Occupational Medicine Part 2

Diagnostic decision making

The determination that a patient’s symptoms are work related often entails extensive ramifications for the patient’s employer,as well as potentially serious public health and medicolegal implications. These may present a significant challenge to the clinician, because for many occupational disorders, there is no gold standard for diagnosis.

The decision-making process should address the following questions:

1. Is the clinical illness—including the history, physical examination, and laboratory findings—consistent with other case descriptions?

2. Is the timing between exposure and clinical onset compatible with the known biologic facts about the hazard?

3 Is the exposure dose within the range of doses believed to cause such effects?

4. Are there special attributes of the particular patient that make it more or less likely that he or she would be so affected?

5. Are there alternative ways of constructing the case that better fit the available facts?

6. Where there remains significant uncertainty about the cause, how important is it to be certain?

Regarding the certainty of identifying the cause, the general legal standard for workers’ compensation purposes is "more likely than not," which is a relatively low hurdle of certainty (i.e., at least 50% certain). However, there may be other situations that demand a higher level of confidence, irrespective of the standard for obtaining compensation benefits. In general, problems involving current working conditions demand a far greater level of certainty than historical ones. For example, a diagnosis of occupational asthma in a spray painter would likely dictate removing the patient completely from exposure to the offending paint or constituent; correct identification of that agent might be crucial to saving his or her career. Similarly, if a surgeon presented with recurrent anaphylactic reactions, it would be very important to determine whether the reactions were to latex, an anesthetic agent, or some extrinsic factor.

In situations where a high level of certainty is needed, it is often worth the effort to refine the diagnostic impression by serial observations, usually while the patient remains exposed, or by utilizing diagnostic challenges of removal followed by reexpo-sure. Using serial functional measurements, such as peak expiratory flow records or serial blood tests, a more certain judgment can be made. This may also be an appropriate circumstance for referral to occupational physicians who specialize in evaluating challenging cases.

Major Occupational Disorders in Developed Countries

The spectrum of occupational disorders of clinical importance is rapidly shifting as a result of several factors: these include changes in the economy, which have brought about a decline in traditional manufacturing and a rise in service-sector activities; better control of many hazards, such as mineral dusts (e.g., asbestos, silica, coal), heavy metals (e.g., lead, arsenic, mercury), and the most toxic solvents (e.g., benzene); rapid introduction of many new technologies whose health risks remain inadequately characterized; and changing demographics in the workplace, in which the proportion of women, minority, and older workers is increasing. In the sections that follow, the disorders that are most important in clinical practice in developed countries are briefly discussed by organ system.

Occupational cancer

Only a small fraction of known chemical agents and a handful of physical and biologic hazards appear capable of inducing neo-plastic change in mammalian tissues. In general, the risk of cancer being induced increases in direct proportion to total dose of toxin to which the person is exposed. Typically, the target organ is relatively specific and is determined by metabolism and transport of the agent. However, a few agents, including ionizing radiation and asbestos, appear to have potential to cause malignancy at more than one human site. There is invariably a long lag time between initial exposure and onset of clinical disease. Only a small number of hazards found in the workplace have been clearly established as carrying substantive cancer risk for workers. An additional group of hazards are suspected, but additional studies are needed. The list of potential carcinogens is expanding; for example, evidence suggests that exposure to cadmium may play a role in the development of prostate cancer.13 Studies provide some indication that workers in print shops, service-station employees, farm-product vendors, horticulturists, farmers, and aircraft mechanics are at increased risk for renal cell carcinoma14,15 [see Table 3].

