Occupational Health and Disability Issues in Primary Care

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Contents 1 Occupational Health and Disability Issues in Primary Care 1.1 MEDICAL PRESENTATIONS OF OCCUPATIONAL DISEASE 1.1.1 Respiratory Disease 1.1.2 Acute Irritant Responses. 1.1.3 Occupational Asthma. 1.1.4 Byssinosis and Other Illnesses Related to Vegetable Dust. 1.1.5 Hypersensitivity Pneumonitis. 1.1.6 Inhalation Fever. 1.1.7 Pneumoconiosis. 1.1.8 Granulomatous Disease. 1.1.9 Industrial Bronchitis. 1.1.10 Emphysema. 1.1.11 Skin Disorders 1.1.12 Low Back Pain Case Management 1.1.13 Musculoskeletal Cumulative Trauma or Repetitive Motion Injury 1.1.14 Cardiovascular Disease 1.1.15 Renal and Urinary Tract Disorders 1.1.16 Hepatic Disorders 1.1.17 Neurologic Problems 1.1.18 Hematologic Disorders 1.1.19 Reproductive Hazards 1.1.20 Infectious Diseases 1.1.21 Stress in the Workplace 1.1.22 Physical Hazards 1.1.23 Noise. 1.1.24 Cold Stress. 1.1.25 Heat Stress. 1.1.26 Vibration. 1.1.27 Decompression Sickness (Caisson Disease). 1.1.28 Radiation Exposure. 1.1.29 Occupational Cancer 1.2 DISABILITY ISSUES 1.2.1 Preplacement Evaluation 1.2.2 Return to Work 1.2.3 Workers' Compensation 1.2.4 Short- or Long-Term Disability Due to a Non–Work-Related Medical Problem 1.2.5 Fitness for Duty 1.2.6 The Determination of Impairment and Independent Medical Examinations 1.3 REFERENCES

[edit] Occupational Health and Disability Issues in Primary Care

John W. Burress

David C. Christiani

What is your occupation?

The above question should be routinely incorporated into the primary care data base (see Chapter 4). Box 11-1 provides a sample occupational history and evaluation form. When an occupational history suggests a potential hazard, further questions should detail the extent and character of exposure. When a correlation between past or current exposures and an adverse health effect is suspected, additional measures or appropriate referrals can confirm or rule out that initial clinical impression. Table 11-1 lists occupations, pertinent toxicants, and possible diseases or adverse effects; Table 11-2 matches presenting conditions with toxicants and potential exposures.

Table 11-1 Representative Job Categories, Toxicants, and Possible Diseases to Consider When Taking an Occupational History

Modified from Rom WN, editor: Environmental and occupational medicine, ed 3, Philadelphia, 1998, Lippincott-Raven.

Rights were not granted to include this data in electronic media. Please refer to the printed book.

Table 11-2 Examples of Occupational Health Conditions

From Goldman RH, Peters JM: The occupational and environmental health history, JAMA 246:2831, 1981.

Condition	Agent	Potential exposures
Intermediate or short-term effects
Dermatoses (allergic or irritant)	Metals (chromium, nickel), fibrous glass, epoxy resins, cutting oils, solvents, caustic alkali, soaps	Electroplating, metal cleaning, plastics, machining, leather tanning, housekeeping
Headache	Carbon monoxide, solvents	Firefighting, automobile exhaust, foundry, wood finishing, dry cleaning
Acute psychoses	Lead, mercury, carbon disulfide	Handling gasoline, seed handling, fungicide, wood preserving, viscose rayon industry
Asthma or dry cough	Formaldehyde, toluene diisocyanate, animal dander	Textiles, plastics, polyurethane kits, lacquer use, animal handler
Pulmonary edema, pneumonitis	Nitrogen oxides, phosgene, halogen gases, cadmium	Welding, farming (“silo filler's disease”), chemical operations, smelting
Cardiac dysrhythmias	Solvents, fluorocarbons	Metal cleaning, solvent use, refrigerator maintenance
Angina	Carbon monoxide	Car repair, traffic exhaust, foundry, wood finishing
Abdominal pain	Lead	Battery making, enameling, smelting, painting, welding, ceramics, plumbing
Hepatitis (may become a long-term effect)	Halogenated hydrocarbons (e.g., carbon tetrachloride), viral hepatitis	Solvent use, lacquer use, hospital workers
Latent or long-term effects
Chronic dyspnea
Pulmonary fibrosis	Asbestos, silica, beryllium, coal, aluminum	Mining, insulation, pipefitting, sandblasting, quarrying, metal alloy work, aircraft or electrical parts
Chronic bronchitis emphysema	Cotton dust, cadmium coal dust, organic solvents, cigarettes	Textile industry, battery production, soldering, mining, solvent use
Lung cancer	Asbestos, arsenic, uranium, coke oven emissions	Insulation, pipefitting, smelting, coke ovens, shipyard workers, nickel refining, uranium mining
Bladder cancer	β-Naphthylamine, benzidine dyes	Dye industry, leather, rubber-working chemists
Peripheral neuropathy	Lead, arsenic, n-hexane, methyl n-butyl ketone, acrylamide	Battery production, plumbing, smelting, painting, shoemaking, solvent use, insecticides
Behavioral changes	Lead, carbon disulfide, solvents, mercury, manganese	Battery makers, smelting, viscose rayon industry, degreasing, manufacturing/repair of scientific instruments, dental amalgam workers
Extrapyramidal syndrome	Carbon disulfide, manganese	Viscose rayon industry, steel production, battery production foundry
Aplastic anemia, leukemia	Benzene, ionizing radiation	Chemists, furniture refinishing, cleaning, degreasing, radiation workers

Box 11-1 - Occupational Health History and Evaluation

Worker's name____________ Social Security #_______Age______Principal occupation (for most of working life)___________ Agenda: major concerns of worker and who need copy (e.g., lawyer) Occupational history in chronologic order✢ (This section includes the following factors: years, job title, employer, job description, notable hazards, exposure severity,† protective equipment, and injuries or lost time.) Specific questions related to possible exposures (The above open-ended questioning is preferable, but memory may be stimulated further with direct questions.) During any of the above jobs, have you missed work or lost time because of a work-related injury or illness? Have you ever changed jobs or transferred to another work area because of health problems or symptoms you relate to work? Have you or any of your co-workers ever experienced health problems that you or someone else related to work? Have you ever noticed a pattern in which a symptom (e.g., cough, headache, rash) would go away over a weekend or holiday, only to return on resumption of any of the above jobs? While at work, have you ever experienced shortness of breath or trouble breathing that was not from exertion? At work or later that night, have you ever experienced cough, wheezing, or trouble breathing that you related to dust or fumes? Have you ever developed a rash, burn, or severe itching from a substance you came in contact with at work? During any of the above jobs, did you ever notice consistently becoming nauseated when exposed to certain substances or fumes? Did co-workers, your family, or you ever notice a consistent alteration in thinking, speech, or ability to focus on a task during or after work at any of the above jobs? At work or while enjoying a hobby, have you been exposed to any of the following chemicals or substances? Check box if yes: □ Acids □ Alcohols (industrial) □ Alkalis □ Ammonia □ Arsenic □ Asbestos □ Benzene □ Beryllium □ Cadmium □ Carbon tetrachloride □ Chlorinated naphthalenes □ Chloroform □ Chloroprene □ Chromates □ Coal dust □ Cold (severe) □ Dichlorobenzene □ Ethylene dibromide □ Ethylene dichloride □ Fiberglass □ Halothane □ Heat (severe) □ Isocyanates □ Ketones □ Lead □ Manganese □ Mercury □ Methylene chloride □ Nickel □ Noise (loud) □ PBBs □ PCBs □ Perchloroethylene □ Pesticides □ Phenol □ Phosgene □ Radiation □ Rock dust □ Silica powder □ Solvents □ Styrene □ Talc □ Toluene TDI or MDI □ Trichloroethylene □ Trinitrotoluene □ Vibration □ Vinyl chloride □ Welding fumes □ X-rays Environmental exposure Where do you live? _________ For how long? _________ □ House □ Apartment □ Other (specify) ____________ How many people live with you? ______________ Do you have any of the following? □ Pets (specify) _____________ □ Humidifier □ Air conditioner What type of heat? ____________ Type of stove?____________________ What hobbies do you enjoy? Have you ever noticed any associated health problems or symptoms? Have you ever moved because of a health concern, bad smell, or hazard? Have people in your neighborhood had complaints about health problems related to pollution? Do you live next to a factory? Do you have a garden? Do you use pesticides on your garden or lawn? What household chemicals do you use? History of present illness (Writehe reports pain instead ofhe has pain. Document key points in patient's own words.) Past medical history (Ask about allergies, organ pathology, hospital stays, etc. Consider if any disease is associated with organ system toxicity from any of the above exposures.) Medications Smoking and substance abuse history Family history Social history Review of systems (This especially includes respiratory, skin, musculoskeletal, and nervous systems.) Physical examination Diagnostic testing (Include laboratory tests, imaging studies, physiologic testing, and pulmonary function tests.) Assessment (Inform worker of your opinion about the severity of exposures and whether a relationship may exist among symptoms, health problem[s], and work.) Plan (Discuss with worker your level of certainty, the need for further testing to confirm diagnoses, or your inclination to refer for consultation.) ✢Appropriate space would be provided on actual form.†Estimate time (hours per days per week) and include markers of exposure severity (e.g., “dust so thick we couldn't see 10 feet” or “noise so loud we had to hsout into each other's ears to communicate”)

Disability issues inevitably arise in primary care patients and are discussed later in this chapter. The primary care physician has several potential roles in occupational health and disability determination. The initial patient history, recorded accurately with sufficient detail including key direct quotes by the patient, gets heavy consideration during any future record review. Other potential roles of the primary care physician include: (1) advocating for appropriate resources for injured or ill workers, (2) performing preplacement evaluations that establish baseline data and distinguish whether accommodations are necessary, (3) providingconsultation to companies and assisting in the education of employees and employers, (4) performing return-to-work or fitness-for-duty evaluations, (5) providing acute injury management, (6) performing impairment evaluations, and (7) assisting with surveillance programs. Primary care physicians should be familiar with the major workplaces in their communities, as well as agencies and experts involved in occupational health and safety (Box 11-2).

