Principles of Ambulatory Medicine, 7th Edition

Chapter 8

Occupational and Environmental Disease and Bioterrorism*

Laura S. Welch

David W. Blodgett

As we enter a new century, we continue to have widespread proliferation of new and potentially toxic chemicals. These hazardous exposures are encountered in homes, schools, the general environment, and especially the workplace. The extent to which such exposures may be causing health problems is a grave concern. Few communities in the United States have escaped public concern over the health hazards of pesticide spraying, asbestos in school buildings, contaminated drinking water, electromagnetic radiation, and toxic waste disposal.

This chapter provides an overview of how environmental diseases occur and outlines an approach for recognizing and addressing them. It emphasizes the workplace, where environmentally induced illness is most commonly recognized. A good estimate is that there are a total of 55,200 U.S. deaths annually that are a result of occupational disease or injury (range: 32,200 to 78,200) (1). Occupational deaths are the eighth leading cause of death in the United States, ahead of suicide (30,575) and greater than the annual number of motor vehicle deaths per year (43,501) (1). Additional occupational illnesses that do not result in death may number an additional 300,000 per year (1,2). Hazardous exposures and resulting illness also occur in the home or community environment. The same principles that apply to workplace exposure also apply to home and community exposure.

Vital Role of Primary Practitioners

Primary practitioners are often the first professionals to recognize the hazards of occupational exposure and to document the link between their patients’ illnesses and their patients’ work. The task of controlling the hazards usually involves public health specialists, but it is vitally important that primary practitioners take the time to report and followup suspected occupational diseases.

Although the United States has for three decades had the Occupational Safety and Health Administration (OSHA) to ensure workplace safety, there are only enough inspectors to visit every workplace once every 100 years. Each year still brings efforts in Congress to weaken the program that does exist. Locked fire exits, exploitation of immigrants, child labor, and sweatshop conditions persist decades after the New Deal took steps to abolish them. Many workers are unaware of their right to request an investigation of potential hazards at work, and concerns for job security deter them from raising complaints about safety with supervisors. Public health surveillance of occupational and environmental disease has been improved by the efforts of the National Institute for Occupational Safety and Health (NIOSH) working with state health agencies, but it remains limited in scope and coverage. For all these reasons, if a patient has an occupational health problem or is exposed to a dangerous situation at work, the patient's physician may be the single most important factor in protecting the patient's and the community's health.

P.119

Pathogenesis of Occupational Disease

The pathogenesis of occupational disease is complex and involves not only the interaction between the host and a toxic exposure, but also a complex set of social interactions.

Toxin–Host Interaction

For an occupational disease to occur, there must be a triad consisting of a toxic agent, a host, and an environment in which the host is exposed. The illness that may result depends on the toxic properties of the substance or energy source, its route of entry, the dosage received by the host, and the susceptibility of the host to the toxin.

Toxic agents can be inhaled, ingested, or absorbed through the skin. With inhalation, the dosage received depends on whether the substance is present as gas, a fume, or a dust. Deposition of dust in the lungs depends to a great extent on particle size and distribution, because smaller particles can more easily enter the alveoli and become trapped. The concentration of the substance in the air (which is related to room ventilation, temperature, and humidity), the rate at which the worker is exercising and breathing, and protective factors such as special clothing or respirator use are other factors that affect the amount of toxin absorbed.

Once the toxic substance is absorbed, there may be an instantaneous effect (as in the case of carbon monoxide poisoning), a brief latent period (as in the case of occupational asthma), or a latent period of years or decades (as in the pneumoconioses). A brief, high-dose exposure may cause serious illness and death and be easy to recognize. Prolonged exposure to a low dosage of a toxin may not cause symptoms at the outset but may produce disease years later.

Impact of Economic and Social Factors

Thousands of new chemicals are introduced into industrial processes every year, but few have been tested to determine their potential toxicity. Even when toxicologic screening tests are done on a compound, they may not predict human disease. Despite the implementation of the Toxic Substances Control Act (TOSCA), which gave the U.S. Environmental Protection Agency (EPA) authority to require pretesting of chemicals, in too many cases, the hazard of a chemical is recognized only after an outbreak of illness. Economic factors play a major role in determining how safe a workplace is. Industrial hygiene programs to monitor exposure are common only in the largest plants. Important decisions, such as improving ventilation or decreasing exposure to noise, may involve significant expense. Workers may be reluctant to complain about working conditions for fear of losing their jobs. This is especially likely during periods of high unemployment, when acceptance of unpleasant and potentially unhealthy working conditions may be the price of having a job. Even when workers are strongly organized, the desire for a safer workplace may be balanced by a concern that increased production costs may result in the decision of a company to relocate its plant to areas where unions are less effective or do not exist. Such anxieties have been heightened by the globalization of manufacturing. Stringent health and safety regulations, with strong enforcement, can put competitors on a more equal footing and protect responsible businesses from being undercut by irresponsible ones.

Diagnosing Work-Related Disease

Although episodes of illness caused or exacerbated by the patient's work are often seen in ambulatory practice, they frequently are not recognized as such. Misdiagnosis of an occupational disease means that the patient does not benefit from correct diagnosis and management and there is no correction of the poor working conditions that may subsequently injure others or even result in death. Two cases illustrate these points.

Case Study: A Teenager with Bronchitis

An 18-year-old woman complained to her physician of a severe cough and some wheezing. The physician treated her with erythromycin and fluids and advised her to stay in bed for a few days. She recovered and returned to work feeling well. Several days later she had a severe recurrent cough with wheezing and dyspnea and saw her physician again. The physician again prescribed erythromycin and rest. She remained off work for a week. She felt better and returned to work. After 2 days she became extremely short of breath and was brought to the emergency room. She had severe bronchospasm and was admitted, improving on bronchodilators and corticosteroids after a few days. An occupational history on admission disclosed that her work involved grinding drill bits made of tungsten carbide containing a small amount of cobalt, a known pulmonary sensitizer. Once the patient was sensitized, each fresh exposure to the dust caused symptoms after a shorter incubation period. Had the first physician considered the diagnosis of extrinsic asthma and inquired about occupational exposures, the patient's subsequent deterioration could have been prevented.

Case Study: A Man with Severe Abdominal Pain

A 28-year-old man presented to the emergency room of a community hospital with a chief complaint of severe abdominal

P.120


pain. There was significant abdominal tenderness with a question of guarding. He reported having seen his family physician on two occasions during the preceding 2 weeks, with severe cramping pain felt around the umbilicus. His physician had prescribed a H2 blocker and tried to schedule a gastroenterologic consultation, which the patient had not set up because of difficulties with his work schedule. The pain that had been intermittent had now become constant, more in the lower quadrants, and more severe for longer than 6 hours. Blood work showed a normal amylase level and a leukocytosis. A surgical consultant suggested the possibility of an appendiceal abscess but believed that the patient was stable enough to await the results of a computed tomography scan. A gastroenterologist was consulted and was the first physician to take an occupational history. The patient had been a painter for several years and was currently working for a contractor repainting the elaborate metal cornices of a building. For more than a month he had been using a vibrating tool to remove old paint, and this created a lot of dust. He did not know whether lead was in the paint. The gastroenterologist suggested a determination of the patient's blood lead concentration and watchful waiting. The computed tomography scan was normal and the blood lead concentration was elevated. Several coworkers were also poisoned, and the patient's son had an increased blood lead concentration from the contaminated work clothes his father had brought home.

