Principles and Protocols for Prevention, Evaluation, and Management of Exposure to Hazardous Materials
Authors: Francis Sullivan, MD, Richard Wang, MD, Ilse Jenouri, MD, Department of Emergency Medicine, Rhode Island Hospital, Providence, RI.
Peer Reviewers: Charles Stewart, MD, FACEP, Associate Professor of Emergency Medicine, Strong Memorial Hospital, Rochester, NY.
Ralph B. Leonard, PhD, MD, FACEP, Associate Professor of Emergency Medicine, Department of Emergency Medicine, Bowman Gray School of Medicine, Winston-Salem, NC.
More and more potentially toxic chemical agents are being used to produce the myriad consumer products that feed, clothe, shelter, transport, and entertain us. On the up side, these chemicals give us clean water and housing, save labor, and provide cures for a variety of illnesses. In controlled and informed use, any hazards these chemicals pose to human or other life can be minimized. However, uncontrolled situations do occur due to accidents or mishaps in the course of the manufacturing process, transport, finished product manufacture, or disposaloverall, an estimated 18,000 events annually in the United States.1,2,3 As a result, our increased dependency carries with it an increased vulnerability to harm from one of three mechanisms: flammability, reactivity, and direct biological effects.1-3 Efforts to improve safeguards must accelerate to keep pace, despite recent progress.
Heightened environmental consciousness led to the creation of the Environmental Protection Agency (EPA) and Superfund legislation, including the Superfund Amendments and Reauthorization Act (SARA). This act required the federal government to identify chemicals considered hazardous. It also mandated creation of Local Emergency Preparedness Councils (LEPC) and ordered local manufacturers to notify the corresponding LEPC of the existence of all listed chemicals within its jurisdiction. Industrial information hotlines proliferated. Occupational Health and Safety Administration (OSHA) regulations also addressed employee training and access to emergency treatment information in the form of Material Safety Data Sheets (MSDS). Household product labeling and the growth of Poison Control Centers further promoted awareness.
Despite these developments, however, the ability to manage toxic exposures or releases varies markedly across the nation and must be considered a work in progress.1,4,5 Included in this evolution are development of specific recommendations for emergency medical services, which address both prehospital and hospital ED components.6 The Joint Commission on the Accreditation of Healthcare Organizations (JCAHO) has incorporated a survey of ED capability and its congruence with statute into the overall hospital inspection process.4 There are recognized practical, administrative, and regulatory incentives to improved ED competence in handling hazardous materials incidents as part of an integrated community program.7-11
With these national directives in mind, the first portion of this review will provide general information that is essential for the emergency physician involved in planning and practice of acute hazardous materials exposure. Principles of care in this context will stress the clinical continuum from incident, to victim extraction, to patient arrival. The second part will focus on specific care issues for agents most likely to be encountered in the ED setting.
The Editor
Introduction and Scope of Problem
Exposure to a hazardous substance can be the result of loss of control of the agent, of inadequacy or failure of personnel protective policies and/or equipment, or of some combination of these factors.1 The properties of the agent and its use dictate exposure-control measures. Approximately 98% of mishaps are the result of human or equipment error, some of which may be foreseeable and preventable. Given the attention, resources, and efficiency compromise required to eliminate exposure events, many successful manufacturing and transport industries operate with little or no margin for error.1 Government regulatory agencies have assumed an increasingly prominent role as advocates for worker and community safety; this is balanced against the natural competitive pressures that force private enterprise to strive for more narrowly defined efficiency and safety standards.10 On an industry level, the recognition of potentially hazardous agents, their proper identification, and safe confinement during storage, use, and transport are standard practice. Employee protection, training, and health-monitoring regulations exist as a result of OSHA statutes.1, 10,12
Once failure of control or exposure occurs, planning must address the limitation of actual exposure and attendant injury. Accordingly, manufacturers are now required by law to maintain MSDS for individual exposure and to create specific disaster plans for larger-scale incidents.