Box 11-2 - Key Occupational Health Agencies, Standards, and Legal References

Agencies and Organizations Occupational Safety and Health (OSHA) The Occupational Safety and Health Act (OSHAct) provides some general protection under specific standards and its “general duty clause” of Section 5(a)(1): “Each employer shall furnish to each of his employees employment and a place of employment which are free from recognized hazards that are causing or are likely to cause death or serious physical harm to his employee.” Enforcement stems from inspections, citations, and fines that can be initiated by a complaint from a worker or a health care provider. The limitations of OSHA are significant and vary, depending on resources allowed for enforcement and resistance to setting new standards. For example, only about 25 hazardous substances and five hazardous situations have specific standards. Also, large segments of workers are not covered by OSHA including federal government employees, self-employed persons, workers on family farms, and workers at workplaces covered by other agencies or federal statutes, such as mining, fishing, railroad, and nuclear industries. Office of Information and Public Affairs: 202-523-8151; OSHA Home Page: http://www.osha.gov or OSHA Technical Center: http://www.osha-slc.gov/SLTC/. National Institute for Occupational Safety and Health (NIOSH) Research and education agency that investigates workplace illness and injuries to determine nature and extent of hazards; does not have enforcement powers. For information and free literature searches: 800-35N-IOSH or http://www.cdc.gov/niosh/homepage.html. Environmental Protection Agency (EPA) Agency responsible for the assessment and control of environmental problems, including pesticides, noise, toxic substances, radiation, and air, water, and solid waste pollution. 202-260-2090 or http://www.epa.gov. Centers for Disease Control and Prevention (CDC) This agency provides information, does research, and investigates outbreaks of infectious disease; it has broadened its scope to address prevention of noninfectious disease issues as well. Call 888-329-4232 or visit CDC Home Page: http://www.cdc.gov. Department of Transportation (DOT) This department has oversight responsibilities for the nation's highways and other modes of transportation. Questions about a DOT examination can be directed to this administration at 800-526-1144 or visit DOT Home Page: http//www.dot.gov. Agency for Toxic Substances Registry (ATSDR) This agency produces excellent booklets on various toxins and does investigative work regarding environmental concerns. Visit http://atsdr1.atsdr.cdc.gov:8080/atsdrhome.html. American Conference of Governmental Industrial Hygienists (ACGIH) This organization publishes threshold limit values (TLVs) for chemical substances and physical agents as well as biologic exposure indices (BEIs). Updated periodically, this reference contains a broader scope of chemicals and is much more current than most of the OSHA standards. Try http://www.aiha.org/. Selected Standards and Legal References Americans with Disabilities Act (ADAct) Important legislation whose goal is to help those with disabilities mainstream into the U.S. workforce. The implications and practical implementations for occupational health are discussed in latter part of this chapter, or see ADA Document Center http://janweb.icdi.wvu.edu/kinder/. Family Medical Leave Act (FMLA) Important legislation allowing up to 12 weeks unpaid leave for those with personal or family needs. A worker must invoke this to obtain job security benefit. Try http://www.osha.gov.oshpubs/employee.html or www.law.cornell.edu. Right to Know Law Hazard Communication Standard (HAZCOM, 29 CFR 1910.1200[a]; final rule 59 FR 6126) stipulates the employer inform workers of potential exposures. Material Safety Data Sheets (MSDSs) must be available. Primary care providers should request pertinent MSDSs to facilitate the evaluation of workers with chemical or other exposures. Toxicologists can usually be accessed via listed emergency numbers on the MSDSs. The MSDS contains first aid information, the properties of the chemical(s) (e.g. pH), and the Chemical Abstract Number (CAS), which can facilitate further research. Many MSDSs are now available online; try http://research.nwfsc.noaa.gov/msds.html. Another standard (29 CFR 1910.20) provides the right to access exposure information previously compiled by the employer, including biologic monitoring. Medical Records Generated by Employer (e.g., as part of surveillance program) HAZCOM 29 CFR 1910.20(e)(2) provides an employee unrestricted access to his or her medical records as well as, upon written consent, access to an analysis of a co-worker's medical records. The employer is obligated to retain records of any “adverse reactions to health” based on HAZCOM 29 CFR 1910.1200[d][1]; for companies dealing with chemicals, access is stipulated under the Toxic Substance Control Act (section 8[c]); visit http://www.hammock.ifas.ufl.edu/txt/fairs/26242. Hearing Conservation OSHA standard CFG 1910.95 provides an “action” level of 85 db, above which an employer is required to provide baseline audiograms, workplace monitoring, employee notification, audiometric testing, and hearing protection.

Occupational exposures can affect any organ system. The most common occupational problems include those of the skin, respiratory tract, and musculoskeletal system. Although primary care physicians focus on individual patients, recognizing a sentinel health problem in one worker in a company or an industry can help protect others. In occupational medicine, medical surveillance programs are implemented to pick up adversely affected individuals (screening) or assess groups to look for significant trends (surveillance) using either biomarkers of exposure (e.g., blood lead level) or biomarkers of effect (e.g., pulmonary function tests). See Box 11-2 for information on key regulations protecting workers such as the Right to Know Laws that ensure an employee's physician access to information on potential hazards (e.g., Material Safety Data Sheets [MSDSs]).

[edit] MEDICAL PRESENTATIONS OF OCCUPATIONAL DISEASE

[edit] Respiratory Disease

Fewer than 5% of occupational respiratory disease cases are correctly identified as being associated with work. When assessed at a one-time clinical visit, symptoms are often indistinguishable from those caused by the myriad of nonoccupational etiologies. Primary care physicians should routinely ask about occupational and environmental exposures whenever a patient has respiratory symptoms. Furthermore, most work-related respiratory diseases are not curable and must be discovered early in their course to avoid future disability. Airborne pollutants at work can interact, additively or synergistically, with smoking to produce disease (e.g., bronchitis).^[1]

The clinical evaluation for an occupational respiratory disease entails at least four elements: (1) complete history, including occupational and environmental exposures;cigarette-smoking history; and a careful review of respiratory symptoms focusing on cough, sputum production, dyspnea, wheezing, chest discomfort, and allergic responses to work or nonwork environments. Attention to a temporal relation to occupational exposure is very important (e.g., symptoms are worse at the end of a workday, better when on vacation); (2) physical examination, with special attention to breath sounds, although patients with significant disease may have normal examinations; (3) chest x-ray (CXR), with attention to parenchymal and pleural disease. For example, linear irregular opacities in the lower fields may suggest asbestosis, whereas rounded opacities in upper fields may suggest silicosis. A NIOSH-certified “B reader” can provide a semiquantitative interpretation of the CXR through comparison with a standardized set of films that focuses on size, shape, concentration, and distribution of parenchymal opacities and pleural thickening or calcification; and (4) pulmonary function tests (PFTs), which help distinguish among various respiratory diseases. Comparing spirometry done before and after work shifts can also be informative (e.g., occupational asthma). Table 11-3 provides a brief summary of work-related respiratory disease.^[1][2]

Table 11-3 Major Types of Occupational Respiratory Disease

Pathologic process	Occupational disease examples	Clinical history	Physical examination	Chest x-ray	Pulmonary function pattern✢
Fibrosis	Silicosis	Dyspnea on exertion, shortness of breath	Clubbing, cyanosis	Nodules	Restrictive or mixed obstructive and restrictive
	Asbestosis	Dyspnea on exertion, shortness of breath	Clubbing, cyanosis, rales	Linear densities, pleural plaques, calcifications	Normal or ↓ DLCO†
Reversible airways obstruction (mucus plugging, asthma)	Byssinosis, isocyanate poisoning, asthma	Cough, chest tightness, shortness of breath, asthma attacks	↑ Respiratory rate Wheeze	Usually normal	Normal or obstructive with bronchodilator improvement Normal or high DLCO
Emphysema	Cadmium poisoning (chronic)	Cough, sputum, dyspnea	↑ Respiratory rate	Hyperaeration bullae	Obstructive
			↑ Expiratory phase		Low DLCO
Granulomata	Beryllium disease	Cough, weight loss, shortness of breath	↑ Respiratory rate	Small nodules	Usually restrictive with low DLCO
Pulmonary edema	Smoke inhalation	Frothy, bloody sputum production	Coarse bubbly rales	Hazy, diffuse; air space disease	Usually restrictive with ↓ DLCO Hypoxemia at rest
↑, Increased; ↓, decreased.

✢Restrictive PFTs: ↓ FEV₁, ↓ FVC, FEV₁/FVC may be normal. Obstructive PFTs: ↓ FEV₁, ↓ FEV₁/FVC, FVC may be normal.

†Diffusion capacity (level) for carbon monoxide.

[edit] Acute Irritant Responses.

Workplace exposures usually elicit specific regional inflammatory effects that depend on characteristics of the irritant, including the concentration of the agent in respired air, its solubility, the duration of exposure, the presence of a carrier aerosol, and the level of physical activity and physical fitness of the worker. These combine to determine the regional site, severity, and timing of irritant response. In general, highly water-soluble agents irritate the upper respiratory tract. They tend to act quickly, causing burning of the eyes, nasal congestion, frontal headache, and runny nose. A dry cough may be seen with throat involvement or, with severe exposure, epiglottic edema; very high exposures can produce bronchospasm and pulmonary edema. Ammonia, hydrogen chloride, and hydrogen fluoride are examples of water-soluble irritants. Odor and immediate symptoms often alert the worker and limit duration of exposure unless the worker inadvertently becomes trapped (e.g., in a confined space). Moderately water-soluble irritants affect the midrespiratory tract to cause bronchoconstriction. Insoluble agents can induce delayed (6 to 24 hours) pulmonary edema via direct toxicity to capillary walls. Bronchospasm may precede effects at the alveolar level. Ozone, phosgene, and oxides of nitrogen are common examples. Persisting sequelae are possible from either single high-dose exposure or episodic low-dose exposures causing irritant asthma (reactive airways dysfunction syndrome).^[1]

[edit] Occupational Asthma.

Asthma is a common clinical entity in the general population. An estimated 2% to 15% of cases are thought to be caused or aggravated by work exposures, but this may grossly underestimate the true prevalence because of both underdiagnosis and employees leaving work settings with exposures that they associate with adverse health effects. A variety of materials have proved to be asthmogenic (Table 11-4). These differ greatly as to period of sensitization required, latency, pattern of asthmatic response, duration of symptoms, and progression. All these factors may differ among individuals, adding to the complexity of the diagnosis.

Table 11-4 Selected Causes of Occupational Asthma✢

Modified from Chan-Yeung M, Lam S: Occupational asthma, Am Rev Respir Dis 133:686, 1986.