TABLE 8.1 Components of an Occupational History

Description of the job
Physical exertion
Body mechanics
Pace of work
Repetitive tasks
Job stress
Exposure to hazards
Risk of trauma
Noise and vibration
Heat and cold
Ionizing and nonionizing radiation
Dusts, fumes, mists
Contamination of skin and clothing
Protective measures
Ventilation and respiratory protection
Protective clothing
Medical surveillance
Effects of exposure
Temporal relationship of any symptoms to work (e.g., relationship to time of day, day of week, change of symptoms on vacation, weekends)
Similar symptoms in coworkers

To avoid the pitfalls these cases demonstrate, the following three strategies are fundamental when evaluating a patient:

  • Ask every patient about his or her job.
  • Consider the possibility that the patient's illness is related to the work or home environment.
  • Followup on one's suspicions. Other people may be in danger.

Taking an Occupational History

Inquiring about a patient's job not only helps identify occupational disease but also provides other information useful in caring for a patient. Clearly the physical demands of the job are important when advising a patient about a health problem such as coronary artery disease or diabetes mellitus. Knowing the patient's work schedule is also important, because shift work affects medication schedules, diet, and family life. Medications can dramatically affect the patient's comfort or safety at work (e.g., diuretics in an interstate truck driver, antihistamines in a construction worker who works at elevation). Financial and psychological stress may result from layoffs, whereas regular overtime may bring about chronic fatigue and psychological problems of its own. Usually, a brief discussion of the current job, including a brief description of how the patient spends the working day, is sufficient. This rarely takes more than 3 minutes. Table 8.1 summarizes the major points to cover in this inquiry.

When some aspect of the medical or occupational history raises suspicions of a work-related condition, further questioning flows naturally. The inquiry should focus on a temporal relationship between symptoms and possible exposure, exposure to an agent known to cause disease, or a pattern of similar illness among coworkers. Because every patient, every job, and every medical presentation is different, there is no single way of taking a history. If the patient uses jargon or job titles that are unfamiliar, it is important to ask for clarification.

The screening history sometimes reveals the need to take a lifelong work history. An account of previous jobs and exposures is especially important when the patient has a chronic illness or the possibility of work-related neoplasia. In such cases, the following approach is recommended (it may save time to have the patient bring this information, written out, to a followup visit after the initial evaluation):

  1. Begin with parents’ jobs and childhood exposures.
  2. Review each of the patient's jobs in chronologic order.
  3. Elicit relevant aspects of each period of employment (Table 8.1).

Diseases That Are Commonly Related to Work

The occupational diseases that physicians encounter depend on the industry in the immediate vicinity and the demographic makeup of their practice. For example, practitioners caring for the elderly may see retired workers with previous exposure in all types of industry. Any organ system can be affected by hazardous exposures. Table 8.2 lists

P.121

P.122

P.123

P.124


clinical problems grouped according to the organ system affected.

TABLE 8.2 Common Medical Problems with Examples of Environmental Causes

Clinical Problem

Causative Agent

Skin

Cyanosis

Methemoglobin formers
Aniline
Anisidine, ortho- and para-isomers
Dimethylaniline
Dinitrobenzene, all isomers
Dinitrotoluene
Monomethylaniline
p-Nitroaniline
Nitrobenzene
p-Nitrocholorobenzene
Nitrogen trifluoride
Nitrotoluene
Perchloryl fluoride
n-Propyl nitrate
Tetranitromethane
o-Toluidine
Xylidine

Contact dermatitis

Many chemicals with irritant or sensitizing properties

Chronic eczematous dermatitis

Solvents
Detergents

Folliculitis

Oil exposure
Grease exposure

Acne

Polychlorinated biphenyls
Chlorinated naphthalenes
Paraffin
Coal tar
Dioxin

Photosensitization

Coal tar
Pitch
Asphalt
Anthracene
Creosote
Fluorescein
Phenanthrene

Granulomas

Beryllium

Corns

Asbestos
Fiberglass

Punctate ulcers

Chromic acid

Painful burns

Hydrofluoric acid (deep pain out of proportion to appearance of burn)

Skin cancer

Soots
Tars
Arsenic
Coke oven emissions
Cutting oils
Sunlight

Nervous System

Central Effects

Altered consciousness

Hundreds of chemicals have
CNS-depressant properties and other
CNS effects

Headaches

Carbon monoxide
Nitrites
Nitrates
Alcohols
Lead
Organic lead compounds
Methemoglobin formers (see Cyanosis)

Behavioral change

Mercury
Lead
Carbon disulfide
Carbon monoxide
Methyl chloride
Methyl bromide

Peripheral Effects

Ataxia, tremor, spasticity

Manganese
Organic lead compounds
Organic tin compounds

Hyperreflexia, micrographia

Mercury
Dichlorodiphenyltrichloroethane (DDT)

Peripheral neuropathy

Peripheral neurotoxins
Acrylamide
Arsenic and compounds
Calcium arsenate
Carbon disulfide
n-Hexane
Lead and inorganic lead compounds
Dimethylaminopropionitrile
Lucel-7 (2-t-butylazo-2-hydroxy-5-methyl hexane)
Mercury
Methyl bromide
Methyl butyl ketone
Thallium, soluble compounds
2,4,6-Trinitrotoluene
Tri-o-cresyl phosphate

Auditory

Decreased acuity and tinnitus

Noise exposure, especially >85 db
Aniline

Acoustic neuritis

Arsenic
Carbon monoxide
Hypoxia
Lead
Organic mercury
Phosphorus
Sodium nitrate

Otitis extrerna

Contamination of earplugs used for noise protection

Ear pain

Acute shifts in pressure

Respiratory

Nasal septal perforation

Chromic acid and other chromates

Laryngeal carcinoma

Asbestos

Laryngitis, bronchitis tracheitis, pneumonitis

Many irritants, including the following:
Ammonia
Chlorine
Oxides of nitrogen
Ozone
Phosgene
Sulfur dioxide
Vanadium pentoxide
Mercury
Manganese
Cadmium dust

Bronchiolitis obliterans

Nitrogen dioxide

Allergic alveolitis

Many different antigens

Bagassosis

Thermoactinomyces vulgaris and Micropolyspora sp.

Bird-breeder's lung

Avian proteins

Byssinosis

Cotton, flax, and soft fiber hemps

Cheese-washer's lung

Penicillium caseil

Detergents

Bacillus subtilis

Farmer's lung

Micropolyspora faeni and Thermoactinomyces vulgaris
Feathers
Feather proteins

Furrier's lung

Keratinized particles of hair

Malt-worker's lung

Aspergillus clavatus

Maple bark-stripper's disease

Cryptostroma corticale

Paprika-splitter's lung

Mucor stolinifer

Bronchospasm

Pulmonary sensitizers (any list is incomplete, because new agents are reported each year)
Castor bean pomace
Cobalt, metal fume and dust
Enzymatic detergents
Grain dusts
Maleic anhydride
Methylene bisphenyl isocyanate
Methyl isocyanate
Nickel, metal
p-Phenylenediamine
Phthalic anhydride
Platinum salts
Polyvinyl chloride (fume from heated film: meat-wrapper's asthma)
Toluene 2,4-diisocyanate
Tungsten carbide
Western red cedar
Plicatic acid

Pulmonary fibrosis

Asbestos
Silica
Beryllium
Talc
Coal dust
Cobalt
Hematite
Kaolin

Benign pneumoconiosis deposits in lung without fibrosis

Aluminum powder
Barium
Graphite
Iron oxide
Tin
Cerium oxide
Silver
Titanium

Pleural effusion

Asbestos
Paraquat
Talc

Gastrointestinal

Gingivitis and gum pigmentation

Mercury
Lead
Bismuth

Dental erosion

Acetic acid
Hydrochloric acid
Lactic acid
Nitric acid
Nitrogen dioxide
Sulfuric acid

