22 Brenda S. Buikema, T. Renée Anthony, and Fredric Gerr The purpose of this chapter is to introduce readers the practice of occupational and environmental health. Specifically, this chapter will define occupational and environmental heath and describe the: Readers of this book should be familiar with the historical figures whose efforts shaped our modern occupational and environmental health practices as well as the occupational and environmental health disasters that serve as lasting reminders of the importance of preventing occupational and environmental illness and injury. In 1587, Paracelsus, often considered the father of modern toxicology, wrote the first known monograph on occupational disease. However, the role of occupational risk factors in the development of disease was not widely appreciated until 1700, when the Italian physician, Bernardo Ramazzini, published the first known textbook of occupational medicine, entitled De Morbis Artificum Diatriba (The Diseases of Workers” in modern translation). Prior to its publication, there were few efforts to link work and illness, despite increasing development of metallurgy and other technologies. Ramazzini recommended that physicians ask their patients about their occupation and the conditions of their work. He also encouraged physicians to visit their patients’ work sites to observe directly their working conditions. In particular, Ramazzini wrote, “Liceat quoque interrogationem hanc adiicere, & quam artem exerceat” (“I may venture to add one more question: what occupation does [the patient] follow?”). Ramazzini recognized noise, dusts, fumes, extremes of heat and cold, and awkward postures as risk factors for occupational disease and used this knowledge to reduce exposure to these hazards as a means of preventing occupational illness. Ramazzini’s work contributed to subsequent efforts of other occupational health specialists and is widely credited with establishing the specialty of occupational medicine. With the industrial revolution, certain workplace exposures became more common, leading to the occurrence and recognition of new occupational diseases. For example, in 1775, the British surgeon, Percival Potts, noted that occupational exposure to soot among chimney sweeps resulted in an increased risk of scrotal cancer, eventually leading to protective legislation for workers in Europe. Government medical positions were created in the second half of the nineteenth century in Great Britain, establishing occupational medicine as a legitimate part of public health and clinical medicine. In 1911, the Triangle Shirtwaist Factory fire in New York City resulted in the death of 146 garment workers, which placed workers’ health and safety concerns into the limelight both locally and nationally, leading to the reform of fire safety codes and the inception of U.S. workers’ compensation programs. This tragedy, resulting from locked fire exits in the factory, also resulted in the creation of the Office of Industrial Hygiene and Sanitation of the U.S. Public Health Service. It was one of the earliest U.S. federal responses to the growing hazards of industrialized work. Just after World War I, Dr Alice Hamilton, the first woman to be a member of the faculty of the Harvard Medical School, became the leading American figure in the field of occupational and environmental medicine. As a pioneering advocate for occupational and environmental public health, she gave congressional testimony in opposition to the addition of tetraethyl lead to gasoline and correctly predicted widespread environmental lead contamination and an epidemic of lead toxicity as a consequence. In 1925, Dr Hamilton wrote Industrial Poisons in the United States and paved the way for growth and maturation of the field. In 1930, contractor profits were placed ahead of workers’ health by allowing dry drilling of silica-containing rock with inadequate ventilation during construct of the 3 mile Hawks Nest Tunnel in West Virginia. The resulting exposure to airborne crystalline silica resulted in the death of hundreds of workers who developed a severe and rapidly progressive form of silicosis (a disease of the lung resulting from inhalation of silica dust and characterized by scar tissue and impaired transfer of oxygen from air to blood). Hundreds more developed permanent lung disease. In terms of lives lost, this incident remains the single largest industrial disaster in U.S. history. In December of 1952, a 5-day temperature inversion in London, United Kingdom, resulted in a dense ground-level fog that trapped soot, tar, and sulfur dioxide from household and industrial coal combustion. London residents developed chest pain, lung inflammation, and increased asthma incidents, with 4000 fatalities initially attributed to the event. While many who died of respiratory illness during the inversion were elderly or had preexisting lung conditions, increased fatality rates for both middle-aged and infant residents were observed during and immediately following the smog event. Today, estimates of 12,000 deaths are attributed to the event. In the wake of this tragedy, the British government began efforts to reduce household coal emissions in the ensuing 1956 Clean Air Act. Such industrial disasters have affected not just previous generations but are still occurring in the current era. For example, in 1984, the unplanned release of methyl isocyanate gas from a Union Carbide plant into a densely populated neighborhood of Bhopal, India, resulted in the immediate death of approximately 2000 people and the onset of permanent lung disease among more than ten thousand residents. Neither the community nor local hospitals knew what was in the gas or were aware of its toxic effects. As a result, regulators in the United States developed a hazard communication standard to ensure that the