Agents	Workers at risk
High-molecular-weight compounds
Animal products: dander, excreta, serum, secretions	Animal handlers, laboratory workers, veterinarians
Plants: grain, dust, flour, tobacco, tea, hops, latex	Grain handlers, tea workers, bakers and workers in natural oil manufacturing and tobacco and food processing, health care workers
Enzymes: Bacillus subtilis, pancreatic extracts, papain, trypsin, fungal amylase	Bakers and workers in detergent, pharmaceutical, and plastic industries
Vegetable: gum acacia, gum tragacanth	Printers, gum-manufacturing workers
Other: crab, prawn	Crab and prawn processors
Low-molecular-weight compounds
Diisocyanates: toluene diisocyanate (TDI), methylene diphenyldiisocyanate (MDI)	Polyurethane industry workers, plastics workers, workers using varnish, foundry workers
Anhydrides: phthalic and trimellitic anhydrides	Epoxy resin and plastics workers
Wood dust: oak, mahogany, California redwood, Western red cedar	Carpenters, sawmill workers, furniture makers
Metals: platinum, nickel, chromium, cobalt, vanadium, tungsten carbide	Platinum-and nickel-refining workers, hard metal workers
Soldering fluxes	Solderers
Drugs: penicillin, methyldopa, tetracyclines, cephalosporins, psyllium	Pharmaceutical and health care workers
Other organic chemicals: urea formaldehyde, dyes, formalin, azodicarbonamide, hexachlorophene, ethylene diamine, dimethyl ethanolamine, polyvinyl chloride pyrolysates	Workers in chemical, plastic, and rubber industries; hospitals; laboratories; foam insulation manufacture; food wrapping; and spray painting

✢Mechanism believed to be immunoglobulin E (IgE), mediated for high-molecular-weight compounds and for some low-molecular-weight compounds. The immunologic mechanism for asthma from many low-molecular-weight substances remains undefined.

Three general patterns of asthmatic response to challenge tests are immediate (onset within minutes, maximal symptoms at 20 minutes, recovery in 1 to 2 hours), late (onset in several hours, peak at 4 to 8 hours, recovery in 24 hours), and dual (a combination of immediate and late). In the workplace these patterns may manifest as (1) maximal deterioration on first working day, (2) daily similar deterioration with overnight recovery, or (3) progressive deterioration throughout the workweek. The intensity as well as duration of exposure may be important for sensitization.

Atopy is a risk factor for occupational asthma from exposure to high-molecular-weight exposures, but not from exposure to low molecular weight (see Table 11-4). For example, isocyanate-induced asthma is as common among nonatopic as atopic workers (5% to 15% of all workers significantly exposed will be sensitized). Major or minor constituents and accidental by-products of substances may be inciting agents. Thus an appropriate clinical suspicion and subsequent history (temporal association with workplace exposure) are crucial in making the diagnosis. The physician should document intermittent respiratory symptoms (cough, chest tightness, dyspnea, wheezing, decreased exercise tolerance) and, if possible, physiologic evidence of reversible or variable airways obstruction (i.e., a peak expiratory flow rate diary pattern showing a consistent 20% drop or cross-shift PFTs with 10% variability in forced expiratory volume in 1 second [FEV₁] temporally related to work). The necessity of these and other measures, including bronchoprovocation with methacholine or dilute aerosols of workplace substances, depends on the strength of the history, whether others have been affected, and knowledge of exposure levels at the workplace. Objective evidence is desired because history alone may not be reliable. It is important to realize, however, that no definitive diagnostic criteria exist. Eosinophil elevation in sputum or blood may help distinguish allergic asthma from nonallergic asthma and bronchitis; skin testing or other immunologic tests for allergens indicate sensitization but may not correlate well with the actual airways exposure and may not even be available for many workplace agents.

Acute care of workers with occupational asthma exacerbations does not differ from that of nonoccupational attacks (see Chapter 72 ). However, further management is required, including cessation of workplace exposure, assessment of risk to other workers, and follow-up to document resolution or lack thereof. Once an individual is sensitized to an agent, even low levels of that agent can trigger an attack. If return to a suspected exposure is anticipated, personal protective devices such as a respirator, along with close monitoring of symptoms and lung function, are certainly warranted but may not prevent exacerbations. Continued exposure may indeed result in generalized airway hyperresponsiveness (i.e., workers become sensitive to exposures outside the workplace to which they had not previously been sensitive) that fails to resolve on cessation of exposure.^[1]

[edit] Byssinosis and Other Illnesses Related to Vegetable Dust.

Unlike occupational asthma, byssinosis (Greek for “white thread”) may produce bronchoconstriction without prior exposure. The mechanism is thought to occur through direct toxicity and to involve endotoxin from gram-negative bacterial contaminants of cotton dust that produce acute symptoms and a decrease in lung function. Workers involved in the initial processing of (in decreasing order of potency) soft hemp, flax, cotton, jute, and sisal are at greatest risk. With cotton, higher “trash” or impurity content material generates more inhalable dust. Ginning and the early stages of yarn preparation, which involve breaking open bales of cotton to separate impurities and then “carding” (aligning fibers into parallel threads), historically have been associated with the greatest prevalence of byssinosis. Engineering controls to reduce dust exposure, such as enclosed and automated carding machines, have greatly improved textile mill conditions in the United States. Processing of cloth, or finishing, is practically free of dust, especially after the cloth has been washed. The diagnosis of byssinosis is based mainly on symptoms of shortness of breath and chest tightness, with or without cough and sputum production. The pattern of symptoms is characteristic, being more pronounced on the first day of the workweek or after a vacation (“Monday morning tightness”). A decrease in FEV₁ may be seen with these symptoms. Further investigation is warranted if the FEV₁ decreases 3% or 75 ml in a group of 20 or more workers. A decrease of 10% or 200 ml or more may be significant for an individual. OSHA standards mandate medical surveillance of preshift and postshift lung function. CXR and skin tests have no characteristic findings. Mild cases probably are reversible, but prolonged exposure to high dust levels may lead to irreversible disease. The advanced stage is characterized by fixed airways obstruction with hyperinflation and air trapping; chronic bronchitis increases the severity. Cigarette smokers also exposed to cotton dust are at particular risk of irreversible airways obstruction.

Also associated with the cotton industry are two conditions known as mill fever and weaver's cough. Mill fever is self-limited, occurs on first exposure to cotton dust environment, and lasts 2 to 3 days. It is a flulike illness, and symptoms include headache, malaise, and fever similar to metal and polymer fume fever. Weaver's cough occurs in outbreaks of acute respiratory illness characterized by a dry cough. It may be associated with mildewed yarn.^[1]

[edit] Hypersensitivity Pneumonitis.

Also known as extrinsic allergic alveolitis, hypersensitivity pneumonitis (HP) is characterized by an interstitial and infiltrative process after exposure to certain organic dusts and chemicals in predisposed individuals. As opposed to bronchoconstriction in asthma with immunoglobulin E (IgE)-mediated (type I) immediate reactions, HP appears to be caused by inadequate control or regulation of cellular (type IV) immune function. Although most individuals exposed to inhaled antigen develop an immune response, only a small percentage develop clinical disease. In one study, for example, only the 10% of pigeon breeders who developed HP had defective suppressor lymphocytes. HP occurs most often in workers exposed to fungi or bacteria found in thermophilic material; however, it is also seen with longstanding exposure to some animal antigens and inorganic haptens (Table 11-5). Atopy is not a risk factor. For unclear reasons, nonsmokers may be more susceptible than smokers.

Table 11-5 Examples of Hypersensitivity Pneumonitis

Disease	Antigenic material	Antigen
Farmer's lung	Moldy hay or grain	Thermophilic actinomycetes
Bagassosis	Moldy sugar cane
Mushroom worker's lung	Mushroom compost
Humidifier fever	Dust from contaminated air conditioners or furnaces
Maple bark disease	Moldy maple bark	Cryptostroma species
Sequoiosis	Redwood dust	Graphium species, Pullularia
Bird-breeder's lung	Avian droppings or feathers	Avian proteins
Pituitary snuff user's lung	Pituitary powder	Bovine or porcine proteins
Suberosis	Moldy cork dust	Penicillium species
Paprika splitter's lung	Paprika dust	Mucor stolonifer
Malt worker's lung	Malt dust	Aspergillus clavatus or A. fumigatus
Fish meal worker's lung	Fish meal	Fish meal dust
Miller's lung	Infested wheat flour	Sitophilus granarius (wheat weevil)
Furrier's lung	Animal pelts	Animal fur dust
Coffee worker's lung	Coffee beans	Coffee bean dust
Chemical worker's lung	Urethane foam and finish	Isocyanates (TDI, HDI), anhydrides

Clinical features vary along a spectrum of acute, subacute, and chronic forms of HP. Acute disease symptoms occur 4 to 8 hours after exposure and include headache, fever, sweating, rigors, anorexia, nausea, vomiting, dry cough, chest tightness, and dyspnea on exertion. On physical examination, there may be fine basilar rales on inspiration without wheezing along with fever and tachycardia. Symptoms generally subside in 48 hours, but repetitive acute episodes may cloud the history. CXR may reveal patchy infiltrates or diffuse micronodular shadowing. PFTs often reveal a restrictive pattern, with FEV₁ reduced in proportion to forced vital capacity (FVC). In an acute attack of HP, there may be decreased diffusion capacity (DLCO) and lung compliance, as well as hypoxemia accentuated with exercise.

With very few exceptions, therapy for HP includes lifelong avoidance of the inciting agent. A trial of systemic corticosteroids while monitoring blood gases and PFTs may be indicated. Full or partial reversal of the lung disease may be possible. The chronic form may be preceded by bouts of acute symptoms or may arise insidiously from repeated low-level exposures, yielding persistent flulike symptoms. Progressive dyspnea associated with cough, malaise, lethargy, and weight loss may develop. Chronic HP may result in restrictive, obstructive, or mixed ventilatory defects with decreased diffusion capacity. CXR suggests interstitial fibrosis; continued exposure may yield a honeycomb appearance on the CXR in end-stage disease.

Prevention of HP includes workplace controls, such as exhaust ventilation or the elimination of conditions that foster bacterial or fungal growth, and early avoidance through medically mandated removal of workers who develop symptoms.^[1][3]

[edit] Inhalation Fever.