Tongue paresthesias

Furfural
Rotenone
Crosol

Green tongue

Vanadium

Nausea and vomiting

Many chemicals including the following:
Central nervous system depressants
Cholinesterase inhibitors
Methemoglobin formers

Constipation

Lead
Barium sulfate
Thallium
Tellurium
Vanadium
Fluorides

Hepatomegaly

Hepatotoxins
Acetylene tetrabromide
Carbon disulfide
Carbon tetrachloride
Chlorodiphenyl
Chloroform
p-Dichlorobenzene
Dimethylacetamide
Dimethylformamide
Dioxane
Ethylene chlorohydrin
Ethylene dibromide
Ethylene dichloride
Hexachloronaphthalene
Kepone
Nitroethane
Octachloronaphthalene
Pentachloronaphthalene
Picric acid
Tetrachloroethane
Tetrachloroethylene
Tetrachloronaphthalene
Trichloronaphthalene
2,4,6-Trinitrotoluene

Jaundice

Hepatotoxins (see Hepatomegaly)
Hemolytic agents
Arsine
Butyl Cellosolve
Naphthalene
Phenylhydrazine
Stibine

Angiosarcoma of liver

Vinyl chloride

Abdominal pain

Antimony
Arsenic
Bromine
Cadmium
Lead
Mercury
Nicotine
Organophosphates
Thallium
Many other chemicals when ingested

Cardiovascular

Myocardial damage

Antimony
Arsine
Carbon disulfide
Cobalt

Ischemic disease

Nitroglycerin
Nitroglycol
Other vasodilating nitrates

Hypertension

Noise exposure
Aminopyridine
Arsenic
Barium
Boron hydride
Carbon disulfide
Cobalt
Diphenyl
Lead
Mercury
Thallium

Vasospastic disorders—“White finger”

Vibrating tools

Raynaud's phenomenon

Vinyl chloride

Genitourinary

Renal disease

Nephrotoxins
4-Aminodiphenyl
Cadmium
Carbon disulfide
Carbon tetrachloride
Chloroform
Dioxane
Ethylene chlorohydrin
Ethylene dibromide
Lead
Mercury
Oxalic acid
Picric acid
Tetrachloroethane
2,4,6-Trinitrotoluene
Turpentine
Uranium

Renal carcinoma

4-Aminodiphenyl
Auramine
Benzidine
β-Naphthylamine
4-Nitrodiphenyl
Magenta

Urinary retention

Dimethylaminopropionitrile

Reproductive

Female sterility

Lead

Male sterility

Glycol ethers
Carbon disulfide
Dibromochloropropane (DBCP)
Lead
Microwaves to testes (radar workers)
Stilbestrol

Hematologic

Anemia

Lead
Hemolytic agents
Arsine
Butyl Cellosolve
Naphthalene
Phenylhydrazine
Stibine
Marrow depressants
Benzene
Dinitrophenol
Tetryl
2,4,6-Trinitrotoluene

Leukemia

Benzene
Radiation
Styrene-butadiene
Ethylene oxide

Musculoskeletal

Osteonecrosis

Phosphorus

Osteomalacia

Cadmium

Osteosclerosis

Fluorine

Acro-osteolysis

Vinyl chloride

Dermatitis and pneumoconiosis are the most commonly reported occupational illnesses. This probably reflects both true incidence (skin and pulmonary epithelium being most in contact with the outside environment) and the greater likelihood of recognition of these disorders as occupational in origin.

The number of chemicals that are toxic to the liver and kidney is so great that a careful exposure history should be taken from all patients with unexplained hepatitis or hepatic or renal failure. Many chemicals can affect the gastrointestinal tract and cause functional disturbances that may be misdiagnosed as peptic disease or irritable bowel syndrome.

Low-level exposure of the respiratory organs to a variety of substances may result in the production of nonspecific upper respiratory tract syndromes that the patient may describe as an intractable cold or as sinus trouble.

Occupational diseases sometimes manifest with striking and unusual signs (e.g., acro-osteolysis in vinyl chloride workers, nasal septal perforation in patients exposed to chromates). More commonly they cause vague systemic symptoms typical of early intoxication or manifest as a disease of ordinary life, such as asthma or eczema.

The following specific clinical situations should always raise the consideration of an occupational or environmental cause:

  • Any unexplained change in personality or behavior.Poisoning with mercury, lead, pesticides, and a wide variety of other central nervous system toxins may be the cause.
  • New onset of asthma in an adult.There is usually a temporal relationship between exposure and symptoms of asthma, but because of the time lapse when an immunologic mechanism is involved, wheezing and dyspnea may not be noted until after the workday is over.
  • Any case of pulmonary fibrosis.A prolonged latent period between exposure and disease onset means that abnormalities that appear on radiographs may be the result of a job the patient had decades ago.
  • Peripheral neuropathy.A toxic neuropathy may be recognizable by an unusual pattern of presentation, but in most cases, only careful history taking will reveal the cause.
  • Overuse syndromes in the extremities.Tendonitis, epicondylitis, and shoulder bursitis often are the result of a pattern of overuse. This can result from occupational or recreational activities. When they are work related, modification of the job is essential.
  • Hearing loss.Noise-induced hearing loss occurs gradually and usually in older workers, so it is rarely recognized in time to prevent severe damage.
  • Inability to conceive.Workers often question whether hazardous exposures at work cause infertility. Several toxins do reduce sperm count or increase time to conception.
  • Lung cancer.Exposures to asbestos and cigarette smoke are very common throughout the United States. Other lung carcinogens may be important in certain parts of the country.
  • Other cancers.Table 8.3 identifies specific carcinogens.

Determining Work Relatedness

The key to identifying occupational disease is to be sure that a toxic or environmental etiology is at least considered. In addition, the patient should always be asked, “Do you think this problem could have anything to do with your work?” and, “Does anyone else at work have this same problem?” Very often, if there is a connection, the patient will be able to identify it.

If neither the physician nor the patient knows whether a syndrome is occupational in origin, resources are available that identify toxic causes of a given symptom complex, toxic exposures of given occupations, and the potential hazards of exposure to given substances (Table 8.4).

FollowUp of Occupational Disease

Physician's Role

If there is suspicion that a patient became ill from an occupational exposure, it is the physician's responsibility to followup. Not only does diagnosing an occupational disease affect therapy and eligibility for compensation for a patient, but it may indicate that the health of others is also in danger. Often physicians overcome their own uneasiness about a patient's job by advising the patient to change jobs. Then, instead of the potentially hazardous job being made safe, another unsuspecting person is brought in to take the risk.

In some circumstances, occupational disease is recognized but the original hazard has been eliminated (e.g., in a patient with asbestosis who worked in a now-closed shipyard). Even in these circumstances, former coworkers need to be informed of the risk resulting from previous exposure.

It is not necessary to wait for absolute proof of etiology before beginning an investigation of a possible workplace hazard. The least-severely affected member of a group of workers may be the one who seeks attention. Moreover, for most occupationally induced diseases, proof of a relationship rests on epidemiologic data rather than on diagnostic study of the individual patient. Often the most practical way to learn whether a patient's problems are caused or exacerbated by his or her occupation is to find out whether coworkers are similarly affected. If the physician identifies

P.125


a possible occupational illness, assistance from others can be sought.

