in other chapters throughout this book.
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Table 34-3 lists forty agents that are known by the International Agency for Research on Cancer (IARC) to be carcinogens in humans (Group 1) and for which there has been or is currently extensive occupational exposure. This list includes agents such as asbestos, arsenic, benzene, vinyl chloride, and coal tars. IARC Group 1 refers to agents or mixtures that are known to be carcinogenic to humans based on sufficient epidemiological evidence usually accompanied by limited or sufficient animal evidence.
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Occupational Respiratory Diseases
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Because inhalation generally represents the most significant route of exposure, many of the major occupational diseases affect the lung and airways. These diseases have been studied extensively and are largely responsible for the creation of the occupational regulatory framework. Deaths due to occupational lung diseases such as asbestosis, coal workers' pneumoconiosis, silicosis, byssinosis, and occupational asthma have been recognized for centuries and led to important legislation such as the 1970 US Occupational Safety and Health Act. These occupational lung diseases continue to have significant associations with morbidity. Table 34-4 lists the crude US death rate and annual deaths for 2005 (the most recent data available) and illustrates that while the death rates are fairly low, there are still about 2460 deaths per year attributable to asbestos, silica, coal dust, and other pneumoconiotic dusts; 2704 malignant mesothelioma deaths; and 67 deaths from hypersensitivity pneumonitis. However, fatalities are just the tip of the iceberg as some occupational lung diseases are rarely fatal, yet may still be debilitating. Every year in the United States, there are 20,000 hospital discharges related to cases of asbestosis, and 188,000 coal workers receive federal Black Lung Benefits (NIOSH, 2006). The US Mine Safety and Health Administration has compiled data on inspector- and mine operator-collected samples in coal mining operations and found that 29.3% of these exceeded the PEL for respirable quartz and 7.5% were over the PEL for respirable coal dust.
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Many of the diseases listed in Table 34-2 are known by other names that refer to a particular occupation or agent. One example is hypersensitivity pneumonitis, an allergic lung disease marked by interstitial lymphocytic pneumonitis and granulomatous lesions. Hypersensitivity pneumonitis is also known as extrinsic allergic alveolitis, farmer's lung disease, bagassosis (sugar cane), humidifier fever, Japanese summer house fever, pigeon breeder's lung, and maple bark stripper's lung, depending on the occupational setting in which it arises. Although we often think of these as the same disease, it is important to recognize that the exposures and physiological responses they induce are complex and may differ in the manifestation of the disease.
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The US Bureau of Labor Statistics tracks data for nonfatal occupational injuries and illnesses, of which, there were 3.3 million in 2009. The vast majority of these were injuries, but there were still over 220,000 occupational illnesses reported in 2009 (USDL 2011c). There were 21,500 reported respiratory conditions arising from exposure to toxic agents and dust diseases of the lung. The former category includes pneumonitis, pharyngitis, rhinitis, and acute lung congestion. Table 34-5 shows data for rates and cases in 2009 by industry division. Poisonings were relatively rare, whereas skin diseases occurred at rates as high as 5.2 per 110,000 workers per year. The manufacturing sector accounted for approximately 29% of all occupational illnesses. Seven industry codes that had respiratory condition incidence rates that exceeded seven per 10,000 full-time workers were ambulance services, police and fire protection, urban transit systems, support activities for water transportation, adhesive manufacturing, grain and oil seed milling, and animal slaughtering. The relevant exposures for the first four of these are combustion products from fires and diesel engines. The rate for chemical manufacturing was much lower, 1.8 cases per 10,000 workers, down by 50% since a decade ago.
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Toxic gas injuries are often characterized by leakage of both fluid and osmotically active proteins from the vascular tissue into the interstitium and airways. Important determinants of the severity and location of injury are the concentration and water solubility of the toxic gas or vapor. Anhydrous ammonia, with its extremely high solubility, primarily damages the eyes, sinuses, and upper airways. The vapors combine with water in the tissue and form ammonium hydroxide, quickly producing liquefaction necrosis. Chemicals with lower solubility, such as nitrogen dioxide, act more on the distal airways and alveoli and take longer to induce tissue damage.