The Federal mandate for LEPCs requires that the plans be filed with the agencies and health care facilities that would be affected by an incident and, in theory, these plans and databases should be integrated into overall disaster planning for the community. Obviously, there are many points at which planning and execution can be faulty.4,5 To compound the problem, 250,000 transports of hazardous materials occur every day, and 23% of hazardous materials accidents involve materials in transit, so any preparation must also be flexible enough to include response to unknown agents originating outside the area. Areas at low risk from fixed-facility exposure remain at risk from materials in transit, making planning important for these regions as well.2,3,4
General Principles of Exposure
The physical chemical properties of a given agent not only determine the effects of exposure but also the behavior of the agent upon release. Therefore, for any given incident, the size and context determine the magnitude of risk. The most important factors affecting dispersal are listed in Table 1. The physical state often plays a dominant role in the degree of dispersal, but the following also are important: vapor pressure, boiling point, vapor density, specific gravity, water solubility, and expansion ratios.1 A useful generalization of the mechanisms by which hazardous materials cause harm is derived from their likely interaction with the environment and/or biological materials. Within this framework, however, these categories are not mutually exclusive. Accordingly, agents may be harmful by virtue of their flammability (in air at a given ambient temperature), their reactivity (with chemicals in the environment, particularly water), and as a result of their direct health effects.
Flammability. Flammability is a general expression referring to the capacity of a material to ignite and burn. It is a critical concept because approximately 65% of hazardous materials have this property. The descriptive parameters are the flash point, flammable and explosive range, and auto-ignition temperature. The flash point is the lowest temperature at which enough of a substance is vaporized to ignite if exposed to a source of additional heat. Only if continued additional heat is added will burning be sustained, but the expression provides a measure of the minimal temperature at which such a process can be initiated. The flammable or explosive range describes the concentration range over which the partial pressures of oxygen and flammable vapor are such that combustion will be supported. Finally, the auto-ignition temperature is that temperature at which spontaneous ignition of a vapor will occur, independent of exposure to spark or flame as required by flash-point ignition. This auto-ignition can obviously result in sustained combustion if the species concentration is within the flammable range.1
Reactivity. Reactivity is another general term denoting the tendency of an agent to undergo an energy-releasing action with other chemical species likely to be encountered. These may include: air, water, extinguishing agents, or other chemical agents used in a particular manufacturing process. Commonly recognized explosive agents have this characteristic. So-called air reactive materials have low auto-ignition temperatures and ignite when a source of oxygen is provided. Water-reactive agents undergo highly exothermic reactions when exposed to water, an important concern when water is used for fire extinguishing or decontamination. Unstable monomers, used in the plastics industry, may undergo uncontrolled polymerization with violent energy release when exposed to heat, light, or certain chemicals or contaminants. Hypergolic materials are a class of species that may react spontaneously on mutual contact without an additional external energy source.1
Toxicity. In contrast to the mechanisms above, in which thermal and/or mechanical energy from a chemical reaction causes harm, toxicity refers to harm done by direct chemical reaction with body tissues, either in a general or highly specific fashion. For example, acids, alkalis, and vesicants may react with tissue to impair both structure and function. Cyanide is an example of a more specific metabolic poison, and hydrofluoric acid exhibits both general and specific toxic behavior. Although zero exposure and absolute protection may be the ideal standards applicable to toxins, the reality of industrial and public-safety professions requires some rational risk assessment. Accordingly, the American Council of Government and Industrial Hygienists (ACGIH) and OSHA have established the threshold-limit value /time-weighted average (TLV/TWA) and permissible exposure limit (PEL), respectively, for long-term exposure. From an emergency medicine perspective, however, the threshold limit value-short-term (TLV/STEL), threshold limit value-ceiling (TLV-C), and the immediately dangerous to life or health (IDLH) standards set by these organizations are more important.1 The tissues at risk of exposure are the eyes, skin, and mucous membrane, and the possible routes of exposure include direct contact, inhalation, and ingestion.