TABLE 8.3 Cancers Known to Be Caused by Environmental Agents

Site/Cell Type

Toxic Agent

Industry/Occupation

Liver/hemangiosarcoma

Vinyl chloride monomer

Vinyl chloride polymerization industry

Arsenical pesticides

Vintners

Nose

Hardwood dusts

Woodworkers, cabinet and furniture makers

Radium

Radium chemists and processors, dial painters

Chromates

Chromium producers, processors, users

Nickel

Nickel smelting and refining

Unknown agent

Boot and shoe industry

Larynx

Asbestos

Asbestos product manufacture, shipbuilding, construction and maintenance work

Lung

Asbestos

Asbestos product manufacture, shipbuilding, construction and maintenance work

Coke oven emissions

Topside coke oven workers

Radon daughters

Uranium and fluorspar miners

Chromates

Chromium producers and processors, users

Nickel

Nickel smelters, processors, and users

Arsenic

Smelters

Silica

Foundries, abrasive blasting

Mustard gas

Mustard gas formulators

Bis(chloromethyl) ether, chloromethyl

Ion exchange resin makers, chemists methyl ether

Pleura and peritoneum/mesothelioma

Asbestos

Asbestos product manufacture, shipbuilding, construction and maintenance work

Bone

Radium

Dial painters, radium chemists and processors

Scrotum

Mineral/cutting oils

Automatic lathe operators, metalworkers

Soots and tars, tar distillates

Coke oven workers, petroleum refiners, tar distillers

Bladder

Benzidine, α- and β-naphthylamine, auramine,

Rubber and dye workers magenta, 4-aminobiphenyl, 4-nitrophenyl

Esophagus

Asbestos

Asbestos product manufacture, shipbuilding, construction and maintenance work

Stomach

Asbestos

Asbestos product manufacture, shipbuilding, construction and maintenance work

Colon

Asbestos

Asbestos product manufacture, shipbuilding, construction and maintenance work

Kidney

Coke oven emissions

Coke oven workers

Hematopoietic/lymphoid leukemia, acute

Unknown

Rubber industry

Ionizing radiation

Radiologists

Myeloid leukemia, acute

Benzene

Refining, chemical, and manufacturing industries

Ionizing radiation

Radiologists

Erythroleukemia, acute

Benzene

Refining, chemical, and manufacturing industries

Investigative and Enforcement Agencies

State Level

Many states have a health department unit for investigation of occupational disease. Some states require physicians to report all cases of suspected occupational disease. Reporting any suspected occupational disease problem to the local health department can be the first step in followup. In many states, NIOSH assists the health department in surveillance and control of specific occupational diseases.

Federal Level

If there is difficulty in clarifying the potential relationship of illness to environment, or if the concerns raised are not addressed by a specific OSHA regulation (see Enforcement Agencies), it may be helpful to request assistance from NIOSH. This institute is the part of the United States Public Health Service (USPHS) Centers for Disease Control and Prevention that conducts research on occupational disease. An employer, a union, or any three employees can request a formal health hazard evaluation

P.126


(HHE) of a workplace. Furthermore, NIOSH has educational resource centers (where consultants are available to help physicians, employers, and workers) in each region of the United States. These centers can provide literature searches and information on available publications and current areas of research, and can refer a physician to others who are experts in the field. Access to regional centers can be provided by the central office.

TABLE 8.4 How to Determine the Potential Hazards of an Exposure

Identify the chemical

(Shortcut: Call local poison center for help. You can find your local poison center through the American Association of Poison Control Centers [http://www.aapcc.org/ ])

Employers are required to provide Material Safety Data Sheets (MSDS) on all materials containing potentially hazardous chemicals. Check with the manufacturer, using the phone numbers on the MSDS.
For energy exposure, ask employer about equipment specifications or measurements of wavelength and intensity.

Clarify potential health effects

(Shortcut: Call NIOSH helpline at 800-356-4674 and press 125 to access a representative directly, or call the general line at 513-533-8328, or visit NIOSH's website:http://www.cdc.gov/niosh/homepage.html ; or visit the ATSDR website: http://www.atsdr.cdc.gov .)

Use one of the general references listed at the end of this chapter for an overview.
Use your medical library or Grateful Med to access Medline and Toxnet (http://www.toxnet.nlm.nih.gov ) at the National Library of

Medicine to check newer information.

Synthesize information

(Shortcut: Identify a consultant through AOEC, [202-347-4976 or http://www.aoec.org ]).

Organize what you have learned from patient history about the exposure: identity of the chemical or mixture, source and wavelength of the energy source, intensity, duration, and time course of exposure.
Compare with dosages known to cause human health effects or animal effects.

AOEC, Association of Occupational and Environmental Clinics; ATSDR, Agency for Toxic Substances and Disease Registry; NIOSH, National Institute for Occupational Safety and Health.

In addition to its investigative function, NIOSH can assist a physician directly in investigating a patient's exposure. Its clearinghouse responds to practitioners’ inquiries with information about the hazards of particular trades and toxic substances. Table 8.4 has contact information.

Enforcement Agencies

Although health departments generally have authority to investigate occupational diseases, regulation of workplace conditions is usually the responsibility of a separate state agency or the local OSHA office in the United States Department of Labor (http://www.osha.gov/fso/osp/index.html). When a state takes over OSHA enforcement, its regulations are required to be as strict as the federal regulations. In every state, every employer is obligated to report workplace-related injuries and illnesses to OSHA.

If other workers may be in imminent danger of being made ill, the physician should communicate this urgently to OSHA and request an immediate investigation. In most cases, OSHA enforcement officers can determine easily whether regulations are being violated at a workplace, and they will provide a followup report to the referring physician. In some cases, the inspection suggests that the patient's illness was job related but that at the time of the inspection no specific OSHA regulation was being violated. If a continuing hazard does exist, OSHA can require changes because the employer has a general duty to maintain a safe workplace. Especially in these situations, physicians may need to be patient but persistent to see that appropriate action is taken.

The Mine Safety and Health Agency (MSHA) is the specific federal agency with responsibility for safety inspection and enforcement of occupational health standards for the mining industry (http://www.msha.gov/).

Consultants

Consultants who are particularly knowledgeable about specific problems are increasingly available to help practicing physicians. Poison centers, through their national network of contacts, can usually identify an appropriate expert for telephone consultation about an acute problem; you can find your local poison center through the American Association of Poison Control Centers (http://www.aapcc.org/). The Association of Occupational and Environmental Clinics (AOEC), a national network of primarily university-based clinics, can be contacted to identify resources available in most parts of the United States (Table 8.4).

Evidence-Based Practice

The Cochrane Library now has a section, the Cochrane Occupational Health Field, that provides evidence-based reviews of occupational health practice (see http://www.hopkinsbayview.org/PAMreferences).

P.127

Workers’ Compensation Programs

Every state has a workers’ compensation act that provides a system to pay for medical expenses related to occupational disease and injury and for employees’ lost earnings. These acts were passed to provide a no-fault system of compensating workers injured on the job and to provide employers with statutory protection from being sued for negligence by their employees.

Although the system sometimes works well for on-the-job injuries, it does not respond well to the needs of a worker with an occupational disease. Here the burden of proof that the disease is work related falls on the worker, and the process of obtaining compensation is often slow and difficult. Because most small employers insure themselves with an insurance company, the insurer may delay action on a claim even when the employer believes the illness was caused by the job. Usually the worker can obtain legal assistance without having to pay an attorney in advance, because provision is made for cases to be taken on a contingency-fee basis (i.e., attorneys receive no fee unless the claim is upheld, and then they receive a fixed percentage of the award). Because illness claims are usually complex, the worker often needs a lawyer.

If a physician concludes, or even strongly suspects, that a patient has an illness caused by or made worse by the patient's job, the patient should be encouraged to file for workers’ compensation (through the employer, the workers’ compensation local office, or a lawyer).