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Occupational asthma may be defined as a “disease characterized by variable airflow limitation, and/or airway hyperresponsiveness, and/or inflammation due to causes and conditions attributable to a particular occupational environment and not to stimuli encountered outside the workplace” (Bernstein et al., 2006). Data from the NIOSH Work-Related Occupational Lung Disease Surveillance System has shown that 20% of occupational asthma cases represented aggravation of preexisting asthma by workplace exposures and 68% of cases represented new-onset asthma caused by occupational exposures. The remaining 12% could not be classified (NIOSH, 2011). The US National Health Interview Survey has provided data on the prevalence of asthma based upon usual industry and smoking status (Table 34-6). These data indicate that asthma prevalence is highest in health services; general merchandise stores; food, bakery, and dairy stores; and eating and drinking places. Also high are hospitals; transportation equipment; printing, publishing, and allied industries; utilities and sanitary; furniture, lumber, and wood products industries; and chemicals and allied products. Interestingly, in some industries, current smokers demonstrate the higher prevalence, while in other industries, the higher prevalence is seen among nonsmokers. This may reflect that many people diagnosed with these conditions quit smoking.
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There are a variety of industries in which there is increased risk of developing work-related asthma. In chemical-based industries, plastic and rubber polymer precursors, diisocyanates, reactive dyes, and acid anhydrides are recognized low-molecular-weight sensitizing compounds. Biocides and fungicides used in metal fabrication and machining, custodial services, lawn and turf growing, and agriculture are also chemicals associated with occupational asthma. A number of metals can induce sensitization and asthma, including chromium, cobalt, nickel, platinum, and zinc. Enzymes pose significant risks for occupational asthma (Heederik et al., 2002). Examples include α-amylase among bakery workers and subtilisin, a protease used in laundry detergents. The enzyme production industry has had to adopt strict environmental and process controls to reduce the incidence of occupational asthma in their production facilities.
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Those working with animals or animal products are at increased risk of developing allergy (Elliott et al., 2005) and occupational asthma (Pacheco et al., 2003). Animal handlers, processors, and laboratory technicians who work with animals can become immunologically sensitized to urine or salivary proteins in many vertebrates; proteins in bat guano and bird droppings; animal dander; serum proteins in blood products; dust from horns, antlers, and tusks; or the shells of crustaceans. Very high rates of sensitization can occur in shellfish processors (Glass et al., 1998). Arthropods such as insect larvae, cockroaches, mites, or weevils are recognized inducers of work-related asthma. Plants and plant products (eg, soy flour, spices, and coffee beans) can also cause asthma among workers. In a variety of occupations, exposure to fungi, especially of the genera Aspergillus, Penicillium, Rhizopus, Mucor, and Paecilomyces, are associated with allergic rhinitis and asthma. These are especially present in sawmills, woodchip handling, and composting facilities (Duchaine et al., 2000; Eduard et al., 1992). Apart from the contaminating microorganisms, certain woods themselves produce chemical sensitizing agents. Examples include western red cedar, redwood, and some tropical hardwoods.
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Asthma emerged in the 1980s as a major occupational health concern among health care workers. In order to reduce the risk of hepatitis B and other infectious diseases, health care workers adopted the use of natural rubber latex gloves for barrier protection. Proteins from the latex of the rubber tree, Hevea brasiliensis, led to immunological sensitization. Thirteen of these high-molecular-weight proteins have been characterized as allergens (Bernstein et al., 2003). Many other plants of less commercial value produce a similar milky fluid when cut, and have similar sensitizing properties. A shift to powder-free and nonlatex examination gloves has reduced the incidence of latex allergy among health care workers and patients.
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Studies of asthma prevalence in occupational settings with exposure to low-molecular-weight chemicals have suggested prevalence rates of 5% to 10% for toluene diisocyanate (Baur, 1996; Becklake et al., 2006), 3.2% to 18% for anhydrides (Venables et al., 1985; Wernfors et al., 1986), 4% for plicatic acid from western red cedar (Chan-Yeung et al., 1984), and 54% in a platinum refinery (Venables et al., 1989). For high-molecular-weight allergens, prevalence among shellfish processors was estimated at 21% to 26% (Desjardins et al., 1995; Glass et al., 1998), 11% to 44% among lab animal workers (Cullinan et al., 1994; Fuortes et al., 1997; Hollander et al., 1997), and 5% to 7% among bakers exposed to wheat and α-amylase (Heederik et al., 2002).