General Principles of Protection and Use of Available Resources
Protection against the risks of hazardous-material exposure obviously begins with prevention and contingency planning, but, in an imperfect world, exposures occur despite these efforts. Minimizing the adverse impact of an accident requires awareness of the potential dangers and is aided by identification and quantification of the materials released. Knowledge of the site and mechanism of the accident, of the appearance and labeling of any containers, and the characteristics of any apparent release should be used to formulate an effective response.1,4,5
A standardized diamond placard and label system covers nine classes of materials in transit. The placards must be color-coded and display the corresponding numerical hazard-class indicator and symbol coding. For many agents, a specific four-digit number is assigned by convention and must be displayed on the placard to facilitate precise identification. In the United States, the Department of Transportation (DOT) requires that this system be used for land transport of any quantity of the most dangerous entities, and for quantities greater than 1000 pounds of those materials posing a lesser threat. Air and water transport regulations differ somewhat, but the labeling system is identical.
The Emergency Response Guidebook, distributed by the DOT, matches the system with the most precise guidance feasible from the amount of information contained on a given label. These features are detailed in the accompanying tables.1,5 (See Table 2 and Table 3.) In this regard, the National Fire Protection Association 704 M marking system adheres to the three basic recognized categories of hazards already introduced. The familiar diamond configuration is used, and it is divided into diamond-shaped quadrants. Three of these, a blue one for health risk, red for flammability, and yellow for reactivity, are labeled with a relative risk scale from zero to four. The fourth, a white diamond at the bottom, contains additional warning information. Industry is encouraged to use this system liberally on containers and storage sites.1
Written information, which may not be as readily available or visible from a safe vantage point, is also required for materials in transit or storage. Shipping papers may not add any additional information to that obtained from a proper DOT label, although for agricultural chemicals, specific risk advice and initial exposure treatment must be included by law. However, if the placard is missing, erroneous, or does not reflect the entire contents of a vehicle, the manifest can be invaluable. The driver and cab should be checked whenever possible. A hazardous materials inventory, LPEC registration, and MSDS are required by law. These sources likewise provide descriptive risk information and advice regarding initial care for exposure.
The increasing power and portability of communication and information-access devices have similarly enhanced the utility of electronic databases and on-line consultation services for support of both scene management and medical care of victims at receiving facilities. In addition to regional poison control centers, there are several other sources that might provide helpful information.1,5 (See rapid reference card inserted in this issue.)
Measuring Health Risks. Quantification of a risk may require use of a number of instruments at the incident site by personnel in full protective gear. In addition, some of the methods may permit detection of unsuspected hazardous agents. These devices are subject to error as a result of a number of factors. Consequently, complementary determinations should be used whenever possible, and the "worst case" results should be used for decision-making. Combustible gas indicators measure the air concentration of a flammable species in terms of the lower explosive level. The determination is valid only for normal oxygen concentrations. A useful adjunct is an oxygen meter or combination meter, which allows detection of abnormal oxygen levels. This capability allows on-scene personnel to make informed interpretations of the combustible gas measurement and also allows planning for self-contained breathing equipment if oxygen concentrations have been reduced below 19.5% due to combustion, other reactions, or as a result of displacement. Unfortunately, the meter may malfunction during exposure to halogen or in carbon dioxide-rich environments. Colorimetric tubes are detection devices used in conjunction with an air aspiration sampling bellows to both identify/confirm and quantitate the concentration of a specific species in the sampled environment. Practical pH detectors are limited to litmus paper or analogues and are of more value as an emergency department index of adequate decontamination than as a useful guide to field rescuer protection and care.1,5
Protective Gear. The information obtained as outlined determines the appropriate protective equipment for emergency response personnel. Respiratory support may require self-contained breathing apparatus (SCBA) due to inadequate oxygen supply and/or toxic agents not removable by filters. When the specific toxic species are knownand both concentrations and ambient temperatures are within the safe performance envelope of a given respirator filteruse of the less cumbersome respirator is an option. Likewise, prudent choices in the arena of skin protection require knowledge of the agents to be encountered, their concentrations, the risk of significant contact, and the co-existent conditions such as temperature, presence of water, fire, and other local features. The initial encounter may require fully encapsulating gear, a cumbersome seamless suit with integrated facemask that prevents all contact with gases and airborne particulates as well as less insidious hazards. An intermediate level of protection is afforded by coveralls that rely upon separate, but securable glove, boot, and face-mask arrangements. The materials of which the suits are constructed are designed with defined permeability, durability, temperature resistance, flexibility, decontamination (reuse) potential, shelf life, and cost.