Certain inhalation exposures can result in acute self-limited flu-like illness. Symptoms begin within hours after an exposure. Welding galvanized steel can release zinc oxide, producing metallic taste at first, and then throat irritation followed by fever, chills, myalgia, malaise, and a nonproductive cough; occasionally headache, nausea, and vomiting occur. The pathogenesis differs from HP; instead of an allergic mechanism, leukocyte recruitment to the lungs with release of cytokines thought to cause the systemic symptoms has been postulated. In addition to zinc, copper and magnesium can produce “metal fume fever.” Inhalation of combustion products of polytetrafluoroethylene (Teflon) can yield “polymer fume fever.” Several bioaerosols can impart a similar clinical syndrome. Examples include contaminated humidifier mist (“humidifier fever”) and inhalation of products from moldy silage, compost, or wood chips (“organic dust toxic syndrome”). Although the reason is unclear, repeated attacks of inhalation fevers may lead to long-term sequelae.^[4][1][3]

[edit] Pneumoconiosis.

Respirable inorganic dust is a causal agent in silicosis, asbestosis, and coal workers' pneumoconiosis. Although the epidemiology and pathology differ, the clinical features are similar, including nonproductive cough initially, followed by progressive shortness of breath with perhaps distant heart sounds, distant breath sounds, and if severe enough, signs and symptoms of right-sided heart failure. Dust less than 5 microns in aerodynamic diameter can reach terminal bronchioles and alveoli; when suspended in air, dust of this size is not visible and can lead to a potentially unrecognized hazard. Secondary prevention to avoid further loss of reserve lung function is of paramount concern, given the lack of cure. Workers should be removed from exposure on finding evidence of pneumoconiosis. However, progression may still continue even after removal from exposure.

Coal workers' pneumoconiosis (CWP) is caused by coal dust, principally carbon, and affects a defined group of workers in an industry. Simple CWP is distinguished from complicated CWP (also called progressive massive fibrous [PMF] and involving about 1% of cases) by the relative size and confluence of nodular opacities on CXR. The pathogenesis of PMF is controversial. Continued reduction in exercise tolerance may be seen. Unlike asbestosis or silicosis, simple CWP generally does not progress after the worker is removed from exposure, although PMF may progress. An upper lobe predominance is seen, similar to silicosis. Coal dust can also produce chronic bronchitis and centrolobular emphysema independent of smoking, but smokers have additional risk when working with coal because of a combined effect. The associated chronic bronchitis can contribute to disability and is dose related to coal dust exposure in both smokers and nonsmokers. Federal mandates provide CXR screening together with a protection program that allows a miner to work in a reduced-dust environment with increased monitoring.

In contrast, silica and asbestos are encountered in multiple industries (see Table 11-1) by a greater number of workers who produce a diverse range of products, making control and surveillance more difficult. Of the two basic types, silicosis exemplifies typically localized and nodular peribronchial fibrosis, in contrast to the diffuse interstitial fibrosis of asbestosis.

The amount of fibrosis in silicosis appears proportional to the free silica content and duration of exposure. For example, acute silicosis stems from an intense exposure that leads to onset of symptoms within weeks and death within a year. A chronic form of silicosis is more common; this form entails CXR findings 15 years after exposure and symptoms even later. Accelerated silicosis falls between these two extremes, with findings within 5 to 15 years. Typically, nodules on CXR show an upper lobe predominance. Silicosis imparts an increased risk of Mycobacterium tuberculosis and atypical mycobacteria infection.

Asbestos exposure leads to several distinct manifestations of lung disease. The most common are benign pleural plagues. Asbestosis refers to the diffuse interstitial pneumoconiosis. Lung cancer and mesothelioma are also associated with asbestos exposure.

Asbestosis results from lung inflammation and fibrosis caused by persisting activation of alveolar macrophages, creating patchy, linear, and irregular fibrosis with a lower lobe predominance. Important to the diagnosis are a history of exposure, somewhat dose related, with an appropriate latency period of about 15 years; a CXR suggesting interstitial fibrosis; PFTs with a restrictive pattern (although obstructive or mixed patterns can be seen); and decreased diffusion capacity, which may be the first sign of early disease. Occasionally, open-lung biopsy is needed for definitive diagnosis. Rales are present in only about 20% of those affected; clubbing is rare and seen in advanced cases only. There is a fivefold increased incidence of lung cancer associated with asbestos exposure alone, a tenfold to twentyfold increase in smokers, but a fiftyfold to ninetyfold increase with both exposures together. Two scientific controversies remaining are (1) whether lung cancer caused by asbestos occurs only in those with the interstitial fibrosis of asbestosis (currently a minority stance) and (2) whether asbestos-related pleural disease alone, without interstitial fibrosis of lung parenchyma, conveys any increased risk of lung cancer.

Pleural calcifications and plaques seen incidentally on CXR suggest asbestos-related disease. These pleural plaques are generally asymptomatic until extensive and severe, when pleuritic chest pain or tightness may be found. When plaques are present, it is appropriate to do follow-up CXR and PFTs every 3 years. If a decrement in PFTs is found and CXR findings suggest parenchymal disease, yearly follow-up is warranted. It is important that patients understand the difference between benign plaques and lung cancer or mesothelioma. Mesothelioma may occur in persons with only a distant, brief exposure to asbestos and no asbestos-related pleural disease or pulmonary fibrosis. A pleural effusion is often the presenting finding of mesothelioma. Some increased risk of gastrointestinal tract cancer secondary to asbestosis exposure has been noted, thus warranting screening.

Exposure to respirable synthetic vitreous fibers (SVFs) (e.g., fibrous glass, mineral wool, ceramic fiber) has been associated with irregular opacities consistent with pneumoconiosis in some studies but not in others. A twofold elevation in lung cancer risk was found in one large study of exposure to SVFs on 30-year follow-up. Current levels of exposure are much less, and studies are ongoing to ascertain a health effect, if any.^[1][2][3]

[edit] Granulomatous Disease.

Exposure to beryllium, talc, and some synthetic fibers can result in granuloma formation clinically similar to sarcoidosis. Beryllium is a metal with very desirable characteristics for many high-tech and space applications (e.g., lightweight, high tensile strength, high melting point, ability to stop neutrons). The pulmonary reaction in berylliosis is out of proportion to the amount of metal dust in the lungs. CXR may reveal an interstitial pattern of groundglass appearance or more discrete, small, rounded opacities; hilar adenopathy is present in 30% to 40% of patients with chronic berylliosis. PFT findings relate to the distribution of granulomas and can be restrictive, obstructive, or normal with reduced diffusion capacity from interstitial involvement. The lymphocyte proliferative test (LPT) from blood and/or bronchoalveolar lavage fluid is both sensitive and specific for berylliosis. Before 1949, fluorescent light manufacturing was the origin of most cases. Machining of beryllium for various high-tech applications is increasing. Of interest, bystander cases or disease in individuals not directly involved in machining but sharing air space has been documented, warranting strict adherence to prevention (e.g., local exhaust).^[1][2]

[edit] Industrial Bronchitis.

Many work exposures can cause chronic bronchitis, including mineral dusts and fumes such as coal and metals, organic dusts such as cotton and grain, plastic compounds such as phenolics and isocyanates, acids, and smoke inhalation. Although smoking is the most common cause of bronchitis, there may be a superimposed occupationally related component.^[1]

[edit] Emphysema.

Emphysema can be the late manifestation of such occupational exposures as coal dust in PMF, cadmium, and isocyanates. However, emphysema does not appear to occur in workers chronically exposed to cotton dust more frequently than would be attributable to cigarette smoking. Whether this response occurs after other occupational exposures is unclear at present.^[1]

[edit] Skin Disorders

Skin disorders account for 20% to 30% of all new cases of occupational illness. Of these cases, 90% are contact dermatitis. Four fifths of contact dermatitis cases are from acute or chronic exposure to an irritant, and one fifth are allergic cases caused by a specific sensitizer (Box 11-3). These dermatoses may be induced or aggravated by the work environment. It is very useful for the primary care physician to determine the occupational cause of the dermatitis both to facilitate management decisions (e.g., when the patient can return to work, whether it is necessary to perform a patch test) and to prevent further illness in that worker or similarly exposed co-workers. The pattern of eruption and type of lesion, together with a thorough occupational and medical history, are therefore crucial. Work-related illness is more plausible if a temporal relationship and an exposure capable of causing the dermatosis exist.

Box 11-3 - Contact Dermatitis: Four Types, Possible Causes, and Examples of Occupations at Risk✢

Rights were not granted to include this data in electronic media. Please refer to the printed book. ✢Modified from LaDou J, editor: Occupational medicine, East Norwalk, Conn, 1990, Appleton & Lange.

The ability of an irritant to cause dermatitis depends both on the agent, including its concentration and duration of exposure to the skin, and the skin itself, including the skin thickness, the presence of hair follicles, existing skin disruption, and underlying skin conditions. Of note, the area of a healed lesion is at greater risk of recurrence of dermatitis for at least 3 months. Also, some agents are particularly toxic in synergy with sun exposure, yielding a phototoxic dermatitis. Certain preexisting skin conditions predispose workers to develop other skin problems more easily. For example, patients with psoriasis may develop additional lesions at the site of mechanical trauma (Koebner's phenomenon), those with atopic dermatitis may experience a flare-up when exposed to an irritant, and those with vitiligo may develop depigmentation at the site of mechanical trauma.

In acute irritant contact dermatitis, there is typically a sharp demarcation of the affected skin areas at the site of the exposure. Then, erythema or vesiculation usually follows. The irritant should be irrigated immediately with water if the agent is water soluble or with mineral or olive oil if it is hydrophobic. Local therapy such as wet dressings may help remove remaining traces of the irritant and ease the discomfort.

In contrast, chronic irritant dermatitis stems from longer exposure to a mildly irritating chemical. Erythema, scaling, pruritus, fissuring, and lichenification of a less well delineated area are characteristic. Chronic irritant dermatitis is the most common occupational skin disease. Aggressive therapy includes high-dose topical or in some instances oral corticosteroids. The prognosis is guarded for some patients with chronic hand dermatitis; the condition may not abate even with a job change, reinforcing the need for early detection.

Chemical burns as a form of contact irritant dermatitis are distinct in that substantial skin necrosis and inflammation result from a one-time, usually brief exposure. Acids coagulate protein through oxidation, reduction, desiccation, or salt formation. Alkalis coagulate protein but also saponify fats and cause liquefaction necrosis. In all cases, copious irrigation with water is warranted initially. Most authorities consider pH neutralization after lavage to be unnecessary. Therapy is similar to burn care, with topical sulfadiazine, nonadherent surgical dressings, and cautious debridement as needed.