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Agricultural workers exposed to grain dust, cotton dust, or atmospheres in swine or poultry confinement barns are at risk for the development of an asthma-like syndrome. This syndrome is an acute nonallergic airway response characterized by self-limited inflammation with neutrophilic infiltrates and increased proinflammatory cytokines and chemokines (eg, TNFα, IL-6, and IL-8), but it does not include persistent airway hyperreactivity as in occupational asthma (Schenker et al., 1998). Asthma-like syndrome includes cough, mild dyspnea, fever, malaise, and cross-shift declines in lung function. Endotoxin in combination with other inflammatory bioaerosols is the likely etiological agent (Douwes et al., 2003; Schwartz et al., 1994, 1995).
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An emerging area of concern is adverse effects of respiratory exposures to manufactured nanomaterials. There are currently over one thousand consumer products that contain nanotechnology-based materials (Nanotechnology Consumer Products Inventory, 2011). Nanomaterials are engineered structures that have a primary size less than 100 nm in at least one dimension. Airborne nanoparticles generally form agglomerates in which groups of particles are held together by relatively weak forces (eg, van der Waals). They may also aggregate forming clusters that are fused, sintered, or chemically bonded to one another (Pettibone et al., 2008). Manufactured nanomaterials find applications in electronics, construction materials including wall and floor coverings, cosmetics, drug delivery, medical imaging, food products, packaging materials, and textiles, to name a few. Occupational exposures occur in the manufacture of the nanomaterials and in their use in fabricating materials and consumer products. Exposures can also occur when nanomaterials are cut or shaped and when product waste is discarded. Engineered nanomaterials may be carbon-based, metal-based, or biological in nature (Adamcakova-Dodd et al., 2010). Biological actions of nanoscaled materials may differ from the comparable bulk materials or micron-sized particles (Nel et al., 2006; Grassian et al., 2007). Inhaled nanomaterials may induce pulmonary toxicity or they can cause adverse effects in other tissues through adsorption and transport, generation of toxic substances by their dissolution or degradation, or by crossing key physiological barriers, or cell and nuclear membranes (Kim et al., 2011). In early 2011, NIOSH issued a new guideline on TiO2 marking the first instance of two guidelines for the same compound based on particle size. In mid 2011, NIOSH has issued for peer review a draft Current Intelligence Bulletin on carbon nanotubes and nanofibers. Other research and regulatory bodies worldwide are studying nanomaterials and conducting human health risk assessments.
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Other Occupational Diseases
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Occupational diseases of the skin are common but less often fatal that those of the respiratory system. Irritant dermatitis and allergic contact dermatitis have the highest incidence of reported skin conditions. Table 34-5 shows data for rates of skin diseases or disorders in 2009 by industry division. These data indicate that agriculture, fishing, and forestry services; and manufacturing carry the highest risks. In the service sector, the education and health services division has the highest rate of skin diseases. This is due to the high rate of skin disorders in hospitals (7.2 per 10,000) and in nursing and residential care facilities (10.6 per 10,000). In 2009, 14% of reported occupational skin disorders were in manufacturing while 21% were in education and health services.
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Occupational toxicants may induce diseases in a variety of body sites distant from the lung or skin. These include tumors arising in the liver, bladder, gastrointestinal tract, or hematopoietic system and are attributable to a variety of chemical classes. Further discussion of other occupational diseases and the toxicants listed in Table 34-2 can be found in the relevant chapters in Units IV and V of this text.
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Nervous system damage can be central, peripheral, or both. It may be acute, as with some organophosphate exposures, or chronic, as with organomercury poisoning or acrylamide-induced neuropathy. Injury affecting the immune system may arise from the immunosuppressive effects of chemicals such as dioxins or toxic metals. Many occupational diseases of the immune system occur due to hypersensitivity leading to respiratory or dermal allergy or systemic hypersensitivity reactions. Autoimmune syndromes have been associated with occupational exposures to crystalline silica and vinyl chloride.