hazards of occupational chemicals were clearly communicated to workers and, in conjunction with emergency response rules, to the neighboring communities and emergency responders. In 1986, an explosion at the Chernobyl nuclear power plant in Ukraine resulted in the immediate deaths of 28 workers and emergency responders, who again did not know the hazards of the radiation exposures they were facing. In 2005, an explosion in a British Petroleum refinery in Texas City killed 15 workers and injured 170 others because of violations of the process safety management standard, and in 2010, 29 coal miners died in a mine explosion at the Upper Big Branch Mine in West Virginia because inadequate ventilation allowed explosive dusts and gases to build in the mine. While these cases illustrate the diversity of large-scale tragedies associated with industrial exposures, it is important to remember that many more workers are chronically exposed to hazardous chemicals that may be associated with health effects that may take years to develop. Over the ensuing decades, multiple occupational and environmental health outbreaks have occurred in the United States and throughout the world. In the United States, the Occupational Safety and Health Act of 1970, which created both the Occupational Safety and Health Administration (OSHA) and the National Institute for Occupational Safety and Health (NIOSH), allowed for greater oversight and regulation of occupational exposures and furthered the field of occupational and environmental medicine in the United States. As a result of the contributions of both early and recent occupational health researchers and practitioners, the health and safety of workers has improved dramatically, especially in developed nations. Industrial and commercial activities create a wide range of human health hazards in both the workplace and the general environment. In the workplace, exposure to machinery, toxic chemicals, physical agents (e.g., noise, heat, and radiation), and biological hazards result in illness and injury. Releases of toxic substances into ambient air and water have adverse environmental and human health effects. When manifesting as a well-defined human disorder, the adverse effect of an exposure to an occupational and environmental hazard is typically categorized as an injury or illness. An occupational injury is an adverse health event of nearly instantaneous onset resulting from a single, short-duration occupational exposure.1 Examples include a burn experienced by a worker who has contact with steam escaping from a ruptured pipe and a broken leg experienced by a worker who falls from a roof. Of more interest to the study of toxicology, injuries from chemical exposures can also occur. Chemical injuries associated with short-term exposures typically require inhalation or dermal exposures to high concentrations of acutely hazardous chemicals. Examples include exposures to (i) airborne hydrogen sulfide, where a single exposure to concentrations above 700 mg/m3 can cause rapid respiratory failure; (ii) dermal contact with phenol, which is rapidly absorbed through the skin and can result in irregular breathing, muscle weakness, and respiratory arrest; and (iii) skin contact with concentrated hydrofluoric acid, which causes both initial redness and pain and can result in hypocalcemia (low blood calcium) and death following contact with as little as 2.5% of the body’s skin. An occupational or environmental illness is an adverse health condition that occurs over some period of time after exposure to a hazardous agent. Examples of occupational and environmental illness include hearing loss among workers who experience prolonged exposure to noise, asthma (an obstructive lung disease) among workers with occupational exposure to the organic chemical toluene diisocyanate, and impaired cognitive function experienced by a child who ingests lead-based paint found in older housing. None of these illnesses occur immediately following the initial exposure. Occupational illness can result from exposure to chemicals (e.g., pesticides from agricultural applications, solvents from printing operations, and metals from welding), minerals (e.g., asbestos from mining, silica from abrasive blasting, coal dust from mining), physical agents (e.g., vibration from construction equipment, radiation from radon intrusion), biological agents (e.g., hepatitis B from tattooing, tuberculosis from hospital patients, and human immunodeficiency virus from needlestick injuries), or psychosocial stressors (e.g., time and productivity demands from automated production lines). Some examples of the large variety of work-related diseases encountered by occupational medicine providers are provided in Table 22.1. Table 22.1 Examples of Organ System, Occupation or Setting, Specific Exposure, and Health Effects for Selected Occupational Diseases The goals of occupational and environmental health are to prevent, identify, and mitigate the adverse effects of occupational and environmental hazards among workers and exposed members of the public. Information on occupational injury and illness is available from several sources, each providing a partial characterization of the full impact of these conditions. The Bureau of Labor Statistics (BLS) of the U.S. Department of Labor is the primary federal entity responsible for collection of work-related illnesses and injuries statistics in the United States (www.bls.gov/). BLS occupational injury and illness information is obtained by compilation of injury and illness reports submitted by eligible employers as required by applicable U.S. OSHA law. There are limitations to these data, however. First, many employers are exempt from federal reporting requirements (e.g., farms with fewer than 11 employees and self-employed persons). Further, underreporting of injuries