Some specific concerns relate to problematic agents. Hydrofluoric acid, used as a rust remover, an etching agent in the semiconductor industry, and a reagent in fluorination processes, produces intense pain and erythema. If the concentration is less than 20%, symptoms may be delayed by several hours. A worker can use a dilute solution without gloves for a prolonged period and then seek medical attention for mild discomfort and redness, only to return later when symptoms peak. Fluoride's affinity for calcium can lead to extensive underlying bone destruction and, most important, life-threatening systemic toxicity from hypocalcemia. If the burn area is greater than 4 cm, admission for cardiac monitoring is indicated. Local calcium gluconate injections and even arterial infusion may be necessary for pain control and management. Calcium gluconate gel (10%) applied topically, preferably at the workplace, can be tried initially. Alkyl mercury compounds, which are used as disinfectants, wood preservatives, and fungicides, are extremely toxic to the central nervous system. If alkyl mercury causes blistering, the necrotic skin should be debrided as soon as possible to avoid continued absorption. Phenol or carbolic acid burns can cause depigmentation but also systemic toxicity. Water irrigation is less effective, and polyethylene glycol diluted with alcohol is recommended to help remove residual phenol. Chromic acid, used in electroplating, etching, and glass cleaning, oxidizes tissue to produce small, painless ulcers called “chrome holes.”

Allergic contact dermatitis may mimic chronic irritant dermatitis in its presentation. Often the work history identifies exposure to a known sensitizer (see Box 11-3). A latent period of about 2 weeks is required after initial exposure. The allergenic chemical binds to a skin protein to become a complete antigen, eliciting a Type IV or cell-mediated immune response. One approach is to prescribe topical steroid therapy along with avoidance of suspected allergen(s). If the worker returns to work and redevelops the dermatitis, the diagnosis is clear. However, workplace exposures are often complex, and effective management, including recommending appropriate restrictions, process modification, personal protective equipment, or job transfer, may be difficult. Patch testing may be necessary and should be performed in a standard manner and interpreted with caution.

Contact urticaria also requires a latency period of weeks to years but differs in that histamine and other vasoactive substances are liberated by the principal mediator IgE and onset is more rapid (see Box 11-3).

Exposure to the protein allergens in natural rubber latex can induce both a Type IV or cell-mediated response producing contact dermatitis and a Type I or IgE immediate hypersensitivity response producing urticaria. The latter can involve respiratory (asthma) and even anaphylactic reactions. Cornstarch powder in gloves can absorb latex allergen and become airborne. Thus exposure routes include inhalation in addition to cutaneous, mucosal, and visceral. Hospitals therefore make efforts to limit latex use to prevent sensitization in health care workers.

Other skin manifestations of occupational exposures include depigmentation from phenols and hydroquinone, chloracne from polychlorinated biphenyls (PCBs), and occupational Raynaud's disease from vibration. Skin cancer, as from exposure to ultraviolet (UV) light, and skin infections, as from herpes simplex, also may result from exposure at work.

Primary and secondary prevention consists of engineering controls, industrial and personal hygiene, gloves, and protective clothing. The type of glove and its resistance to the offending agent should be considered (Box 11-4). Despite these efforts, assiduous avoidance may still be necessary.^[4][3]

Box 11-4 - Preferred Gloves for Use with Specific Irritant Chemicals

Heavy rubber: inorganic acids, organic acids, soaps and detergents Nitrile: aromatic solvents, chlorinated solvents Neoprene: aliphatic solvents, vegetable oils

[edit] Low Back Pain Case Management

Work-related low back pain occurs frequently, roughly 20% of work injuries that present for care, and accounts for more than 30% of the cost of all claims. The disproportion is typically due to the high cost of a minority of cases that experience prolonged or indefinite disability. Chapter 127 covers the diagnosis and care of low back pain. When considered work-related, the physician should be attentive to aspects of management that can prevent a worker from becoming “disabled.” First, it is important to have the initial history carefully documented. Second, the physician should consider more frequent follow-up (e.g., weekly) to deal with workplace issues, refine modified duty restrictions, and document progress. Third, it is important to elicit the worker's own perception of his or her low back pain, correct misconceptions, and provide realistic information as to the prognosis. Fourth, if progress is slower than anticipated, it is useful to document inconsistent objective signs, positive Waddell's signs (suggesting symptom magnification or malingering as noted in Chapter 127 ), and poor cooperation with therapies. When recovery is delayed, the physician should assess the patient for an underlying depression. Appropriate referrals, judicious diagnostics, and communication with the employer and/or case manager are prudent steps. A fine line can exist between being supportive and enabling disability or the “sick role.” It is important to assess any ergonomic hazards that might lead to recurrence or similar injury in co-workers (Box 11-5). When appropriate and with the worker's consent, it can be very constructive to engage the employer in discussion as to the worker's condition and potential modified duty assignments. Doing so can greatly facilitate successful transition back to work. See the section on “Disability Issues” for more details.^[4]

Box 11-5 - Factors Associated With Low Back Pain

Related to Job Manual handling tasks (almost two thirds of compensated cases) Lifting (about one half of claims; most often from floor) Twisting (about one fifth of cases) Bending (one tenth of cases) Falling (one tenth of cases) Reaching Excessive weights Prolonged sitting Vibration Related to Individual Prior episode (threefold risk if occurred within 3 years) Job dissatisfaction (very important; based on longitudinal questionnaire data) Smoking (accelerates disk degeneration) Obesity and genetic factors

[edit] Musculoskeletal Cumulative Trauma or Repetitive Motion Injury

Cumulative trauma or repetitive motion injury results from microtears to soft tissues and an inflammatory response. Depending on both the demands of the work setting and an individual's healing capacity, these lesions frequently are not allowed to heal properly and may progress.

Cumulative trauma disorders (CTDs) account for about 3% of the total workers' compensation claims. The focus on CTDs stems from an increasing prevalence, especially in some industries such as meatpacking, with an estimated 15% of workers affected. Table 11-6 shows the types of CTDs associated with different jobs. Work-related factors that increase the likelihood of CTDs include repetition, forceful exertion, incentive-and machine-paced work, awkward joint posture, mechanical pressure, vibration, cold, and job dissatisfaction. The primary care physician should make a specific and accurate diagnosis (Table 11-7). The history should include questions aimed at substantiating a work-related cause, if one exists, including a temporal relationship between the onset of symptoms and performing a predisposing job task, as well as the absence of alternative explanations such as a fall or a sports-related injury. Especially with recurrent or recalcitrant CTDs, a systemic medical condition causing increased vulnerability should be considered (e.g., hypothyroidism). The overall goal is to prevent progression and permanent loss of function. See the individual chapters in Part Two, Section IX for specific diagnoses and therapies. Sometimes the patient can return to work on “modified duty.” However, if symptoms persist, a trial of “active rest” away from work for at least 2 weeks may be necessary. See Disability Issues for more details, including return-to-work issues.^[5][4][1]

Table 11-6 Partial List of Cumulative Trauma Disorders and Associated Occupations

Rempel DM: Work-related cumulative trauma: disorders of the upper extremity, JAMA 267:838, 1992.

Disorder	Occupation
Tenosynovitis	Food packer
	Buffing/grinding worker
	Cashier
	Data entry clerk
	Musician
Wrist tendinitis	Small parts assembler
	Package assembler
	Butcher/meat packer
	Reporter/editor
	Espresso maker
De Quervain's tenosynovitis	Sewer/cutter
	Packer
	Electronic assembly worker
Trigger finger	Labeler
Epicondylitis	Musician
	Construction worker
	Electrician
	Butcher/meat packer
Carpal tunnel syndrome	Butcher/meat packer
	Cake decorator
	Postal worker
	Assembly worker
	Garment/sewing worker
	Rock driller
	Grocery checker
Ulnar nerve entrapment	Glass cutter
	Telephone operator
Shoulder tendinitis	Overhead assembly worker
	Punch press operator
	Butcher/meat packer
Hand-arm vibration syndrome	Forest worker
	Chipper/grinder
	Rock driller

Table 11-7 Tests for Common Cumulative Trauma Disorders

Rempel DM: Work-related cumulative trauma: disorders of the upper extremity, JAMA 267:838, 1992.

Disorder	Diagnostic tests/indicators
De Quervain's tenosynovitis	Finkelstein test
Tendinitis	Localized tenderness
	Pain with passive stretching
	Pain with contraction of associated muscles
Carpal tunnel syndrome	Percussion test (Tinel's sign)
	Wrist flexion test (Phalen test)
	Von Frey pressure test✢
	Electrodiagnostic study
Tenosynovitis	Localized pain with tendon motion or stretching
Cubital tunnel syndrome	Elbow flexion test
	Percussion test (Tinel's sign)
	Electrodiagnostic study
Lateral epicondylitis	Cozen test†
Neck tension syndrome	Muscle spasm of trapezius
	Pain with active resistance of neck motion
Cervical root syndrome	Spurling test‡

✢Semmes-Weinstein monofilaments.

†Pain at lateral epicondyle with resisted wrist extension and radial deviation while forearm is pronated.

‡Compression on top of head with neck in 20 degrees at extension.

[edit] Cardiovascular Disease

The extent of cardiovascular disease attributable to workplace exposure is unknown. Several toxic agents have been shown to affect the heart adversely through several different mechanisms (Table 11-8). Acute overwhelming exposures to carbon monoxide (CO), halogenated solvents, and organophosphate pesticides can result in death. However, today's primary care physicians are much more likely to encounter patients with chronic low-level exposures, such as those with exacerbation of coronary heart disease by CO exposure. A young worker with an unusual presentation of cardiovascular disease should prompt a detailed occupational history, with emphasis on those toxins known to cause heart disease. If the influence of a cardiotoxin is suspected, an exposure measurement at work may be necessary. Other workers may also be similarly exposed and affected. Some workplace cardiotoxins can act through more than one mechanism. For example, chronic CO exposure may accelerate atherosclerosis; induce carboxyhemoglobin formation, which can burden existing heart and lung disease via decreased tissue oxygenation; and cause congestive cardiomyopathy from chronic high-level exposure. Nitrates from explosive and certain pharmaceutical manufacturing processes exert their effects on withdrawal because of rebound vasospasm of the coronary arteries. A worker with an occupational exposure to nitrates might experience headaches temporally associated with work. Heart disease in certain professions (e.g., firefighting) may be compensable on the basis of special laws in some states.^[4][3]

Table 11-8 Classification of Cardiovascular Diseases and Possible Toxic Causes

Modified from LaDou J, editor: Occupational and environmental medicine, Stamford, Conn, 1997, Appleton & Lange.