If a claim is pursued and won (even though it takes time), the patient is usually guaranteed lifetime medical coverage from workers’ compensation funds for that illness. Compensation may lift some of the financial burdens from the patient and the patient's family, particularly in cases of chronic or fatal illness.

To some extent, the workers’ compensation system has failed because of inadequate physician diagnosis and follow-through. Most of the economic and social costs of industrial disease are borne not by the companies that may have acted irresponsibly but by the victims and the taxpayers, including businesses that are trying to protect their employees properly. A 2005 report from the RAND Corporation found that about one-third of all disabled people in their fifties receiving benefits from Social Security Disability became disabled because of their jobs; this proportion was 50% among the men.

Physicians are often reluctant to become involved with workers’ compensation, believing that a claim may tie them up in court. This is an unsubstantiated fear, because the medical record usually provides sufficient medical evidence and the physician does not have to appear at the hearing. If the record does not provide adequate information, the attorneys involved are almost always willing to take a statement at the physician's convenience. Physicians should note, however, that many patients are reluctant to file for workers’ compensation because of fear of reprisal, lack of management response to prior reports, and a desire to stay in their usual job rather than being transferred to a different job because of a medical condition (3).

Part-Time Occupational Health Physician

A primary care practitioner may become involved in a workplace at the invitation of the employer or the union representing the employees. Many small- and medium-size workplaces need the assistance of part-time physicians to conduct effective programs to detect and prevent occupational disease. A physician who takes on an occupational health role should become thoroughly acquainted with the goals and procedures of the proposed program, as well as the applicable regulations. Table 8.5 lists the principal responsibilities that an occupational physician

P.128


might be asked to assume and the sources of regulations that guide these physician responsibilities. The American College of Occupational and Environmental Medicine (ACOEM; http://www.acoem.org) sponsors regular training sessions to keep its members and interested physicians up-to-date in these roles.

TABLE 8.5 Responsibilities for the Part-Time Occupational Health Physician

Responsibilities

Regulations to Be Familiar With

Source of Information and Training

Preplacement and fitness-for-duty examinations

Americans with Disabilities Act

Equal Employment Opportunity Commission (http://www.eeoc.gov )

Transportation (DOT) requirements

American College of Occupational and Environmental Medicine training courses (http://www.acoem.org or 847-818-1800)

Testing for substance abuse

DOT regulations

American College of Occupational and Environmental Medicine Medical Review Officer training courses (http://www.acoem.org or 847-818-1800)

Surveillance

Occupational Safety and Health Administration (OSHA) regulations

http://www.osha.gov

Care of injured or ill workers

Workers' compensation procedures for one's state

Find your state's contact information athttp://www.dol.gov/esa/regs/compliance/owcp/wc.htm

Rules governing access to medical records

Some physicians in occupational medicine regard themselves as responsible to the management of the company that pays them, rather than to the patients they serve. In some instances, physicians have withheld information from patients about work-related diseases. In other cases, physicians modify their therapy for illnesses and injuries to meet the needs of production rather than the needs of the patient. Both the ACOEM and the International Labour Organization (ILO) have developed ethical guidelines for occupational physicians, and many abuses have been ended. Table 8.6 summarizes the principal ethical responsibilities of an occupational health physician as outlined by ACOEM.

TABLE 8.6 ACOEM Code of Ethical Conduct

This code establishes standards of professional ethical conduct with which each member of the American College of Occupational and Environmental Medicine (ACOEM) is expected to comply. These standards are intended to guide occupational and environmental medicine physicians in their relationships with the individuals they serve, employers' and workers' representatives, colleagues in the health professions, the public, and all levels of government, including the judiciary.

Physicians should:

1. accord the highest priority to the health and safety of individuals in both the workplace and the environment;

2. practice on a scientific basis with integrity and strive to acquire and maintain adequate knowledge and expertise upon which to render professional service;

3. relate honestly and ethically in all professional relationships;

4. strive to expand and disseminate medical knowledge and participate in ethical research efforts as appropriate;

5. keep confidential all individual medical information, releasing such information only when required by law or overriding public health considerations, or to other physicians according to accepted medical practice, or to others at the request of the individual;

6. recognize that employers may be entitled to counsel about an individual's medical work fitness, but not to diagnoses or specific details, except in compliance with laws and regulations;

7. communicate to individuals and/or groups any significant observations and recommendations concerning their health or safety; and

8. recognize those medical impairments in oneself and others, including chemical dependency and abusive personal practices, which interfere with one's ability to follow the above principles, and take appropriate measures.

Physicians and Health Care Institutions as Employers

Promulgation of the OSHA Blood-Borne Pathogens Standard has reminded physicians and health care organizations of their responsibilities to those they employ and supervise. Most hospitals and state and local medical societies have available information and instructional material to simplify compliance with the requirements for protective equipment, immunization, and education. The basic components of universal precautions to protect health workers from infected body fluids are summarized in Chapter 39, and postexposure actions to address the risk of acquiring hepatitis or human immunodeficiency virus infection are summarized in Chapters 18 and 39, respectively.

Hazards at Home and in the Community

Exposures at Home

The average American home is a Pandora's Box of potentially harmful exposures. Between kitchen, bathroom, garage, and garden, family members may have access to caustics, a variety of aerosols, pesticides, solvents, paint removers, adhesives, and electrical equipment. These types of exposure should be considered when warning about childproofing for toddlers and when evaluating dermatoses and allergic reactions. Exposures at home may also produce illness in ways that come less readily to mind (Table 8.7). Case reports document poisoning from inappropriate use of cosmetics and vitamin supplements. Many hobbies can involve exposure to chemicals with fewer protections than workers in industry enjoy. For example, lead poisoning has been documented from ceramics, stained glasswork, and cosmetics; paint strippers containing methylene chloride can produce carbon monoxide poisoning sufficient to aggravate angina and precipitate

P.129


infarction; and injudicious combinations of cleaning materials can release hazardous fumes. Homes themselves may have hazards. For example, lead-containing paints are a risk to both children and do-it-yourself enthusiasts, and formaldehyde-urea foam insulation can release sensitizing fumes. In cases of illness caused by such exposures, physicians need to take a careful history to recognize the cause.

TABLE 8.7 Common Hazards at Home

Heating and air conditioning
Water damage and mold
Insulation and lack of ventilation
Vitamins and health foods
Cleaning chemicals
Lead-containing paint
Electric appliances
Water supply
Hobbies
Home repair
Neighborhood pollution sources

Heating and ventilation systems deserve special mention. Even up-to-date heating systems can produce carbon monoxide poisoning if flues are blocked or inadequate air for combustion is provided. Because symptoms of early carbon monoxide poisoning are nonspecific and mimic those of stress and depression, a high level of suspicion is critical, especially early in the heating season. With the current emphasis on increased insulation and barriers to air infiltration, houses are often poorly ventilated by fresh air. The increasing use of wood, coal, and kerosene heaters may make matters worse. Use of scrap lumber treated with chemical preservatives is an additional hazard.

Leaking roofs and windows can lead to water damage to ceilings and walls. Condensation onto concrete slabs under carpet also can cause damp conditions. Water damage is the major cause of disruption of lead-containing paint and can give rise to significant growth of mold.

Office and commercial buildings are also increasingly tight, as heated or cooled air is recycled. Many epidemics of illness caused by chemical or biologic agents circulated through the air are being reported. Building-associated illness can be caused by exposure to particulates, chemical fumes from cleaning materials and office equipment, and mold spores or other biologic antigens. Because symptoms are often nonspecific, diagnosis may depend on recognizing a temporal pattern or symptoms in coworkers. Evaluation of the ventilation system often reveals inadequacies, and in many situations, improved ventilation may be all the therapy that is needed.