Table 3 Established Occupational Carcinogens

Cancer Site




Insulation, textiles

Ionizing radiation Arsenic

Uranium mining Refining

Polyaromatic hydrocarbons

Coke ovens

Nickel Chromium

Nickel refining Tanning, pigments


Alkylating agents

Chemical industry


Mining, stonecutting

Ceramic fibers


Formaldehyde Beryllium

Chemicals, plastics Nuclear weapons, aerospace industry



Acrylonitrile 1,3-Butadiene


Rubber, plastics

Pleura and peritoneum


Construction materials

Wood dust


Upper respiratory tract




Refining Plating

Friction products


Chemicals, plastics

Urinary bladder

Benzidine and related

amines Polyaromatic hydrocarbons

Dyes, chemicals Aluminum reduction


Vinyl chloride monomer Arsenic

Plastics Pesticides

Upper GI tract



Coal dust Acrylonitrile

Mining Plastics

Hematologic system


Ionizing radiation

Chemicals, rubber Defense industry

Ethylene oxide

Chemicals, sterilizers

Soft tissue


Chemical industry


Vinyl chloride

Chemical industry


Chemical industry

Respiratory tract disorders

The respiratory tract is a frequent target of toxic effects. Complaints referable to the lungs or upper respiratory tract often require a careful evaluation for occupational causes. The presence of other possible causal factors, such as common allergy and smoking, does not exclude the possibility of an occupational cause and may, in fact, increase the likelihood of one.

Acute Disorders and Recurrent Disorders

The most prevalent acute effects—inflammatory reactions of the mucosae of the upper or lower airway system—are caused by environmental irritants.16 An extraordinary array of agents are irritating, including simple inorganic gases (e.g., ammonia and chlorine), organic solvents, acid and alkaline mists, metal fumes (i.e., tiny particles of metal and metal oxide that occur when vaporized metals hit cool air), mineral dusts (e.g., fibrous glass and coal), and almost all the pyrolytic products of combustion. The anatomic site of irritation for dusts, mists, and fumes depends on the deposition of particles; for gases, it depends on water solubility (i.e., the more water soluble the gas, the more it will dissolve in the upper respiratory tract). Expression of symptoms, from mild burning of the eyes, nose, and throat to small airway and alveolar injury associated with the acute respiratory distress syndrome, depends on dose, duration of exposure, and the potency and composition of the irritant; there is also substantial host variability. The period from the time of exposure to the onset of symptoms is very brief for the upper respiratory structures and can be from minutes to hours for lower structures.

Most of the consequences of acute irritation are self-limited; the upper respiratory tract is particularly resilient, although patients who work in areas of poor air quality will experience frequent recurrences, punctuated by commonplace complications such as sinusitis. Such cases require steps to modify exposure. More severe insults may result in fixed scarring of airways or lung parenchyma; late inflammatory sequelae such as bronchi-olitis obliterans are occasionally reported. A newly recognized and probably common outcome of significant lower airway injury is the occurrence of persistent mucosal irritation and bron-chospasm, a variant of asthma induced by a single exposure or repeated exposures to irritants. Initially dubbed reactive airways dysfunction syndrome,17 this disorder is best classified as nonim-mune occupational asthma or simply asthma without latency. Unfortunately, the condition tends to be highly resistant to therapy, and patients derive only modest benefit from inhaled steroids or other bronchodilators. Typically, cough with some phlegm, chest discomfort, and occasionally even dyspnea persist despite early and intensive therapy. Reassurance and reduction of further exposures to irritants are the mainstays of treatment.

Occupational asthma, including the nonimmune- and the immune-mediated varieties, is prevalent.18 There are now over 200 established causes of presumed immune-mediated asthma19; these are usually categorized as proteins and other high-molecular-weight antigens (e.g., animal danders, latex antigens, and grains) and small molecules such as the isocyanates—the ubiquitous chemicals used in polyurethane products. Typically, the classic antigens differentially affect those with atopy and are associated with identifiable IgE antibody responses to the sensitiz-er.20 In such cases, the greatest diagnostic dilemma is distinguishing occupational sources from other causes of asthma, though the periodicity as documented by history or peak expiratory flow records (PEFR) aid in identifying a relation to work. Latex has become a particularly important cause, especially when rendered airborne in association with the use of powdered gloves.21,22 More troublesome are the low-molecular-weight agents such as toluene-2,4-diisocyanate (TDI) and other iso-cyanates, for which atopy is not a risk factor.19,23 Onset is often insidious, with cough and chest discomfort relatively more common than in asthma of other causes. Far more often than with the IgE-mediated agents, symptoms may be delayed some hours after exposure, so patterns may include nocturnal complaints. Once the physiologic hallmarks of asthma are established, the history and PEFR are the keys to specific diagnosis. Studies have shown that detailed histories can be inconclusive; in some cases, objective measurements can establish the diagnosis of occupational asthma.24 Specific inhalation tests may be valuable, but they should be performed only under medical supervision.