Rights were not granted to include this data in electronic media. Please refer to the printed book.

[edit] Renal and Urinary Tract Disorders

The heightened susceptibility of the kidney to toxic agents stems from its enormous blood flow, concentrating function, high metabolic rate, vast glomerular endothelial surface, and conversion of conjugated substances back into their toxic form. The physician is at a disadvantage in identifying early kidney injury given the lack of sensitivity of blood urea nitrogen (BUN) and creatinine testing and the lack of early warning symptoms. Much research is underway to establish more effective methods of early detection. At present, functional abnormalities must be extrapolated from abnormal urinalysis findings, 24-hour urine test for protein and creatinine clearance, and ultrasound; additional tests include fractional sodium excretion, urine chemistry, β₂-microglobulin, and renal biopsy (see Chapter 144 ). Very high short-term exposures can cause acute renal failure (e.g., high level exposure to carbon tetrachloride or inorganic mercury). However, the unknown extent of chronic renal failure and hypertension caused by occupational and environmental toxins has potentially greater impact. In general, lower and more long-term exposure to toxins may lead to accelerated loss of renal function and possible chronic renal failure. Table 11-9 groups toxins according to site of action. Some toxins such as cadmium and mercury bioaccumulate in the kidney. Several mechanisms (direct, indirect, immunologic) and exposure routes (ingestion, inhalation, dermal) are possible. Bladder cancer can result from aromatic amines such as aniline dye, presumably related to the concentration of such chemicals in the trigone area.

Table 11-9 Renal Toxicants Grouped by Site of Action and Associated Occupations

Site of action	Toxicant	Occupations
Glomerulus	Silica	Stone cutting, sandblasting
	Solvents	Use of paints, degreasers, and fuels
Proximal tubule	Lead (inorganic)	Battery manufacture, smelting, lead abaters
	Cadmium	Manufacture of alloys, glass, paints, and electrical equipment, smelting
	Mercury (inorganic)	Manufacture of mirrors, batteries, alloys, and scientific equipment, mining; dental office work
	Halogenated aliphatic hydrocarbons (e.g., CC14)	Solvent use, dry cleaning, work with fumigants
Interstitium	Uranium	Mining, refining
Acute tubular necrosis	Cadmium	Welding of cadmium-plated metal (other heavy metals are possible toxicants, including chromium, mercury, and vanadium)
	Arsine gas	Coal or metal processing, semiconductor manufacturing (secondary to hemoglobinuria)
Accelerated atherosclerosis (prerenal)	Carbon disulfide	Manufacture of rayon and neoprene tires
Bladder (cancer)	Aromatic amines	Manufacture and use of synthetic dyes

[edit] Hepatic Disorders

The primary care physician should be alert to possible hepatoxic interactions involving different workplace chemicals, ethanol ingestion, medications, drugs, and infections (see Chapter 104 ). Common occupational liver disease includes acute toxic hepatitis from chlorinated hydrocarbon solvents, halogenated aromatics, and epoxy resins. Table 11-10 lists toxicants according to type of hepatic injury.^[4]

Table 11-10 Chemical Toxicants Associated with Occupational Liver Disease

Modified from LaDou J, editor: Occupational and environmental medicine, Stamford, Conn, 1997, Appleton & Lange.

Rights were not granted to include this data in electronic media. Please refer to the printed book.

[edit] Neurologic Problems

Work-related neurotoxicity can be peripheral, central, or both. It is important to assess the patient for (1) workplace chemicals or substances used, (2) circumstances of use, (3) duration of exposure (i.e., brief from a spill or long term), and (4) other disease processes or nonoccupational exposures that might explain the problem. Findings are often nonspecific. Box 11-6 lists symptomatic presentations of common neurotoxins.

Box 11-6 - Symptomatic Presentations of Some Common Neurotoxins

Lead: impaired CNS functioning is manifested by fatigue, irritability, and difficulty concentrating; peripheral motor neuropathy affects upper (e.g., wristdrop) more than lower extremities; classic abdominal colic also present. Mercury: elemental form causes shyness, anxiety, inability to concentrate, irritability, and tremor (coarse, rapid); organic form causes severe neurologic effects, including sensorimotor neuropathy, ataxia, tremor, deafness, visual field constriction, and mental disturbances. Organophosphate insecticides: anticholinesterase inhibition leads to autonomic overactivity acutely, with nausea, vomiting, and diarrhea (mild exposure), versus cholinergic crisis, with convulsions, miosis, and involuntary defecation/urination (severe exposure); delayed neuropathy and CNS dysfunction out of proportion to initial symptoms occur with acute high level. Organic solvents: CNS depression or anesthesia on acute inhalation; propensity to affect frontal cortex (e.g., decreased attentiveness); chronic exposure may yield encephalopathy, characterized by irritability, impaired mentation, impaired attentiveness, headache, possible ataxia, and depression abating over months; also, possible irreversible toxic encephalopathy. CNS, Central nervous system.

Peripheral nerve dysfunction usually manifests itself first as numbness or tingling of the distal lower extremities, then the upper extremities. A progression to weakness is seen next, from distal to proximal. In the most severe cases, muscle atrophy and fasciculation occur. The symmetric, distal, and graded neurologic loss extending proximally often results from axonal degeneration secondary to presumed metabolic derangement within the neuron, with the longest fibers affected first. However, new study techniques have revealed that peripheral nerves are vulnerable at multiple sites (e.g., altered vasa nervorum from lead, defective slow axoplasmic transport with acrylamide).

Variations in the onset and course depend on the exposure characteristics. Acute exposure to a toxin may have a delayed onset (e.g., acrylamide in 2 to 3 weeks from accumulation of microfilament, organophosphates in 1 to 2 weeks from the “aging” of a specific esterase enzyme), which then presents in an acute manner and follows a monophasic course.

Chronic low concentrations of toxic exposure may yield an insidious, progressive neuropathy with a slow recovery once exposure is stopped. Peripheral neuropathies caused by n-hexane, methyl n-butyl ketone (MBK), and acrylamide may progress for 3 to 4 weeks after cessation of exposure. In general, most toxic peripheral neuropathies are mixed sensorimotor, and most resolve if identified early and if further exposure is avoided. Examples of exceptions include lead-induced neuropathy, which affects the motor system primarily, and acrylamide-induced injury, which may not resolve. Along with physical examination findings, sensory and motor nerve conduction velocity (NCV) tests, electromyography (EMG), and even nerve biopsy may be of assistance. Subtle neurologic loss may only be detected by serial examinations over time. Other causes of peripheral neuropathy should also be considered (see Chapter 167 ).

Central nervous system (CNS) dysfunction most often results from a high concentration of a toxin in an acute exposure. Often the offending agent is readily known, and other workers may be similarly affected. CNS depression or narcosis may be entirely nonspecific. Recovery is usually rapid and complete, but permanent damage or death does occur in severe cases (e.g., when a worker is trapped in a confined space).

Chronic low-level exposure causing CNS dysfunction, as with organic solvents and chronic toxic encephalopathy, is more challenging diagnostically. Reported symptoms may include headache, vertigo, blurred vision, tremor, decreased coordination, irritability, and fatigue. Clinical findings may include difficulty with concentration, memory, reasoning, and complex concept formation. Depression may occur secondary to the toxic effects or as a reaction to the resultant impairment. Formal neuropsychologic testing may pinpoint deficits and can be repeated to document recovery while the patient is not exposed to toxins. In general, chronic CNS toxic exposures do not result in radiologically or pathologically identifiable structural lesions, except with CO and toluene, which create multiple, small, white matter lesions, as identified on computed tomography (CT) scanning.

Examples of other neurologic disorders stemming from an occupational exposure include a parkinsonian disorder in workers exposed to carbon disulfide, CO, and manganese; facial weakness and numbness in trichloroethylene exposure; and bladder neuropathy and sexual dysfunction from the catalyst dimethylaminopropionitrile (DMAPN).^[4][1][2][3]

[edit] Hematologic Disorders

Workplace exposure to hematotoxins can lead to one or more abnormalities (Box 11-7). The classic example is benzene. Benzene previously was used frequently as an effective solvent. Chronic low-level exposure through inhalation was found to cause blood dyscrasias, such as aplastic anemia, leukopenia, and thrombocytopenia. Benzene is now considered a leukemogen by NIOSH and the International Agency for Research on Cancer (IARC), a program of the World Health Organization (WHO). NIOSH has recommended that use of benzene as a solvent or diluent in open operations be prohibited, and in 1987 OSHA set a permissible exposure limit (PEL) of 1 ppm. Benzene is a good example of how cycles of toxicity have occurred since the 1800s; new chemicals are introduced and their industrial advantages exploited before full appreciation of the human toxicity is realized.

Box 11-7 - Hematotoxins Grouped According to Effect With Associated Agents and Occupations

Red Blood Cell Survival Hemolysis and methemoglobinemia Oxidative chemicals (e.g., aniline, toluidine); nitrates; trinitrotoluene (TNT); naphthalene: rubber, dyes; fertilizer/explosives manufacturing; fumigants in clothing industry Hemolysis (altered red cell membrane suspected) Heavy metals (e.g., arsine); lead; copper: semiconductor, smelting, refining, plus chemical industries; lead abaters, painting, construction, battery manufacturing; leather industry (India) Metabolism of Red Blood Cell (Porphyria) Herbicides and fungicides (e.g., hexachlorobenzene; 2,4-dichlorophenol; 2,3,7,8-tetrachlorodibenzo-p-dioxin [a herbicide contaminant]): manufacturing and use Others (e.g.,o-benzyl-p-chlorophenol, vinyl chloride, lead, cleanser and disinfectant use, plastics industry) Formation of Red Blood Cell (Aplasia) Aplastic anemia (e.g., benzene); ionizing radiation; arsenic; TNT: rubber and shoe manufacturing; petroleum and chemical production; nuclear power plant workers; glass, herbicide, and paint manufacturing Morphology and function (Myelodysplasia, Leukemia) Benzene, ionizing radiation (see above for occupations) Coagulation (Thrombocytopenia) Pyrethrin, lethane, DDT; turpentine; toluene diisocyanate: use of insecticides, organic solvents, and hardeners (e.g., autobody painters) Decreased Oxygen Saturation CO and methylene chloride (breaks down to CO): forklift operators, use of combustion engines indoors, firefighters, auto mechanics

Differences in individual susceptibility to specific toxins clearly exist. For example, people with glucose-6-phosphate dehydrogenase (G6PD) deficiency who are exposed to chemicals that produce an oxidative stress develop cyanosis and a life-threatening hemolytic anemia.^[4]

[edit] Reproductive Hazards

This section emphasizes providing the primary care physician with an approach using clinical risk assessment for this complex topic. One difficulty in attributing adverse reproductive outcomes to a specific occupational hazard is the high rates of background infertility (one in eight couples), spontaneous abortion (20% of pregnancies between 4 and 28 weeks, as high as 75% of all conceptions), major birth defects (3%), and low birth weight (7%). There is differential vulnerability of the reproductive process, both male and female, at the different stages, reflecting the precisely regulated hormonal milieu in which the progressive sequence of gametogenesis, transport, fertilization, implantation, and embryo-fetal growth and development occurs. Furthermore, breast milk concentrates many lipophilic toxins that may adversely affect infants. Knowledge of the physical, chemical, and infectious agents hazardous to human beings of both genders is growing but remains limited (Table 11-11). Animal reproductive toxins are generally considered probable reproductive toxins in humans; regulatory agencies apply “safety factors” of 100 to 1000 to animal data to establish arbitrary allowable levels.