It is evident that preplanning for an incident is invaluable in choosing the best equipment to confront these situations. A four-stage classification of protective equipment has been developed by the EPA, (potentially allowing simplified, generic recommendation for a given incident) and is presented in Table 4.
Level A protection is mandated when skin, mucous membrane, eye, and inhalation exposure risks are high, the IDLH level is exceeded, and exposure duration and extent exceeds the STEL. Level B affords less skin, mucous membrane, and eye protection than level A, and is certainly the minimal level of protection acceptable for entry into an incompletely evaluated site. Level C equipment is advisable only for known entities in concentrations within the absorbable range for respirator filters and for which little risk of additional rescuer exposure is likely.1, 4, 13,14
Rescue, Assessment, and Decontamination
The following discussion suggests several unique aspects of caring for hazardous materials incident victims. First, the incident must be recognized as potentially dangerous. In response, the appropriate public safety resources must be assembled and deployed, ideally within a unified incident command structure. Secondly, it should be stressed that victim rescue may not be feasible within a practical time frame without presenting unacceptable risk to the responding personnel, and the information available to assess that risk may be limited. Therefore, optimization of preplanning and use of the informational and consultation services mentioned are crucial. Finally, safe rescue should focus on rapid removal of the victim, even though this may compromise injury prevention or treatment measures. Not only may the situation create a potentially unsafe scene, but protective equipment will make most traditional assessment and therapeutic interventions impossible.1,15,16 The more demanding the incident, the greater likelihood that only victim body recovery, not patient rescue, will be possible.
Similar competing concerns govern decontamination procedures. A nine-station decontamination scheme is outlined in Table 5. However, critical victim injuries and/or multiple victims may dictate that only gross decontamination be performed before transport. This decision requires that information about the offending agent or agents be reasonably accurate and that further decontamination advice is readily available to facilities receiving incompletely sanitized patients. It also requires adequate safeguarding of emergency medical services (EMS) and ED personnel and equipment, which mandates some advance preparation and training.1,11,12,16 The sequential steps for proper decontamination are standardized, even if discrete stations partly overlap, operate in parallel or in "relay" fashion, or the final steps are performed at a receiving facility. Otherwise, there is a high probability of inadequate patient treatment, substandard protection of responding personnel, and contamination of the encountered health care providers. The requirements for this plan of action are summarized in Figure 1.
Field Decontamination. Field decontamination begins with a head-to-toe brush or wipe-down of the clothed victim, followed by a thorough washdown in a contained area. Clothing removal effectively eliminates 75% of contact with many agents. Jewelry and contact lenses are removed as promptly as possible. Finally, victims should be gently scrubbed with a soft brush or sponge for five minutes. Water, with or without detergent, should be used unless another solvent or intervention is recommended, with particular attention to wounds, skin folds, hair, and nail beds. Examine the patient for orifice, mucosal, and eye involvement, and intervene where feasible, ideally using swabs and flush. Irrigate the eyes for five minutes. Protect the patient against hypothermia.