Exposures from Sources in the Community

Physicians are increasingly being asked for advice relating to concerns about contaminated drinking water and air and the cleanup of toxic wastes. Many communities dependent on groundwater have had their supplies threatened by illegal dumping of chemicals or by leakage from licensed landfills.

There is no substitute in such situations for enlisting the assistance of appropriate experts, and physicians in a community may be expected to take the lead in getting help from state and local agencies. Often there is a continuing role for practitioners to play in facilitating the resolution of problems. In many cases, knowledgeable specialists have difficulty in translating what they have to say into language that the lay public can understand. Physicians who spend a good part of their days translating medical science into advice for their patients in the office are well suited to serve in this role. At the same time, community members may need someone who can represent their acute personal concerns to the authorities in a reasoned way. A physician can serve as advocate and critical reviewer for the community by making sure that the statements and positions of all of those involved are supported by factual evidence and by calling on independent expertise when appropriate. The Agency for Toxic Substances and Disease Registry of the USPHS has made a commitment to support physicians in communities affected by environmental contamination with information and assistance. Emergency help is available 24 hours a day by telephone at the Centers for Disease Control and Prevention (CDC) Emergency Operations Center, 770-488-7100.

Air Pollution

Patients with respiratory disease are especially concerned about the effects of air pollution. Patients often develop symptoms of respiratory tract irritation during periods of severe pollution, and patients with cardiac or respiratory disease may suffer exacerbations. Prudent advice is called for in such situations. Advice to move to less-polluted areas is rarely practical, and such advice should be given only after a great deal of thought about the impact of a move on the patient's entire life. Durable solutions to problems caused by air pollution depend on efforts to limit industrial discharges and, importantly, the emissions of automobiles. Pollution of indoor air in workplaces and in public facilities from cigarette smoking is an equally important challenge to the medical profession and to each community. In recent years, the increase in smoke-free public places has significantly reduced exposure to this form of air pollution. In most states, the American Lung Association is leading the struggle for clean air.

Hazardous Materials: Accidents and Disposal

Physicians with no special background in toxicology or public health may be pressed into service in cases of accidental emissions of toxic fumes or of accidents involving transport of hazardous materials.

In responding to such emergencies, a practitioner should clarify immediately that the hazard is being contained as effectively as possible, that people not needed at the scene are not being exposed, and that orderly procedures for the care of casualties are being set up. Many communities have developed a coordinated plan for response to hazardous materials incidents. Usually the local emergency response system (fire department or 911 system)

P.130


will alert a hazardous materials (HAZMAT) team. Table 8.8 provides a checklist for physicians and others involved in hazardous materials incidents.

TABLE 8.8 Checklist for Physicians and Others Involved in Hazardous Materials Incidents

What toxic and hazardous substances have been identified?
What are the concentrations in air, water, and soil?
What are the known health hazards at these concentrations?
What are the potential hazards of fire, explosion, or chemical interactions?
How many people have been exposed and how many are likely to become exposed in the near future?
What groups in the exposed population are likely to be most susceptible to health effects?
How many exposures are resulting in hospital admissions?
Outpatient visits?
What clinical findings, if any, are being observed?
What technical resources are available on short notice to assist in evaluation and control? Is there a local Hazardous Materials Team?
Is the community adequately handling the casualties?
What is the capacity of local hospitals, clinics, and physicians to absorb the additional caseload?
Should hospital disaster plans be mobilized?
Are intensive care or specialty services adequate or available to the degree needed?
Are local physicians experienced and knowledgeable about this kind of problem? If not, what is the best way to obtain expert help quickly?
Is this community covered by a repository (such as a tumor registry or population-based research study) that could be used to monitor the exposed population in the future?

Environmental and Bioterrorism

Recent events, including those of September 11, 2001 and the anthrax attacks later that year, make it clear that the medical profession must be prepared to respond to intentional disasters, including biologic, chemical, and radiologic terrorist attacks. Response by the medical profession to terrorism events will require early identification of ill or exposed persons, rapid implementation of therapy, application of special infection control considerations, and collaboration or communication with the public health system. Clinicians will also play a critical role in managing postexposure treatment and prophylaxis, and managing the psychological and emotional impact of the event. The challenge will be to differentiate those who are truly exposed from those who are not exposed, but are worried they might be. A working knowledge of the agents most likely to be used in a terrorist event becomes critical. The epidemiologic setting of cases plays a pivotal role in guiding diagnostic tests and treatment.

Epidemiologic clues to intentional terrorist events include the following:

  1. The presence of an unusual number of cases.
  2. Unusually severe disease or unusual routes of exposure.
  3. Unusual geographic areas, unusual season, or absence of normal vector.
  4. Multiple simultaneous epidemics of different diseases.
  5. Outbreaks of unusual zoonotic diseases in local animals.
  6. Unusual strains of organisms or antimicrobial-resistance patterns.
  7. Higher attack rates than expected in persons with common exposures.

Chemical and radiologic casualties are usually readily recognized because of the nature of the agents involved.

Contacting Public Health Officials

Once a potential outbreak or significant cluster or event has been identified, prompt consultation with public health authorities is critical. Most health departments maintain on-call services and can be reached 24 hours a day. The CDC also maintains a 24-hour Emergency Response Hotline at 770-488-7100. The American College of Physicians (ACP) is also a good source of information (see “clinical information” at http://www.acponline.org; last accessed October 26, 2005).

Bioterrorism

The CDC divides potential biologic agents into categories according to risk. Category A agents are those considered to be of greatest risk, and most of them have been used as weapons in the past. These agents are shown in Table 8.9, along with a summary of distinguishing characteristics, and diagnosis and treatment recommendations.

Agents that are “effective weapons of mass destruction” are easily disseminated or transmitted from person to person, relatively easy and inexpensive to produce, cause mortality or widespread infection, and may result in panic and social disruption.

Chemical and Radiologic Terrorism

Decontamination is the most important first step in patient care in a chemical or radiologic event. For greatest effect, decontamination should begin within 1 to 2 minutes of exposure. Decontamination can be summarized as strip, flush, and run. A patient's contaminated clothing should be removed and appropriately disposed of. The patient should then be flushed with copious amounts of water, saline, or soap and water, including the eyes.

TABLE 8.9 Summary of Bioterrorism Agents, Key Characteristics, and Treatment

Agent

Signs and Symptoms

Incubation Period (Range)

Transmission

Infection Control

Diagnosis

Treatment for Adults

Post Exposure Prophylaxis for Adults

Anthrax
Bacillus anthracis

1. Inhalation

2. Cutaneous

3. Gastrointestinal

1. Flulike symptoms (fever, fatigue, muscle aches, dyspnea, nonproductive cough, headache), chest pain; possible 1–2 day improvement, then rapid respiratory failure and shock

2. Intense itching followed by painless papular lesions, then vesicular lesions, developing into eschar surrounded by edema

3. Abdominal pain, nausea and vomiting, severe diarrhea

1. 1–6 days (up to 6 wks)

2. 1–12 days

3. 1–7 days

1. None

2. Direct contact with skin lesions may result in cutaneous infection

3. None

1. Standard precautions

2. Contact precautions

3. Standard precautions

1. Chest radiograph evidence of widening mediastinum; obtain sputum and blood culture

2. Peripheral blood smear may demonstrate gram-positive bacilli

3. Culture blood and stool

1. and C. Combined IV/PO therapy for 60 days
Ciprofloxacin 500 mg q12h or doxycycline 100 mg q12h, and 1 or 2 additional drugs: vancomycin, rifampin, clindamycin, chloramphenicol, clarithromycin, penicillin, or ampicillin