Table 11-11 Human Evidence for Adverse Reproduction or Developmental Effects of Selected Agents

Modified from LaDou J, editor: Occupational and environmental medicine, Stamford, Conn, 1997, Appleton & Lange.

Rights were not granted to include this data in electronic media. Please refer to the printed book.

Specific issues should be addressed for the pregnant worker. In particular, the altered physiology of pregnancy should be considered (Table 11-12). In some cases, removal of the worker from exposure may be indicated; for example, some toxins such as lead are regulated for the worker's protection. In general, the goal is to inform the worker of potential problems so that decisions can be made rationally. The degree of uncertainty should be conveyed so that the worker can decide on what is an “acceptable risk.”^[4][1][3]

Table 11-12 Hypothesized Occupational Health Impact Physiologic Changes in Pregnancy

Modified from LaDou J, editor: Occupational medicine, East Norwalk, Conn, 1990, Appleton & Lange.

Some known physiologic changes	Agent or condition	Example of possible impact	Suggested occupational accommodations
General
↑ Fatigue or stress	Inflexible hours	May be aggravated	Scheduling flexibility
	Shift work		Frequent rest breaks
↑ Nausea	Ketones or acrylates	↑ Sensitivity to chemicals with strong, unpleasant odors	Improve ventilation
	Exhaust fumes		↑ Respiratory protection
↑ Metabolic rate	Carbon tetrachloride	↑ Hepatotoxicity (especially if metabolically activated)	Minimize exposure
	Protective gear
		↑ Discomfort or heat intolerance
Cardiovascular
↑ Uteroplacental flow	Hemolytic agents (e.g., arsine)	↓ Maternal oxygen-carrying capacity	Minimize exposure
	Asphyxiants (e.g., CO or agents metabolized to CO [e.g., methylene chloride])	↓ Fetal oxygenation leading to hypoxia
↑ Myocardial irritability	Chlorinated hydrocarbons (e.g., tetrachloroethylene)	↑ Dysrhythmias or myocardial infarction	Minimize exposure
↑ Autonomic control of vasomotor tone	Anesthetic agents	↑ Arterial pressure	Minimize exposure
	Organic solvents	Preeclampsia
↑ Renal blood flow	Cadmium	↑ Renal toxicity	Minimize exposure
Respiratory
↑ Respiratory rate	All airborne chemicals	↑ Absorbed dose per unit time	Minimize exposure
↑ Tidal volume
↑ Hyperemic engorgement, capillary dilation	Formaldehyde	↑ Sensitivity to irritants and allergens	Minimize exposure
	Sulfur dioxide
Musculoskeletal
↑ Lower back pain	Heavy lifting	Difficulty lifting	↑ Mobility for postural changes
↑ Lumbar lordosis, symphyseal  and sacroiliac loosening	Ergonomically poor chairs and workstations	Aggravation of pain	↓ Maximum lifting: 20%-25% in last trimester
Shifted center of gravity			Well-designed chairs and workstations

[edit] Infectious Diseases

Illness from infectious agents of all categories can occur in the workplace. The jobs at risk include those involving contact with infected persons; laboratory workers in contact with infected human or animal tissue, secretions, or excretions; business travelers in contact with endemic disease; and workers in contact with infected animals. The occupational history may help reveal the origin of a puzzling infectious disease. Table 11-13 provides a selected list of infectious diseases by occupation.

Table 11-13 Selected Work-Related Infectious Diseases by Occupation

From Gantz NM: Infectious agents. In Levy BS, Wegman DH, editors:Occupational health: recognizing and preventing work-related disease and injury, ed 4, Philadelphia, 2000, Lippincott Williams & Wilkins.

Rights were not granted to include this data in electronic media. Please refer to the printed book.

The Bloodborne Pathogen Standard mandates a risk assessment discussion with a qualified provider after an exposure. Triple drug prophylaxis for those human immunodeficiency virus (HIV) exposures of greatest risk (e.g., large bore deep needle stick from a patient with high viral load) warrants immediate attention. The CDC updates recommendations periodically. Currently baseline labs should be performed on the worker exposed (HIV, hepatitis B virus [HBV] surface antigen, HBV antibody titer, hepatitis C, alanine aminotransferase [ALT]) and the source patient if possible. Hepatitis B passive immunization (HBIG) should be considered in high-risk exposures to workers without immunity; otherwise active immunity is checked and updated. No prophylaxis is available for hepatitis C, which carries an intermediate infection risk per needle stick exposure (3.5%) compared with HIV (0.3%) and hepatitis B (30%). Labs on the exposed worker are repeated at 6 weeks and 3 months. Safe sex practices should be recommended through the 3-month period.

Health care workers should not become complacent, since the degree of protection offered by universal precautions and other procedural and engineering controls is not absolute. Studies have found that during surgery, approximately one needle stick occurs in 2% to 5% of cases despite universal precautions. It may be helpful to consider total career risk of contracting a bloodborne pathogen when planning control strategies. In addition to the exposure rate from injury, other factors may affect career risk including seroprevalence of patients served, cases or tasks with potential exposure per year, frequency of extenuating circumstances (e.g., emergencies or combative patients), and efficacy of transmission (e.g., 30% for HBV, 0.3% for HIV-infected patients but transmission higher as CD4 count decreases and viral burden increases). Thus maximizing engineering and procedural controls is warranted.

Other potential infectious agents that pose occupational risks for health care workers are listed in Box 11-8. Pregnancy may be a contraindication to care for HIV-infected patients because of cytomegalovirus risk. Tuberculosis (TB) prevalence is increasing again; multidrug-resistant strains pose considerable risk where endemic, such as in New York City. Many countries have epidemic multidrug-resistant TB (e.g., the Philippines). Therefore immigrants and those traveling from such areas of the world require careful assessment and management (see Chapter 74 ). The Centers for Disease Control and Prevention (CDC) has published guidelines that emphasize point-of-contact identification of those with suggestive symptoms. If TB is suspected, the patient should wear a mask and be taken immediately to a negative-pressure room. Health care facilities are categorized according to the number of TB skin test conversions in their health care workers and the prevalence of TB in the community served. Engineering controls, such as UV light and use of special filters in the ventilation system, are recommended to decrease the bioaerosol content of waiting areas. It is recommended that health care workers use respirators during high-risk procedures, such as administering nebulizers, which might induce coughing, or performing a bronchoscopy or intubation in a patient suspected of having TB. Many occupations require international travel. Traveler's diarrhea is the most common health problem in those who visit developing countries. Dietary precautions remain the most important preventive measures, but the development of resistance to some antibiotics and the advent of the fluoroquinolones as new first-line therapy have changed the management. See Chapter 111 for the indications of prophylaxis and more information.

Box 11-8 - Some Infectious Agents That Are Occupational Risks for Health Care Workers†

Rights were not granted to include this data in electronic media. Please refer to the printed book. †From Gantz NM: Infectious agents. In Levy BS, Wegman DH, editors: Occupational health: recognizing and preventing work-related disease and injury, ed 4, Philadelphia, 2000, Lippincott Williams & Wilkins.

Workers exposed to animals are at risk of developing zoonoses, diseases primarily of animals that are transmitted to humans. Examples include leptospirosis, plague, tularemia, rabies, murine typhus, and psittacosis. Workers involved in earth-moving jobs are at risk of deep fungal infections (e.g., blastomycosis, histoplasmosis, coccidioidomycosis) resulting from inhalation of spore-containing dust in endemic areas. Superficial candidal infection may be a hazard in bakers and other workers whose hands are often wet.

In patients with flulike symptoms, physicians should consider the inhalation fevers such as metal fume fever and polymer fume fever, which can masquerade as an infectious disease (see Respiratory Disease).^[1][3]

[edit] Stress in the Workplace

The influence of occupational stress on health appears to be substantial. In the workplace, individual and environmental factors interact to produce circumstances that may elicit stress responses (Box 11-9).

Box 11-9 - Workplace Stress‡

Stressors Factors related to individual Conflicting nonoccupational demands Inadequate communication skills Moral or ideologic conflict with goals of organization Insufficient social support mechanisms Emotionally laden life events Extreme personality traits Factors related to work environment Organizational change within company Relationship to supervisors Conflictive corporate atmosphere Poor communication within company Promotion or lack thereof Underloading or overloading of job demand, mental or physical Excessive expectations of functional level Lack of control or decision latitude Role conflict or ambiguity Inadequate resources to accomplish job Inadequate authority to accomplish job Responsibility for others Rotating shift work Machine-paced work Boring, repetitive work Noise and vibration Ergonomic problems Poor aesthetics Odors, temperature extremes, bad lighting Obvious safety hazards Manifestations of Stress Early Decreased satisfaction, absenteeism, anxiety, tension, irritability, trouble concentrating, decreased family participation, marital discord, altered social activity, decreased stamina, increased time required to recover from physical demands, increased accidents Late Clinical depression, cumulative trauma disorders, adjustment disorders, substance abuse, somatic symptoms, exacerbation of existing medical and psychiatric conditions, cardiovascular disease, gastrointestinal distress (especially peptic ulcer), accidents, increased workers' compensation claims, violence ‡Courtesy of Stover Snook, PhD, Liberty Mutual Insurance, ergonomic research; lecturer, Harvard School of Public Health.