EMS personnel must wear chemical-protective coveralls, as well as face, hand, and foot coverings, unless they are advised that a higher level of protection is indicated. There should be a single access point and restriction of participating personnel to the absolute minimum required for care. The scene commander or his designee directs the timing of high-priority emergency medical intervention, which is dictated by the nature of the exposure, the condition of the patient, the incident size and victim number, and the relative training and protective equipment of the extraction, decontamination, and EMS teams. Anticipation of communications constraints and performing periodic drills are essential for balancing safety and patient care concerns. Transport of victims after only gross decontamination (brush and/or washdown and clothing removal) may be indicated. The rescue vehicle can be prepared by sealing all storage areas and then isolating the patient compartment with plastic or specialized chemical barrier draping. However, time and other constraints may require the use of other unprepared vehicles (not necessarily ambulances) and portable equipment if care of limited sophistication is all that can be given anyway.
Assessment is more challenging because of impediments associated with protective gear. EMS providers must recognize symptoms and signs of toxin exposure. These effects include: altered consciousness, airway compromise from swelling and/or secretions, lower airway respiratory distress, and cardiovascular instability. Aggravating medical illnesses and confounding traumatic injury, especially that due to blasts or burns, can make the situation even more confusing. For critically injured patients, a primary survey and its mandated interventions are followed by rapid "packaging" and continued assessment and therapy en route. No effective secondary decontamination can be done in the vehicle.1,4,5
Scene command should notify receiving hospitals of inbound patients and provide dynamic information regarding identified materials, victim number, and extent of injury and field decontamination. Emergency medical services personnel can add detail regarding the situation and care of individual patients, but cannot be expected to provide all of the information alone.1,4,5,16
Advance notice of arrival allows receiving facilities to implement Hazmat plans and to begin to match the response to anticipated needs based upon the exposure nature and victim number. It also promotes early involvement of regional poison control centers. The master protocol should address all components of a complete response as detailed in Table 6.
ED Decontamination. If EDs receive patients with only gross prehospital decontamination, or whenever the need for further decontamination is unknown, a contained outdoor space is identified, or a clearly demarcated area of the department is maintained. Ideally, this area is entered by a separate door and is separately ventilated. Provision for a warm water supply, wash collection, and contaminated equipment isolation is made. The choice of site used for a given incident is determined by victim number as well as by facility capability. Security must control access and restrict involved personnel to the minimum required for patient care. Pregnant staff are excluded from participation. Further decontamination processes and victim care may be very labor intensive, so that even with a single victim, routine staffing may need to be supplemented.
It is essential to be able to communicate with the decontamination area personnel from the outside; intercoms, bull horns, and designated messengers are all possible solutions. Protective clothing for the ED staff can range from barrier suits adequate for perimeter staff to level C gear for those involved in initial patient care as advised by consultation resources. Prehospital personnel can be a useful source of assistance during the transition period (and may be essential if completely contaminated patients present primarily to the facility). Commercially available decontamination stretchers are valuable but expensive; military litters are a practical, disposable alternative.
In general, priorities and considerations for care and decontamination in the ED do not differ from those for prehospital care. Management of life-threatening developments or injuries may have to occur concurrently with the decontamination, so dedicated advanced life support equipment is essential. Invasive interventions require additional attention to the problem of spreading contamination internally. With advance planning, resources for skin, mucosal, orifice, and eye decontamination should be superior to those available in the field. Stocking standard decontamination solutions, swabs of various sizes, irrigation lenses, and pH paper are all simple and effective preparations that should be made in advance. In general, patients require a five-minute wash with gentle scrubbing and 5-15 minutes of eye irrigation.
Management Protocols for Common Exposures
The hazardous materials most often responsible for exposure in the United States include ammonia, herbicides, volatile organic materials, and acids.2,3 Nitrogen oxides, hydrogen sulfide, and insecticides are other frequent offenders. An overview of principles that are toxin-specific assists planning, serves as a guide for field care, and becomes the basis for informed use of the many online and textbook resources providing the details necessary for optimal patient care.