Current evidence suggests that correct diagnosis of occupational asthma makes a difference. People who are removed early from further contact have a better likelihood of reducing their dependence on medication; many will become nonasthmatic over time.19,20 Most who remain exposed will develop persistent nonspecific bronchial hyperreactivity, as well as possible fixed obstructive changes. These patients will typically fail to recover after they are removed from contact with the agent, and their conditions may even worsen; this is the basis for an aggressive posture toward early evaluation and management.

Acute infectious diseases occur in an extraordinarily wide variety of workplaces, from health care to industrial and agricultural settings. Anthrax and other agents of bioterrorism, as well as emerging infectious diseases such as severe acute respiratory syndrome and influenza A (H5N1) are of particular concern to workers.

Allergic alveolitis, with its more benign variants, such as humidifier fever, continues to occur sporadically in a wide range of settings. This disorder was traditionally associated with agricultural exposures to molds and bacilli. Cases are now reported to occur in manufacturing and other industrial settings because of the appearance of a few chemicals that appear capable of inducing the immune response (e.g., plastic resin constituents) and because of the contamination of many industrial processes with microorganisms.27 The office environment continues to be an occasional source of this condition as well, though the reservoir of causal microbes may be obscure; such organisms may potentially reside in heating and air-conditioning systems remote from the patient’s work area.28

Chronic Conditions

The pneumoconioses continue to occur, in part because of their very long latency from first exposure and because pockets of very poor industrial conditions continue to exist even in developed countries. Construction activities have been particularly problematic. In general, asbestosis, silicosis, and coal workers’ pneumoconiosis are diseases that occur after extensive work exposures. The diagnosis can usually be made on the basis of clinical findings and the history of exposure, once the patient’s lifetime job history is obtained.

The granulomatous diseases, including CBD and so-called hard metal disease, are less common but important and increasingly recognized disorders of sensitization. CBD is clinically almost identical to idiopathic sarcoidosis except that all cases involve the lung and that the prognosis—even after the patient is removed from exposure to beryllium metal, compound, or fumes—is generally unfavorable. All patients with sarcoidosis should be asked if they work with metals, and the least suspicion should prompt specific testing; there is a highly sensitive test that can distinguish sarcoidosis from CBD on blood or bron-choalveolar lavage (BAL) fluid.29 Hard metal disease is a giant cell alveolitis induced through an idiosyncratic reaction in workers exposed to the metal cobalt.30 Most often, it occurs in workers making or using tungsten carbide, the very hard metal used for machine tools. Onset may be insidious and may include asthmatic symptoms, because cobalt is asthmogenic as well. Recognition of the parenchymal process by BAL or biopsy is crucial because hard metal disease is progressive, often refractory to treatment with steroids, and often lethal; there is anecdotal evidence favoring the use of cytotoxic drugs. Once hard metal disease is diagnosed, the patient should be promptly removed from any further exposure.

In 1998, a novel form of interstitial fibrosis related to an industrial exposure was reported: flock worker’s lung, named after the nylon flocking used for making feltlike textiles.31 Cases of flock worker’s lung are distinctive, with pathologic evidence of both parenchymal fibrosis and lymphocytic bronchiolitis. The reporting of flock worker’s lung underscores a key principle of occupational medicine: that new occupational diseases and other clinical consequences of work continue to be uncovered.32

Dermatologic disorders

Despite increased recognition of the need to reduce contact between the skin and the chemical and physical environment, dermal conditions remain responsible for significant morbidity in the workplace. Most disorders are caused by direct exposure of the skin to workplace irritants, sensitizers, pigments, carcinogens, and materials that interfere with normal dermal function by disrupting sebaceous and follicular secretions (e.g., oils that cause acne) or solvents that erode protective lipids. Trauma, foreign bodies, ionizing and nonionizing radiation, and extremes of temperature may modify or disrupt skin growth, vascular integrity, or both. On occasion, systemic exposure may have a dermal consequence, as in urticarial responses to inhaled antigens, pigmentary alterations from the deposition of metals (e.g., silver), and the much-described though rarely seen chloracne, a variant of acne induced by dioxins and related chemicals. Workers who are at increased risk for allergic contact dermatitis include tanners, cast-concrete product workers, leather-goods workers, footwear workers, machine and metal product assemblers, electrical and telecommunications equipment assemblers, print-shop workers, and machine and engine mechanics.33 Several excellent texts of occupational skin diseases are available.34-36

