Search

Lead, cadmium, mercury and arsenic are widely dispersed in the environment. Adults are primarily exposed to these contaminants in the workplace. Children may be exposed to toxic metals from numerous sources, including contaminated air, water, soil and food. The chronic toxic effects of lead include anemia, neuropathy, chronic renal disease and reproductive impairment. Lead is a carcinogen in three animal species. Cadmium causes emphysema, chronic renal disease, cancer of the prostate and possibly of the lung. Inorganic mercury causes gingivitis, stomatitis, neurologic impairment and nephrosis, while organic mercurials cause sensory neuropathy, ataxia, dysarthria and blindness. Arsenic causes dermatitis, skin cancer, sensory neuropathy, cirrhosis, angiosarcoma of the liver, lung cancer and possibly lymphatic cancer.

Concern for the protection of workers' health is not new to medicine. Physicians in the 1400's raised awareness among colleagues as to the need to prevent the diseases of employment in mines. Society has responded to increasing levels of evidence as to the relationships between disease and certain worksites by making employers accountable for the individual and social costs incurred by poor workplace hygiene. This has occurred by the development of workers' compensation and occupational health and safety regulatory programs. The impact of these efforts has been to significantly reduce occupational disease and safety problems in industry. Increasing resources have also been given to the training of physicians in occupational medicine and research into links between occupations and disease. Increasing pressure to reduce public spending and to deregulate are challenging government's ability to continue research, training, technical information distribution, consultation and regulatory cleanup efforts to improve work conditions and thus reduce the incidence of occupational safety and health problems.

The capacity of cardiac patients to work in their occupations reflects a complex interaction of medical and nonmedical factors. Medical considerations include prognosis and the ability of patients to tolerate the physical, environmental and psychological aspects of their occupation. Nonmedical factors include the patient's satisfaction with the job, economic motivation to work and perceived risk of continued work. Patients' perceptions of their capacity to work and the risks of such work are especially important determinants of occupational work status after myocardial infarction and coronary operations. Symptom-limited treadmill exercise testing carried out three to four weeks after the acute event not only clarifies prognosis and quantitates functional capacity but helps patients to realistically assess their capacity for work. Approximately half of postinfarction patients are found by such testing to have a very low first-year mortality of less than 2 percent. Functional capacity is well maintained in these patients: they do not require formal reconditioning in order to resume their occupational work soon (three to five weeks) after infarction. Exercise testing performed soon after myocardial infarction and coronary artery operation affords practical guidelines for clearing a person to return to work and obviates much of the medically unwarranted disability that follows these events.

Neither clinical nor laboratory evaluation can distinguish occupational neuropathies from neuropathies due to other causes. A worker may suffer either from mechanical injury of individual nerves or from a toxic polyneuropathy that is usually axonal in type. A thorough occupational and environmental history and the recognition of clusters of cases are important in determining the diagnosis. Electrophysiologic studies are helpful in detecting neuropathies in patients who have been occupationally exposed to neurotoxins but have no symptoms. Prevention of occupational neuropathies depends on clinical vigilance, industrial hygiene surveys, biologic monitoring and periodic examination of workers exposed to neurotoxic chemicals. The development of more sophisticated methods of prevention and early detection of peripheral nerve involvement depend on understanding the mechanisms of action of toxins and the pathophysiology of the lesions they cause.

Because large surface areas of the skin are exposed directly to the environment, skin is an organ particularly vulnerable to occupationally induced disease. Statistics show that, excluding accidental injury, nearly half of all occupational illnesses occur in this organ; a fourth of all workers suffering from occupational skin disease lose an average of 10 to 12 workdays. The constant evolution of new industrial chemicals and methods of manufacture continue to bring new skin hazards and disease into the workplace. Occupational health physicians and practitioners, who usually have minimal training in dermatology, must diagnose and treat unfamiliar diseases in a setting of even less familiar, often overwhelming, technology. A thorough understanding of cutaneous defense mechanisms, clinical patterns of occupational skin disease and methods for establishing accurate diagnoses is essential.

The liver plays a central role in toxicology. It is the primary organ of detoxification and elimination by metabolism of many chemicals. Many workplace chemicals can affect the liver in animals; fewer have been proved to do so in humans. The diverse hepatic effects observed in humans from occupational exposure to chemicals range from fatty infiltration, acute hepatitis and cholestasis to cirrhosis and angiosarcoma. Three important workplace chemicals, prototypes for the toxicities of many others, are carbon tetrachloride, vinyl chloride and the polychlorinated biphenyls (PCB's). These three are described in some detail to highlight principles of occupational toxicology. Most of the hepatic effects produced by chemicals in the workplace have clinical, laboratory and morphological features common to many other forms of liver disease. Therefore, only an astute physician who takes an occupational history will recognize the association between a patient's workplace and liver disease.

Diffuse malignant mesothelioma is a signal tumor of asbestos exposure. Mesothelioma incidence has been steadily rising during the past two decades, reflecting the increases in asbestos use during and following World War II. The onset of the disease follows exposure by 25 to 40 years. The dose-response relationship appears to be much lower than that for asbestosis or lung cancer—it is not known whether current levels of exposure will entail a risk for disease 30 years hence. There is no synergistic or additive interaction with smoking for this tumor. Current knowledge indicates that pleural plaques, per se, do not increase the risk for this tumor beyond that of the previous asbestos exposure alone. Durable fibers with high aspect ratios, especially amphiboles, are associated with experimental tumor induction. Treatment modalities including surgical procedures and chemotherapy with doxorubicin and 5-azacytidine offer prospects for palliation.