Ammonia. Ammonia is ubiquitous in industrial applications, particularly in the manufacture of fertilizers, plastics, pesticides, detergents, and explosives. This clear, colorless gas has an odor detectable below hazardous concentrations. It is lighter than air, so it dissipates readily, but is easily liquefied and very water-soluble thereby forming caustic ammonium hydroxide. It is reactive with acids, halogens, and some metal salts. It is not highly flammable. Ammonia toxicity results from the caustic action of ammonium hydroxide, which is already present or is formed by contact with body surface moisture. Acute exposure to the skin or mucous membranes thus produces an inflammatory response dependent upon the concentration and the tissue sensitivity. Exuberant conjunctival reaction and tearing occur with ocular exposure, and respiratory contact may progress from rhinorrhea and erythema to life-threatening upper and lower airway obstruction and pulmonary edema. Long-term sequelae of significant acute exposure includes corneal scarring, cataracts, glaucoma, and chronic pulmonary disease. Chronic exposure may cause low grade conjunctivitis and bronchospasm.6,18
Attempted rescue of ammonia-exposure victims may require Level A protection. The victim may continue to pose a hazard outside the exposure area inasmuch as clothing or skin contamination with ammonium hydroxide may be transferred directly or through vaporization of ammonia. Level D precautions are adequate for the decontamination staff. Asymptomatic victims with no co-exposure do not constitute a hazard and probably require no decontamination. Others must have their clothing removed and body totally flushed, including eye rinsing. If the possibility of ingestion exists, conscious victims should be given eight ounces of water to dilute the material. Airway compromise and bronchospasm must be addressed as quickly as possible.6
ED care first focuses on life support and adequacy of field decontamination. Monitor for airway compromise, treat bronchospasm with inhaled bronchodilators, and observe the patient for at least six hours for evolution of laryngeal or pulmonary edema. Significant skin burns or respiratory distress are indications for admission. Anesthetize the eye and irrigate for 15 minutes or until pH has normalized. Perform as complete eye an examination as possible, including fluorescein staining, and consult ophthalmology. Eye injuries require reevaluation by an opthalmologist within 24 hours.6
Hydrogen Sulfide. Hydrogen sulfide is a colorless, flammable gas with a characteristic "rotten eggs" odor. It is found in natural gas, in sewer gas, in decaying matter, and in a variety of industrial applications. It is heavier than air and, therefore, can be particularly dangerous in unexpected encounters. Olfactory fatigue occurs quickly so that ocular and mucous membrane irritation may be especially important as a warning of continued exposure. Further evolution of symptoms is dose-dependent, and ranges from gradual onset of cough, headache, and nausea to weakness, dystaxia, pulmonary edema, and coma. The compound acts as a cellular poison, similar in action to cyanide, by binding to cytochrome oxidase.6 Evacuation of victims may require SCBA use but no other protective gear by rescuers. Decontamination can be delayed, depending upon acuity, since the victims will not pose a significant hazard to others. Early flushing of the eyes is important. Aggressive field management of respiratory failure may be required.6 ED interventions may include respiratory support and central nervous system care. Some authorities recommend intravenous treatment with 10 mL of 3% sodium nitrite to create sulfhemoglobinemia, an intervention also used for cyanide toxicity. Hyperbaric therapy has been used in several cases, but its true use remains undefined. Careful attention to continued eye decontamination is crucial as is assessment for corneal burns. Minimally symptomatic patients may be observed for six hours and discharged if no respiratory or ocular symptoms develop.6, 29
Nitrogen Oxides. This family of gases, with the exception of nitrous oxide, has a characteristic toxicity and is found in settings in which nitrogen compounds are oxidizedsilage and fuel combustion, metallurgy, and in many industrial synthetic processes. The most common members of this group, which share a sharp irritating odor, are nitric oxide, a colorless gas, and nitrogen oxide, a reddish brown gas or yellow liquid. Neither gas is flammable or highly reactive.6
Both agents cause skin and mucosal irritation, partly through water dissolution and the formation of nitric acid, which can cause severe burns. Low water solubility of these gases allows them to reach the lower airways. There, symptoms range from cough and mild dyspnea to insidious progressive edema and bronchospasm. More concentrated exposures accelerate and intensify the process, producing dangerous upper airway burns as well. Direct vasodilatory effects cause hypotension. Higher-dose exposure can create methemoglobinemia.6
Rescuers may need Level B protection. Victim field decontamination is limited to a five-minute skin and eye flush, since there is no further hazard to responding personnel. Intubation may be indicated if symptomatic upper airway burns are evident. Hypotension may require intravenous therapy. Supplementary oxygen and bronchodilator therapy are important interventions during transport.