Overwhelmingly, the major skin problem in the workplace remains dermatitis, either irritant induced or caused by allergy. Many agents may be responsible, including organic and inorganic chemicals, plastics and rubber, oils and lubricants, metals and construction materials, paints, and coatings.37 Both allergic dermatitis and irritant-induced dermatitis are more likely to affect persons with atopic conditions, dry skin, or other dermal risk factors. Distinguishing between the two is less important than recognizing occupational precipitants in the first place; both are difficult to differentiate from other commonplace skin disorders, such as eczema. The key to correct diagnosis is the history of skin contact and the temporal relation between contact and manifestations. Unfortunately, there is seldom a perfect or obvious correlation between the two, and some sleuthing is necessary, especially to discern the extent to which chemical contact may spread to places like the groin or areas where hand contact occurs. Airborne exposure may cause lesions in apparently untouched areas, such as the face; such occurrences are signs of likely hypersensitivity. Vexingly, symptoms do not always abate dramatically over weekends or during short periods in which exposure is avoided; removing the patient from the toxin for a week or two may be necessary to observe response. This, combined with observation of the patient during reexposure, is often the most valuable diagnostic test. Patch testing, performed by an experienced clinician aware of the exposures of concern, may be useful in difficult cases, though the clinician should keep in mind that irritants may yield false negative results and that even many healthy atopic persons will experience reactions to common contactants, such as nickel.38 Often, complete isolation from offending agents is economically infeasible, and materials that previously were well tolerated become sources of irritation and exacerbation. Combinations of work modification, aggressive treatment of flares and complications, and careful attention to routine skin care are necessary to control disease.

Disorders of the urinary tract

Although innumerable toxins are known to cause acute injury to the kidney, exposures to chemical and physical agents at concentrations found in the workplace rarely cause such effects (exceptions include cases involving overwhelming accidental over-exposure or ingestion). Of far greater concern are recurring exposures to agents at more typical workplace exposure levels that have subclinical effects but can lead to late nephropathy. Although there remains a vast burden of unexplained nephro-pathology in the population and despite epidemiologic data suggesting an occupational cause,39,40 chronic renal injury resulting from workplace exposures remains poorly characterized.

The best-established effects on the urinary tract are those caused by exposure to heavy metals, especially lead, mercury, and cadmium; each of these metals is associated with a unique pattern of effects. Workers whose jobs entail exposure to lead include traffic police, hazardous-waste incineration workers, industrial workers, and furniture strippers; workers at risk for exposure to mercury include gold-mine workers, workers at chloral-kali plants, workers exposed to hazardous waste, and construction workers; workers at risk for exposure to cadmium include those involved in the manufacture of batteries. Long-standing heavy-lead exposure results in a pattern of injury difficult to distinguish pathologically and clinically from the effects of hypertension; signs and symptoms include nephrosclerosis and evidence of both glomerular and tubular defects. The ability to clear urate is impaired early in the course and may be a clue; saturnine gout may occur a decade later. There is debate about the possibility of low-level or brief exposures to lead predisposing to hypertension or enhancing the degree of renal injury associated with essential hypertension or gout.41,42 Proponents of this view stress the importance of assessment of lead exposure in patients with mild chronic renal insufficiency.

Long-term occupational exposure to inorganic mercury— principally through exposure to mercury vapor—may result in renal alterations involving the tubules and glomeruli. The monitoring of urinary mercury is useful for controlling such risk.

Cadmium exposure in jewelry making, battery production, and other metal-processing operations leads to bioaccumulation of cadmium in the kidney, which results in proximal tubular injury with excessive excretion of p2-microglobulin and other tubular proteins. Later, a pattern of renal tubular acidosis may occur, which subsequently may lead to the development of renal insufficiency. Because the tubular dysfunction is only partially reversible,45 it is important to carefully monitor cadmium exposure, which is best done with regular blood and urine cadmium testing.46 Renal damage can occur at relatively low levels of cadmium exposure.47

Organic solvents have been implicated in renal tubular and renal parenchymal injury48; despite uncertainty of their role in renal toxicity, growing evidence suggests the need for evaluation of these substances in all new cases of unexplained nephropathy.

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