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Occupational diseases of the cardiovascular system include atherosclerosis, a variety of arrhythmias, problems with coronary blood supply, systemic hypotension, and cor pulmonale (right ventricular hypertrophy usually due to pulmonary hypertension as with chronic obstructive pulmonary disease). Liver diseases such as carbon tetrachloride-induced fatty liver and hepatocellular death due to toxic concentrations of acetaminophen have classically been used to illustrate chemical mechanisms of cellular injury leading to organ failure. These are thoroughly discussed in Chap. 13. Occupational diseases of the reproductive system can be gender- and organ-specific; but several toxicants—including carbon disulfide, lead, and vinyl chloride—may affect both sexes.
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Exposures to infectious agents are a part of a variety of occupations (Thorne and Duchaine, 2007). Veterinarians, health care workers, and biomedical researchers studying infectious agents have exposures that are largely known and infection control strategies can limit their risks. For others, such as farmers and foresters, specific risks may be less obvious. Zoonotic diseases such as Q-fever, rabies, leptospirosis, and brucellosis may affect abattoir workers, zookeepers, animal handlers, and veterinarians. Foresters, field biologists, and natural resource workers who spend time in wooded areas experience tick- and mosquito-borne illnesses at a higher frequency than that of the general population. These illnesses include the arboviral encephalitides, Rocky Mountain spotted fever, Lyme disease, and ehrlichiosis. Occupational infections may arise as a result of work settings, bringing people into close proximity with other people or animals, thus facilitating the transmission of microorganisms. Occupational infectious diseases attributable to the clustering of people affect workers in such facilities as day care centers, schools, health care settings, correctional facilities, dormitories, military barracks, or shelters for the homeless, among others. Industrial settings can place large numbers of workers in a shared space, leading to increased transmission of diseases. This is especially true for diseases with annual outbreaks, such as influenza and Norwalk-like viruses. Exposures to chemicals may increase the susceptibility of workers to infection through irritation of mucosa or the pulmonary epithelium or through immunosuppression leading to impaired host defense.
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Both industrial and nonindustrial occupational environments may pose occupational hazards due to the presence of chemical or biological agents. Reports of work environments with ineffective ventilation or decreased ventilation rates and increased utilization of synthetic building materials have demonstrated a rise in complaints associated with occupancy in buildings. In some cases, service sector workers in a problem building develop specific clinical conditions with recognized etiology. This is defined as building-related illness. In other cases, symptoms are nonspecific and disappear when the worker leaves the problem building. When this occurs with sufficient prevalence, it is termed sick building syndrome. This can arise from volatile and semivolatile chemicals released from office materials, building materials, floor coverings, furniture, cleaning products, and microorganisms. Office buildings and residential settings comprise a complex ecology consisting of people, molds, mites, volatile organic compounds of microbial and nonmicrobial origin, and sometimes plants, pets, cockroaches, and other vermin (Thorne and Heederik, 1999b). Molds, house dust mites, and animal proteins are potent human allergens that can lead to allergy and asthma. Exposure to chemicals and biomolecules such as endotoxin may enhance this process (Douwes et al., 2003). Workers in laboratory animal facilities exhibit a high prevalence of allergy to rodent urinary proteins. In some cases, the occupied space of a building may be clean and dry, but local amplification sites for molds may develop. These may arise in ventilation systems, utility closets, subfloors or basements that serve as return air plenums, or in local sites of water damage. Such sites can become sources of microorganisms and aeroallergens of sufficient volume to generate significant bioaerosol exposures throughout the environment. Airborne viruses, bacteria, and fungi are responsible for a variety of building-related illnesses arising from organisms that are pathogenic to humans. Nonpathogenic microorganisms may induce symptoms or diseases through inflammatory processes, by stimulating innate or adaptive immune response, or by releasing noxious odors, allergenic compounds, or bioactive macromolecules. These may combine with industrial chemicals released into the air to create complex exposure environments.