Hospital care may include the interventions mentioned above for respiratory and cardiovascular support. Check methemoglobin levels and, if over 30%, give methylene blue, 1-2 mg/kg of body weight, intravenously over 10 minutes. Repeat the dose in an hour if indicated. For severe toxicity, consultants may advise exchange transfusion. The role of high-dose steroids for lung injury and bronchospasm is unproven. Irrigate the eyes for an additional 15 minutes, assess for pH and corneal staining, and arrange ophthalmologic consultation. Hospitalize any symptomatic patient, since respiratory deterioration may continue over a period as long as 36 hours.6
Volatile Organic Agents. Common agents in this category include benzene, toluene, xylene, acrylonitrile, ethylene oxide, and formaldehyde.
Toluene and Benzene. Benzene is widely used as a synthetic base for the manufacture of plastics, rubber, dyes, detergents, and pharmaceuticals. It has an odor that is detectable below the acute toxic concentration. Benzene vapor is heavier than air, highly flammable, moderately reactive, and a potent biological systemic toxin by inhalation. Toluene is used as a solvent in many industrial settings, is readily detectable by odor, forms a very flammable vapor, is moderately reactive, and has an acute direct toxic biological effect profile similar to that of benzene. Xylene finds application as a degreasing agent and solvent in similar settings and is the dominant solvent for pesticides. It shares the physicochemical and toxicologic profile of benzene and toluene.
Central nervous system (CNS) effects are pronounced, ranging from dizziness, visual blurring, and tremors to dystaxia, confusion, coma, and death. Cardiac dysrhythmia and pulmonary edema may occur. Gastrointestinal effects of ingestion are nausea, vomiting, and diarrhea. Absorption of as little as 15 mL of benzene can cause death. Skin and mucous membrane irritation, sometimes progressive to blistering, may result from skin contact. Skin absorption is slow for all of the agents but may contribute to systemic toxicity.6,20
Evacuation of victims exposed to these agents requires Level A protection if extended contact with liquid agent and unsafe vapor levels are anticipated, Level B protection if only limited contact can be assured. Removal of contaminated clothing by the evacuating team and determination of safe vapor levels should allow continuation of decontamination and emergency care by personnel in Level D gear, who should flush the skin and hair of the victim for three minutes, wash with mild soap, and rinse. Support personnel may be required to intervene for airway control, ventilation assistance, bronchospasm, and cardiac dysrhythmias.
ED care should provide a continuation of field interventions. Address bronchospasm, monitor for and treat dysrhythmias with beta-blockers. Begin definitive care of eye and skin burns. Sympathomimetic agents should be avoided when possible or used extremely carefully in the treatment of bronchospasm or hypotension; beta-1 agonists are least likely to stimulate the sensitized myocardium. Perform lavage in patients treated within 30 minutes of significant volume ingestion, followed by giving activated charcoal. Careful provision must be made for collection and disposal of any emesis or lavage material. Admit patients for encephalopathy, dysrhythmias, respiratory symptoms, or suspected significant ingestion. Acute tubular necrosis and pulmonary edema may develop. Aspiration pneumonitis may occur after a 72-hour delay. Patients not meeting admission criteria should be observed for 6-12 hours. Dysphoria, fatigue, and some dystaxia and sluggishness may persist for several days. Arrange for eye injuries to be followed up in 24 hours. Patients with significant benzene exposure will require follow-up surveillance for bone marrow toxicity.6