and illnesses by employers has been identified across many industrialized nations. Underreporting of occupational disease is common due to the chronicity and latency of many occupational diseases (discussed in the following text). In addition to the BLS, occupational illness and injury information can also be obtained from state and federal workers’ compensation reports; however, substantial variability in compensation programs across states limits the utility of this information. As with BLS data, long latent interval diseases from occupational exposures may be neither recognized nor captured by worker’s compensation systems. The data that are collected can be analyzed by industry, exposure type, and reported adverse health effect. Ideally, this information is used for prevention efforts. For example, the OSHA recently issued an alert to workers in the salon industry to notify them of excessive levels of formaldehyde in professional hair care products (http://www.osha.gov/SLTC/formaldehyde/hazard_alert.html). Despite limitations in its completeness, valuable information about the pattern and distribution of work-related injuries and illnesses can be obtained from BLS data. According to 2009 BLS data, 1,238,490 people experienced an injury or illness at work in private industry and state and local government agencies that required one or more days away from work. In private industry in 2009, 14,350 injuries and illnesses requiring time off from work were attributed to exposures to chemicals and chemical products. The breadth of illness and the extent of workers with these illnesses provide unique challenges to all occupational and environmental health specialists. Illness resulting from occupational and environmental exposures is often overlooked and underreported. This is unfortunate, since neither prevention nor effective treatment is possible unless the link between the exposure and the illness is recognized. A discussion of special characteristics of occupational and environmental illness is provided in the following text that, when understood, will assist in better recognition and prevention of these disorders. Simply stated, the clinical and biological characteristics of a disease that results from occupational or environmental exposures are no different than those of the same illness resulting from other causes. Examples are numerous—lung cancer resulting from occupational exposure to asbestos is identical to lung cancer resulting from exposure to tobacco smoke or radon gas. Anemia from occupational exposure to lead may be identical to that resulting from iron deficiency or other diseases. Hearing loss caused by occupational exposure to noise is indistinguishable from hearing loss resulting from nonoccupational exposure to noise. Perhaps more than any other single fact, the similarity of occupational illness to nonoccupational illness makes it especially important to maintain a high level of vigilance (in medical terms, a high “index of suspicion”) for occupational causes of common illness. Occupational and nonoccupational factors can act together in the causation of disease. For example, regular smokers of cigarettes have about a 10- to 15-fold increase in lung cancer risk. Persons with a history of occupational exposure to asbestos have about a fivefold increase in lung cancer risk. However, among persons exposed to both cigarettes smoke and asbestos, the risk of lung cancer is 50 or more times that of persons who have no exposure to either hazard. In this example, we see that the risks are not simply additive, but actually multiply by each other. Such synergy of the effect of multiple exposures has been well characterized for only a few combinations of exposure, but likely occurs often. The adverse health effects of specific exposures may not be observed for many years after cessation of the exposure. The time period separating the onset of exposure to the clinical manifestation of illness is called a “latency period.” For example, some persons exposed to airborne silica dust may not manifest scarring of the lung (i.e., silicosis) until more than a decade has passed (although it can occur both earlier and later than 10 years). Latency periods vary greatly across toxicants and illnesses. For example, organophosphate pesticide poisoning may occur within minutes or hours following exposure, whereas cancers resulting from occupational and environmental exposures (e.g., lung cancer from occupational exposure diesel exhaust) occur after a latency period of years to decades. As emphasized elsewhere in this book, the dose of a toxicant absorbed by an individual is a critical determinant of the resulting adverse health effects. For exposure–effect associations that are stochastic in nature (i.e., probabilistic), the dose is a primary determinant of the risk of disease. Stochastic dose–response relationships are observed for carcinogenic agents—as the dose of the carcinogen increases, the probability of developing cancer increases (however, the severity of the cancer itself is not a function of the dose). Alternatively, for deterministic exposure–effect associations, the dose affects the severity of the disease. For example, the severity of the acute adverse effects of organophosphate pesticide exposure is highly dependent on the dose received. Virtually, all exposed persons, at sufficient doses, will exhibit well-characterized signs of toxicity. Considerable variability in both risk and severity of disease is observed among exposed persons even after dose has been considered. Such variability may be due to other environmental exposures in both work and nonwork settings (as noted earlier), individual characteristics (e.g., physical conditioning, nonoccupational health behaviors, and overall health status), and differences in genetic makeup across individuals. For example, workers