2. 7–10 day course of: ciprofloxacin 500 mg PO q12h or doxycycline 100 mg PO q2h

Prophylaxis for 60 days: ciprofloxacin 500 mg PO q12h or doxycycline 100 mg PO q12h
Alternative: amoxicillin 500 mg PO q8h

Botulism; botulinum toxin

Afebrile, excess mucus in throat, dysphagia, dry mouth and throat, dizziness, then difficulty moving eyes, mild pupillary dilation and nystagmus, intermittent ptosis, indistinct speech, unsteady gait, extreme symmetric descending weakness, flaccid paralysis; generally normal mental status

Inhalation: 12–80 h
Foodborne: 12–72 h (2–8 d)

None

Standard precautions

Obtain serum, stool, gastric aspirate, and suspect foods prior to administering antitoxin; differential diagnosis includes polio, Guillain-Barré, myasthenia, tick paralysis, CVA

Limited supply of antitoxins; supportive care and ventilatory support; avoid clindamycin and aminoglycosides

Limited supplies of antitoxins

Pneumonic plague
Yersinia pestis

High fever, cough, hemoptysis, chest pain, nausea and vomiting, headache; advanced disease: purpuric skin lesions, copious watery or purulent sputum production; respiratory failure in 1–6 d

2–3 d (2–6 d)

Yes, droplet aerosols

Droplet precautions until 48 h of effective antibiotic therapy

A presumptive diagnosis may be made by Gram, Wayson, or Wright stain of lymph node aspirates, sputum, or cerebrospinal fluid with gram-negative bacilli with bipolar staining

10 d of therapy with: streptomycin 1 g IM q12h or gentamicin 2 mg/kg, then 1.0–1.7 mg/kg IV q8h
Alternatives: doxycycline 200 mg PO load, then 100 PO mg q12h or ciprofloxacin 400 mg IV q12h

7-day course of doxycycline 100 mg PO q12h or ciprofloxacin 500 mg PO q12h

Pneumonic Tularemia;Francisella tularensis

Sudden onset of acute febrile illness, progressing to pharyngitis, bronchiolitis, pleuropneumonitis, hilar lymphadenitis. Initially flulike syndrome with fever (100.4–104°F, 38–40°C), chills, headache, coryza, sore throat. Dry or slightly productive cough, substernal tightness, pleuritic pain; hemoptysis rare. Radiograph with bronchopneumonia, often with pleural effusions and hilar lymphadenopathy. Other forms of disease: glandular, oculoglandular, pharyngeal, typhoidal ulceroglandular

3–5 d (1–14 d)

None; laboratory personnel potentially at risk: use BSL-2 for routine diagnostic procedures, BSL-3 if aerosol or droplet production possible

Standard precautions

Culture using selective media (BCY, cysteine or S-H enhanced). Blood (rarely positive), sputum, pharyngeal washings; Gram stain may show poorly stained, pleomorphic, gram-negative coccobacillus. Serology preferred confirmatory test. Rapid diagnostic tests available

Treatment for 10–14 d: streptomycin 1 g IM q12h or gentamicin 5 mg/kg/d IV
Alternatives: doxycycline 100 mg IV q12h × 14 d or chloramphenicol 15 mg/kg IV q6h × 14 d or ciprofloxacin* 400 mg IV q12h × 10 d
May change to PO when clinically improved

Prophylaxis for 14 d: doxycycline 100 mg PO q12h or ciprofloxacin 500 mg PO q12h

Viral hemorrhagic fevers
Filovirus Ebola hemorrhagic fever
Marburg hemorrhagic fever
Arenavirus Lassa fever
Junin (Argentinian) Machupo (Bolivian) Others

Distinguish a classification of viruses thought to have potential for use as a bioterrorism agent. All hemorrhagic fever viruses can cause capillary leak syndromes. Malaise, fever, myalgias, prostration, conjunctival injection, petechiae, ecchymoses, shock, diffuse hemorrhage, neurologic dysfunction, and pulmonary collapse

Ebola: 2–21 d
Marburg: 3–14 d
Lassa 6–15 d (5–21 d)
Junin and Machupo 7–16 d

Transmissible via contact and droplet exposure from blood and body fluids; rare airborne transmission. Follow BSL-4 practices

Private room preferred; airborne precautions with N95 respirators or PAPRs.
Contact precautions

Early postexposure nasal swabs and induced respiratory secretions for hemorrhagic fever RT-PCR, ELISA EM, and viral isolation (requires BSL-4 laboratory)

Aggressive supportive care and management of hypotension; blood replacement products for disseminated intravascular coagulation

None available at present; research is ongoing

Smallpox variola virus

Prodromal period with malaise, fever, rigors, vomiting, headache, and backache. After 2–4 d, skin lesions appear and progress uniformly from macules to papules to vesicles and pustules, mostly on face, palms, and soles, and subsequently the trunk

12–14 d (7–17 d)

Yes, airborne droplet nuclei or direct contact with skin lesions until all scabs fall off (3–4 wk)

Airborne (includes N95 mask) and contact precautions

Swab culture of vesicular fluid or scab, send to BSL laboratory

Supportive care

Early vaccine critical (in <4 d); call CDC for vaccinia.
Vaccinia immune globulin in special cases

BSL, biosafety level. See CDC website, http://www.cdc.gov/od/ohs/biosfty/bmb14/bmb1453.htm for guidelines for biosafety in microbiological and biomedical laboratories (BMBL).
PAPRs, power air purifying respirators; RT-PCR, reverse transcriptase-polymerase chain reaction; ELISA, enzyme-linked immunosorbent assay; CDC, Center for Disease Control.
This table is based on information from the following references: Bartlett J, Henderson D, Inglesby T, et al. Smallpox as a biological weapon: medical and public health management. JAMA 1999;281(22):2127–2137; Borio L, Inglesby TV, Peters CJ, et al. Hemorrhagic fever as a biological weapon: medical and public health management. JAMA 2002;287:2391–2405; Dennis DT, Henderson DA, Inglesby TV, et al. Botulinum toxin as a biological weapon: medical and public health management. JAMA 2001;285:1059–1070; Dennis DT, Henderson DA, Inglesby TV, et al. Plague as a biological weapon: medical and public health management. JAMA 200;283:2281–2290; Dennis DT, Henderson DA, Inglesby TV, et al. Tularemia as a biological weapon: medical and public health management. JAMA 2001;285:2763–2773; Henderson DA, Inglesby TV, O'Toole T, et al. Anthrax as a biological weapon: medical and public health management. JAMA 2002;287:2236–2252.

P.131

P.132

P.133

P.134

P.135

P.136

Those treating chemical or radiologic exposures must not become victims themselves. Under no circumstances should contaminated patients be brought into regular patient treatment areas such as emergency departments or hospitals prior to decontamination. Chemical agents that are most likely to be used in an attack can be classified according to mechanism of action. Table 8.10 summarizes these agents, including a sketch of their characteristics and treatment modalities.