Noise-induced hearing loss is a major and entirely preventable public health problem. Effective prevention of this disorder has yet to be achieved in the United States but would improve the overall hearing health of the population more than the treatment of all other otologic disorders combined. Losses that are mild to moderately severe and maximal at 3, 4 or 6 kHz are typical but not pathognomonic. Individual differences in susceptibility are substantial but unpredictable. Hearing conservation programs are now required by the Occupational Safety and Health Administration for almost all employees whose daily exposure to noise exceeds a time-weighted average of 85 dBA (A-weighted sound pressure level). The permitted exposure level is 90 dBA time-weighted average, above which engineering or administrative controls or hearing protectors are required. Workers with lesser exposures (85 to 90 dBA time-weighted average) who have hearing changes must be similarly protected. Many, but not all, elements of required hearing conservation programs have been specified recently by the Occupational Safety and Health Administration. Medical supervision and otologic referral are important components of hearing conservation programs because otologic problems other than noise-induced hearing loss are common in industrial populations. Compensation for noise-induced hearing loss, which is awarded through state workers' compensation boards, as well as certain federal sources, varies widely.

Taking a medical history is an art that requires skill, experience and practice. There is now increasing recognition of the importance of workplace and environmental factors in causing or aggravating common medical conditions. Because of limited training in evaluating workplace and environmental hazards, general physicians may find it difficult to target a general medical history to detect essential occupational details.

More than 13.5 million American workers, close to 20 percent of the work force, are assigned to evening or night shifts. In some industries such as automobile, petrochemical and textile manufacturing the proportion of shift workers is greater than 50 percent. As the popularity of shift work and other “alternative work schedules” grows, concern is increasing over the disturbance created in the lives of workers and their families by these economically and socially useful innovations. Twenty percent of workers are unable to tolerate shift work. Daily physiologic variations termed circadian rhythms are interactive and require a high degree of phase relationship to produce subjective feelings of wellbeing. Disturbance of these activities, circadian desynchronization, whether from passage over time zones or from shift rotation, results in health effects such as disturbance of the quantity and quality of sleep, disturbance of gastrointestinal and other organ system activities, and aggravation of diseases such as diabetes mellitus, epilepsy and thyrotoxicosis. Worker selection can reduce the number of health problems resulting from shift work. The periodic examination of shift workers is recommended.

Much of the data collected by industrial hygienists on levels of airborne contaminants in the workplace is of marginal relevance to the needs and interests of physicians practicing occupational medicine. Several factors influence data collection. Regulatory agencies require rigid interpretation of exposure levels, yet concentrations of contaminants in the air environment vary considerably. This discrepancy suggests a different approach to dealing with the regulatory problem, one which recognizes its inherent statistical nature. Increased attention also should be devoted to basing sampling intervals more directly on toxicological measurements. These changes would result in the collection of environmental data of greater relevance to physicians, toxicologists and epidemiologists because such information would allow more realistic estimates of the hazard of a cumulative exposure for a given work population.

There are fundamental approaches that can be used by health professionals to study the contribution of occupational exposures to cancer occurrence. It would be helpful for clinicians who see patients with cancer to be aware of the methods used to identify those types of cancer that are related to work. Such physicians may be asked by companies or unions to collaborate on the design of epidemiologic studies in work settings or to assist in interpreting results, or they may be consulted by patients from such work environments. Understanding these approaches is essential in order to anticipate, detect and prevent cancer caused by occupational exposures.

Penetrating ionizing radiation fairly uniformly puts all exposed molecules and cells at approximately equal risk for deleterious consequences. Thus, the original deposition of radiation energy (that is, the dose) is unaltered by metabolic characteristics of cells and tissue, unlike the situation for chemical agents. Intensely ionizing radiations, such as neutrons and alpha particles, are up to ten times more damaging than sparsely ionizing sources such as x-rays or gamma rays for equivalent doses. Furthermore, repair in cells and tissues can ameliorate the consequences of radiation doses delivered at lower rates by up to a factor of ten compared with comparable doses acutely delivered, especially for somatic (carcinogenic) and genetic effects from x- and gamma-irradiation exposure. Studies on irradiated laboratory animals or on people following occupational, medical or accidental exposures point to an average lifetime fatal cancer risk of about 1 x 10(-4) per rem of dose (100 per 10(6) person-rem). Leukemia and lung, breast and thyroid cancer seem more likely than other types of cancer to be produced by radiation. Radiation exposures from natural sources (cosmic rays and terrestrial radioactivity) of about 0.1 rem per year yield a lifetime cancer risk about 0.1 percent of the normally occurring 20 percent risk of cancer death. An increase of about 1 percent per rem in fatal cancer risk, or 200 rem to double the "background" risk rate, is compared with an estimate of about 100 rem to double the genetic risk. Newer data suggest that the risks for low-level radiation are lower than risks estimated from data from high exposures and that the present 5 rem per year limit for workers is adequate.