who are exposed to a hepatotoxic agent such as carbon tetrachloride are at higher risk of liver toxicity if they are also regular consumers of ethyl alcohol, which is also known to be toxic to the liver. In order to maintain the health and productivity of working people, occupational health providers are committed to three major prevention goals: (i) prevent hazardous exposures from occurring to minimize or eliminate the risk of occupational and environmental disease, (ii) identify early evidence of harm (i.e., preclinical disease) in order to prevent additional exposure and further harm, and (iii) diagnose and treat diseased individuals to prevent further health deterioration. Specific activities of occupational and environmental health professionals are described in the following text for each of these goals. The first prevention goal is called primary prevention. Primary prevention is accomplished by lowering the risk of an occupational or environmental disease among healthy (i.e., disease-free) persons. To do so, occupational health professionals must recognize hazardous exposures and take steps to control them before resultant health consequences occur. Primary prevention in the workplace is often implemented by occupational health professionals specializing in industrial hygiene. Industrial hygienists are trained to anticipate, recognize, evaluate, and control exposures in the workplace to prevent sickness, impaired health and well-being, or significant discomfort among workers. For example, after recognizing hazardous airborne mercury concentrations in a work environment, industrial hygienists will identify and characterize the source of the vapor and work with engineers to find a safer substitute, change the facility ventilation, or otherwise contain the substance. Industrial hygienists have prioritized exposure reduction approaches into a hierarchy of controls, described in Table 22.2. The most effective control measures focus on elimination or reduction of the hazard with methods that require no change to workers’ behavior. Administrative controls, such as implementing work/rest cycles on hot days, require supervision reinforcement and workers’ participation to minimize health risks. The final level of control, that is, use of personal protective equipment (e.g., respirator masks), relies on the worker to properly use and maintain protective equipment. While these are often effective to reduce exposures, they place the burden of protection on the worker and are usually considered the last line of defense for primary prevention. Primary prevention in occupational and environmental health may also be implemented by substituting less hazardous chemicals for ones in current use. For example, over the past several decades, safer water-based latex paints have been used as a substitute for more hazardous solvent-based paints in residential and commercial building construction. This trend has substantially decreased exposure to organic solvents among construction painters. Substitution does not always eliminate health hazards of a particular industrial sector, however, as the new chemical may introduce unexpected hazards. For example, the commercial dry cleaning industry has focused on replacing perchloroethylene, a chemical hazardous to the nervous system and suspected of being cancer-causing agent, with 1-bromopropane (1-BP). However, workers handling the new chemical also exhibited neurological effects, including light-headedness and loss of sensation in the arms and legs (peripheral neuropathy). NIOSH investigations identified that exposures to 1-BP exceeded recommended exposure limits and recommended additional ventilation to reduce worker exposure. While the hazards of the substituted chemical, 1-BP, were well documented, sometimes, chemicals with ingredients of unknown toxicity are substituted for chemicals with known toxicity. In these cases, industrial hygienists must work with toxicologists to perform hazard assessments with appropriate analogous chemicals to anticipate hazards of substitution chemicals.
OCCUPATIONAL AND ENVIRONMENTAL HEALTH
22.1 HISTORY OF OCCUPATIONAL HEALTH
22.2 DEFINITION AND SCOPE
Organ System
Occupation or Setting
Exposure
Disease
Respiratory
Shipyard, insulation installer/remover
Asbestos
Pulmonary fibrosis, lung cancer
Foundry, sand casting
Silica
Pulmonary fibrosis, lung cancer
Agriculture, farmer
Organic dusts
Hypersensitivity pneumonitis
Painting and coatings
Toluene diisocyanate
Asthma
Coal mining, coal dust
Coal dust
Coal workers’ pneumoconiosis
Neurological
Automobile repair, mechanic
Organic solvents
Cognitive impairment
Storage battery manufacturing
Lead
Kidney disease, neurological disease, anemia
Construction, agriculture, others
Noise
Hearing loss
Dermatological
Healthcare workers, agricultural workers, others
Soaps, solvents, sensitizing agents, physical agents
Contact dermatitis, skin cancer
Hematological
Petroleum refining
Benzene
Anemia, leukemia
Kidney and bladder
Plating, battery manufacturing
Cadmium
Renal impairment
Tanning and dying
Aniline dyes
Bladder cancer
Cardiovascular
Rayon manufacturing
Carbon disulfide
Atherosclerosis
22.3 DATA SOURCES AND THE BURDEN OF OCCUPATIONAL AND ENVIRONMENTAL ILLNESS AND INJURY
22.4 CHARACTERISTICS OF OCCUPATIONAL ILLNESS
The Biological, Clinical, and Pathological Characteristics of Occupational Illness Are Often Indistinguishable from Those of Illness of Nonoccupational Origin
The Cause of Many Occupational Illnesses Is Multifactorial
The Adverse Effects of Occupational Exposure May Begin after a Predictable Interval from Onset of Exposure
The Dose of a Toxicant Is an Important Predictor of Health Effects
People Vary Substantially in Their Responses to Occupational and Environmental Exposures
22.5 THREE PREVENTION GOALS
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