TABLE 8.10 Recognizing and Treating Poisoning by Chemical Agents

Agent Type

Agent Names

Mechanism of Action

Key Characteristics

Signs and Symptoms

Treatment

Further Considerations

Nerve agents

Cyclohexyl sarin (GF)
Sarin (GB)
Soman (GD)
Tabun (GA)
VX
Some insecticides (cholinesterase inhibitors)
Novichok agents/Soviet V

Inactivate acetylcholinesterase enzymes, causing both muscarinic and nicotinic effects

SLUDGE
-Salivation
-Lacrimation
-Urination
-Defecation
-Gastric
-Emptying
Pinpoint pupils
Seizures

Miosis (pinpoint pupils)
Blurred/dimmed vision
Headache
Nausea, vomiting, diarrhea
Copious secretions/sweating
Muscle twitching/fasciculations
Dyspnea
Seizures
Loss of consciousness

Decontamination
Atropine
Pralidoxime (2-PAM) chloride

Onset of symptoms from dermal contact may be delayed
Repeat antidote administration may be necessary

Asphyxiant/blood agents

Arsine
Cyanogen chloride
Hydrogen cyanide

Arsine: causes intravascular hemolysis/resulting renal failure
Cyanogen chloride/hydrogen cyanide: cyanide binds with iron in cytochrome a3preventing intracellular oxygen utilization
Increased anaerobic metabolism, creates excess lactic acid with resulting metabolic acidosis

Possible cherry-red skin (40%)
Possible cyanosis
Possible frostbite

Confusion
Nausea
Patients may gasp for air, similar to asphyxiation but more abrupt onset
Seizures prior to death
Metabolic acidosis

Decontamination
Oxygen
For cyanide, use antidotes: sodium nitrite, if available, then sodium thiosulfate
Arsine has no specific antidote
Supportive care

Arsine and cyanogen chloride may cause delayed pulmonary edema

Choking/pulmonary-damaging agents

Chlorine
Hydrogen chloride
Nitrogen oxides
Phosgene

Acids or acid-forming agents that react with cytoplasmic proteins and destroy cell structure

Chlorine is a greenish-yellow gas with pungent odor
Phosgene gas smells like newly mown hay or grass

Eye and skin irritation
Airway irritation
Dyspnea, cough
Sore throat
Chest tightness
Wheezing
Bronchospasm

Decontamination
Remove from scene
Semi-upright position
If signs of respiratory distress are present, oxygen with or without positive airway pressure may be needed
No specific antidote

May cause delayed pulmonary edema, even following a symptom-free period that varies in duration with the amount inhaled
May lead to acute respiratory distress syndrome

Blistering/vesicant agents

Mustard/sulfur mustard (HD, H)
Nitrogen mustard (HN-1, HN-2, HN-3)
Lewisite (L)
Phosgene oxime (CX)

Exact mechanisms are unknown
Mustard: forms metabolites that bind to enzymes, proteins and other cellular components
Lewisite: Binds to thiol groups in many enzymes

Mustard (HD) has an odor like horseradish, burning garlic, or mustard
Lewisite (L) has an odor like geranium
Phosgene oxime (CX) has a pepperish or pungent odor

Severe skin, eye, and mucosal irritation
Skin erythema and blistering
Tearing, conjunctivitis, corneal damage
Mild respiratory distress to marked airway damage

Decontamination
Oxygen p.r.n.
British anti-Lewisite (BAL) may decrease systemic effects of Lewisite
Mustard has no specific antidote

Possible pulmonary edema
Mustard has an asymptomatic latent period
Lewisite has immediate burning pain, blisters later
Phosgene oxime causes immediate pain
Monitor electrolyte balance
Neutropenia and sepsis

Incapacitating/behavior-altering agents

Agent 15/BZ

Competitively inhibits acetylcholine, which disrupts muscarinic transmission in central and peripheral nervous systems (atropinelike action)

May appear as mass drug intoxication with erratic behaviors, shared realistic and distinct hallucinations, disrobing and confusion
Hyperthermia
Mydriasis

Dry mouth and skin
Initial tachycardia
Altered consciousness, delusions, denial of illness, belligerence
Hyperthermia
Ataxia (lack of coordination)
Hallucinations
Mydriasis (dilated pupils)

Decontamination
Evaluate mental status
Restraints as needed
Monitor core temperature carefully
Specific antidote physostigmine may be available

Hyperthermia and self-injury are greatest risks
Hard to detect because it is an odorless and non irritating substance
Possible serious arrhythmias

Cytotoxic protein agents

Ricin
Abrin

Inhibit protein synthesis

Exposure by inhalation or injection causes more dramatic course

Latent period of 4–8 h, followed by flulike signs and symptoms
Progress within 18–24 h to nausea, cough, dyspnea, pulmonary edema (inhalation); gastrointestinal hemorrhage with emesis and bloody diarrhea; hepatic, splenic and renal failure (ingestion)

Decontamination
Maintain fluid/electrolyte balance
Maintain adequate oxygenation
Provide pain management

Rapid progression of signs and symptoms
Death possible within 36–48 h
5-d survival indicates recovery is likely

This table is based on information from Brennan RJ, Waeckerle JF, Sharp TW, et al. Chemical warfare agents: emergency medical and emergency public health issues. Ann Emerg Med 1999;34(2):191–204; Sidell FR. Chemical agent terrorism. Ann Emerg Med 1996;28:223–224; and Sidell F, Patrick WC, Dashiell TR. Jane's chem-bio handbook. Alexandria, VA: Jane's Information Group, 1998.

When a radioactive weapon is used in an attack, ionizing radiation presents the highest threat to health beyond the initial blast. Ionizing radiation can be alpha or beta particles, or X or gamma rays. The lowest lethal dose of radiation exposure is approximately 200 rem. With appropriate medical care, the lethal dose increases to about 360 rem.

Proper decontamination and shielding procedures can minimize the effects of external exposure to radioactive agents. Internal exposure, primarily from alpha and beta particles taken into the body by breathing particles in the air, absorption through the skin, or by ingesting in water, soil, or food, must also be addressed. Internal contamination can be treated using chelating or blocking agents. Potassium iodide is a blocking agent; it prevents end-organ uptake of radioactive iodine. Chelating agents bind metals into complexes, preventing tissue uptake and promoting urinary excretion. Calcium disodium edetate and penicillamine are used to treat radioactive lead poisoning. Pentetate calcium trisodium (CaDTPA) and pentetate zinc trisodium (ZnDTPA) are used for americium, curium, and plutonium poisoning.

The Larger Emergency Response Picture

As part of the overall Federal National Response Plan (NRP), public health officials and the medical community have the primary responsibility to prepare for and respond to bioterrorism events. This responsibility is included under emergency support function (ESF) number 8 in the NRP. Each hospital is now required to maintain a current Emergency Operations Plan (EOP) that details how the institution will operate in emergency situations.

National syndromic surveillance projects collect emergency department visit data on cases with descriptor “syndromes” that might indicate a terrorist event. Additionally, over-the-counter sales data is collected to monitor medication use for syndromes associated with bioterrorism agents.

The Strategic National Stockpile (SNS) is a national repository of antibiotics, vaccines, and emergency medical equipment maintained by the CDC. The SNS is designed for delivery within 12 hours to any location in the United States. Current plans call for local responders to “go it alone” for the initial 72 hours after an event. Pre-event planning becomes critical to effectively respond to future emergency situations.

Specific References

For annotated General References and resources related to this chapter, visit http://www.hopkinsbayview.org/PAMreferences.

  1. Steenland K, Burnett C, Lalich N, et al. Dying for work: the magnitude of U.S. mortality from selected causes of death associated with occupation. Am J Ind Med 2003;43:461.
  2. Markowitz SB, Fischer E, Fahs MC, et al. Occupational disease in New York state: a comprehensive examination. Am J Ind Med 1989;16:417.
  3. Pransky G, Snyder T, Dember A, et al. Under-reporting of work-related disorders in the workplace: a case study and review of the literature. Ergonomics 1999;42:171.


If you find an error or have any questions, please email us at admin@doctorlib.org. Thank you!