The ability to predict a stress response in an individual remains poor. Efforts to minimize the influence of this occupational hazard are more successfully directed at recognizing early manifestations and at primary and secondary prevention by addressing the offending factor(s).

Ideally, a workplace should provide sufficient flexibility to allow workers to change their job description through redesign or transfer as necessary. Often this is not the case, however, and job security may be threatened, adding further stress. Violence in the workplace often represents a failure to address stressful issues.

[edit] Physical Hazards

Physical conditions such as temperature, noise, vibration, high pressure, and radiation at the workplace can adversely affect the worker. The physician concerned about prevention of a suspected physical hazard is encouraged to refer to the recommended threshold limit values (TLVs) published by the American Conference of Governmental Industrial Hygienists (ACGIH).

[edit] Noise.

Noise is a common physical hazard, affecting about 10 million U.S. workers. An estimated 17% of production workers have at least some hearing impairment. The 90 dB time-weighted average (TWA) limit of the 1983 OSHA standard may not be sufficiently protective. The primary care physician should be aware that an “action” level of 85 db TWA exists (Section 1910.95 amendment) that mandates both a baseline audiogram and a hearing conservation program (see Box 11-2). Prevention is important because the greatest damage is done in the first 10 years of exposure, typically when the worker is young and has enough hearing reserve to allow the hearing loss to go unnoticed. The impact of a hearing impairment may be greatest in the retirement years, when conversational difficulty may lead to decreased socialization and to depression. There also may be an association between chronic noise exposure and the development of hypertension from a stress response.

A patient may present to the primary care physician with complaints of tinnitus, difficulty hearing the telephone ring, and inability to hear conversation in a crowded room or distinguish words, such as “six” from “sit” (consonants have a higher frequency than vowels). Often a family member first notes the hearing change. It is useful to differentiate acute from chronic and conductive from sensorineural hearing loss. Conductive hearing loss may result, for example, from a slag burn of the tympanic membrane of a welder.

This discussion focuses on noise-induced hearing loss (NIHL). Especially in chronic, bilateral sensorineural hearing loss, it is important to inquire about environmental and occupational noise exposure. The noise source can be continuous or from recurring short impulses. The decibel scale is logarithmic, with loudness doubling every 3 dB; sound at 90 dB is actually 10 times louder than at 80 dB. The evaluation of the worker includes a thorough head and neck physical examination, with attention to hearing, including the ability to distinguish whisper, Weber's and Rinne tests with a 512-Hz tuning fork, and audiometry.

Typical NIHL reveals a “notch” between 3000 and 6000 Hz. Interestingly, the anatomy of the cochlea is such that the first turn occurs at the 4000-Hz level. Two possible explanations for temporary threshold shift (TTS) include the cochlea hair cells being “knocked over” or metabolically exhausted by noise trauma. A TTS should delay testing or should be repeated after at least 16 hours without further noise insult. If the deficit persists, it is considered a permanent threshold shift (PTS).

A basic audiogram quantitates hearing thresholds at the proper frequencies (with hearing loss graded as mild, 20 to 40 dB; moderate, 40 to 60 dB; severe, 60 to 80 dB; profound, greater than 80 dB). An audiologist can assess speech discrimination (expressed in percentage of words repeated correctly; normal, 88% to 100%) and other tests as appropriate. The physician addressing a possible occupational etiology should look for a standard threshold shift (STS), meaning a greater than 10-dB average change relative to a baseline audiogram over the 500-, 1000-, 2000-, and 3000-Hz ranges in either ear after adjusting for aging using the appropriate tables (available in the OSHA regulation). This should be placed on the company's OSHA 200 log and should mandate hearing protection. To ensure compliance, the physician may refer to the OSHA standard (Section 1910.95) or request consultation. The ACGIH TLVs for noise, both continuous and impulse noise exposure, offer a more protective guideline for workers. Although it varies with the frequency, the ideal attenuation efficacy of personal protective devices is approximately 25 dB for waxed cotton, 35 dB for earmuffs, and 45 dB when combined.^[6][4]

[edit] Cold Stress.

Workers at risk of cold injury, whether systemic or localized, include meatpackers (refrigerated work areas) and those with outdoor jobs in winter cold. Elderly employees, intoxicated workers, those taking certain medications, or those with such chronic diseases as diabetes, adrenal insufficiency, and cardiovascular disease may be at increased risk. Cold also predisposes people to cumulative musculoskeletal trauma when repetitive, forceful movements are used. The ACGIH TLVs take into consideration windchill, physical exertion, task, and contacted surfaces. Early warning signs of cold stress include extremity pain. Systemic hypothermia can occur in water that is 72° F (22.2° C) and lower and with air temperatures of 65° F (18.3° C) and lower. The diagnosis requires a core body temperature less than 95° F (35° C).^[6][4]

[edit] Heat Stress.

Workers at risk of hyperthermia include smelters, steel workers, blast furnace operators, glassblowers, and those with outdoor summer jobs, especially farmers, ranchers, fishermen, and construction workers. Predisposing factors include health conditions or medications that inhibit the sweating mechanism, such as obesity, dehydration, cardiac disease, and anticholinergics (e.g., tricyclic antidepressants). There are four clinical states of progressive heat stress: heat cramps, heat syncope, heat exhaustion, and life-threatening heatstroke. Several dermatologic problems caused by heat are also possible. ACGIH TLVs take into consideration solar load, relative humidity, air velocity, protective clothing requirements, caloric expenditure, and task. The TLVs apply to acclimatized workers who are physically fit, and work/rest schedules are recommended for the various conditions and temperatures. Extra caution is advised for workers who are unacclimatized, which requires about 1 week, and for those in poor health, such as those with reduced circulatory response. A core temperature greater than 102.2° F (39° C) in the first trimester of pregnancy should be avoided (e.g., more than about 10 minutes in a sauna for an otherwise active woman); core temperature greater than 100.4° F (38° C) may be associated with temporary infertility in either gender. It may be advisable to have medical clearance for occupations known to involve significant heat stress.^[6][4]

[edit] Vibration.

An oscillating source imparts mechanical energy to another structure to produce a vibration. Every structure has an inherent vibration level at which resonance, or amplification, occurs, including the human body and its specific parts. The vibration frequency determines the effect on the exposed individual. Motion sickness develops at 0.2 Hz; whole-body vibration in the 1-to 30-Hz range, although worst at about 5 Hz; hand, arm, and shoulder involvement in the 30-to 100-Hz range; and hand involvement above 100 Hz. In general, the higher the frequency, the more absorbed by the contacting body part. Other characteristics, such as peak acceleration and direction relative to the body, play important roles and also lead to overlap among the categories just listed. Vibration is considered an ergonomic stress along with force and repetition. Effects from whole-body vibration may include circulatory and internal organ problems, persistent anemia, low back pain, and disk calcification.

Hand-arm vibration syndrome (HAVS), a vibration-induced Raynaud's phenomenon, occurs in workers using tools (e.g., pneumatic impact tools such as jackhammers) that impart local vibration within the resonance frequency of the hands and arms; cold stress can increase the likelihood and severity of HAVS. Early stages usually are reversible, but advanced cases can progress to permanent loss of hand function. In general, workers should avoid continuous exposure, use minimal hand grip force, keep hands warm and dry, avoid smoking, and use antivibration tools and gloves.^[6][4][3]

[edit] Decompression Sickness (Caisson Disease).

Decompression sickness can occur when the body moves from a higher-pressure environment (where nitrogen is more concentrated in tissues) to one of normal atmospheric pressure. Mechanical and physiologic effects of expanding gases cause damage unless sufficient time is allowed for their gradual dissolution. Caisson workers who work in a pressurized enclosure for underwater constructionand divers are at risk. It is recommended that workers have preplacement examinations, looking for predisposing conditions such as obesity, vascular disorders, chronic lung disease, dehydration, or recent bone fractures. Three types of decompression illness are distinguished: type 1 involves the large joints (the “bends”), leading to a stooped posture from pain, and may be immediate or delayed up to 12 hours; type 2 involves pulmonary (the “chokes”) as well as CNS manifestations and with possible permanent sequelae from tissue infarction or massive air emboli; and type 3 is characterized by aseptic necrosis of bone, especially the head or shaft of the humerus, and often has associated CNS manifestations. Treatment of types 1 and 2 consists of placing the patient in Trendelenburg's position with a slight left tilt to minimize risk of cerebral embolism, giving 100% oxygen, and providing hyperbaric chamber oxygenation. Contact the National Diving Accident Network for further assistance at 919-684-8111.^[2][3]

[edit] Radiation Exposure.

Ionizing radiation imparts sufficient energy when absorbed to produce ions and free radicals. Exposure to ionizing radiation occurs in many occupations, such as nuclear power plant and submarine industries, cathode ray and vacuum tube manufacturing, health care professions, and uranium mining. The average amount of energy deposited per unit length of path is called the linear energy transfer (LET) of radiation. Radiobiologists distinguish high-LET radiation (e.g., neutron, alpha) from low-LET radiation (e.g., gamma, x-ray) by determining the relative potency that causes damage to tissues, cells, and chromosomes. Effects are categorized as acute radiation syndrome, acute localized radiation injuries, delayed effects (e.g., radiodermatitis, atrophy), and low-dose effects, which include an increased risk of some cancers. For example, the association between ionizing radiation and an increase in leukemia (latency of 5 years) is well accepted, and a 15% increase in the risk of brain cancer (latency of 10 years) with ionizing radiation has been reported. Lifetime and yearly limits of 5 and 2 rem, respectively, are regulated and measured with a badge that quantifies cumulative low-LET (principally gamma) radiation. Thus far, tests cannot readily measure personal exposure to neutrons and ingested particles; their contribution to the risk of cancer is not well defined.^[2]

[edit] Occupational Cancer

An estimated 30% to 40% of people in the industrialized world will develop a malignancy during their lifetime. Occupational and environmental exposures play an important role, although estimates vary widely regarding the proportion attributable to these exposures. Table 11-14 lists workplace substances known or suspected to cause cancer. The signs, symptoms, and course of occupational cancer are indistinct from non–work-related tumors of the same type. However, a few otherwise very rare tumors are considered sentinel or almost pathognomonic for specific occupational exposures, such as mesot