Acrylonitrile. Acrylonitrile is used in the manufacture of acrylic fiber, styrene plastics, and adhesives. These materials are, in turn, used in the production of clothing, furniture, automobiles, and in the building industry. The mechanism of toxicity includes release of cyanide. Its unpleasant odor is inadequate as a warning for acute exposure. It forms a vapor that is heavier than air. Materials containing acrylonitrile may release this agent during combustion or other chemical changes.6 Significant absorption may occur via the skin and respiratory tract. Effects may be minimal or profound, immediate or delayed. Irritability and malaise may progress to confusion, psychosis, and coma; weakness and cramping may progress to seizures. Arrhythmias and cardiovascular collapse may occur. Cough and dyspnea are common. Skin and mucosal inflammation may lead to blister formation. Severe acidosis characterizes cyanide poisoning, which may be immediate and direct, or a delayed result of hepatic metabolism of the agent. Hepatotoxicity can evolve over days. Encephalopathy and myocardial dysfunction may occur in severe poisoning.6
Evacuation personnel should wear Level A protection. Initial decontamination measures are identical to those for the aromatic organic agents previously discussed. Severely symptomatic patients can be assumed to be acidotic and treated with sodium bicarbonate. If available, immediate use of a cyanide antidote kit is appropriate. If there is any suspicion of cyanide poisoning, online guidance may be required. Amyl nitrite pearls are administered by inhalation every three minutes until 0.20 mL/kg of 3% sodium nitrite can be given intravenously over five minutes, monitoring for development of hypotension is important. Sodium thiosulfate, at a dose of 1.65 mL/kg (maximum of 50 mL) is then infused over 10 minutes.6,21,22
ED care should concentrate on optimizing advanced life-support measures, further correction of the acidosis guided by blood gas analysis, and initial or continued treatment for cyanide toxicity. Repeat sodium nitrite and thiosulfate if measured methemoglobin levels do not exceed 20%. Perform gastric lavage if an ingestion occurred within 30 minutes; this is followed by standard doses of activated charcoal. N-acetylcysteine, 140 mg/kg load, then as guided by toxicologic consultation, is indicated for potential hepatoprotective effects. Blood cyanide or thiocyanate levels may be added to routine laboratory testing, but are of value primarily for diagnostic confirmation and documentation. Skin and eye injury evaluation and treatment measures are the same as those discussed under aromatic agent exposure.
Any patient with significant exposure should be admitted. Symptomatic patients and all those receiving treatment for cyanide poisoning require continued observation and treatment in an intensive care unit.6, 21,22
Ethylene oxide. Ethylene oxide, employed as a sterilizing agent in medical and food processing settings, is also used industrially as a solvent, as a plasticizer, or other reagent. It is a colorless gas that is heavier than air, extremely flammable, and very reactive with a wide range of acids, alkalis, and common metal chlorides and oxides. The concentration required for odor detection exceeds that at which acute toxicity occurs. It is highly water soluble. Biologic toxicity reflects these properties; it causes immediate inflammation of skin and mucous membranes and wreaks deeper havoc through alkylating macromolecules.6 Neurologic manifestations of exposure may be delayed and include coma, seizures, and peripheral neuropathy. The respiratory tract exhibits a range of symptoms from mild upper tract irritation to global mucosal inflammatory response and pulmonary edema. Slowly evolving or delayed cutaneous and ocular effects can be severe. In addition, an allergic response in previously sensitized persons may confound the respiratory and cutaneous presentation.6
Evacuation personnel must wear Level A gear. Initial decontamination procedures are the same as indicated for aromatic organic agents. No special protective equipment should be required by emergency medical staff. Standard field and ED care for allergic reactions, airway compromise, respiratory distress, altered mental status, seizures, burns, and eye injuries is appropriate. Observation for 12 hours or admission is reasonable even for mild cases, since delayed neurological and respiratory difficulties may occur. Admit victims with extensive burns or respiratory distress to intensive care.6
Formaldehyde. Formaldehyde is used extensively in the manufacture of plastics, insulation, and resins, which are found in textiles, paint, furniture, carpets, plywood, and particle board. Secondary release from these materials may occur. The nearly colorless gas is flammable, slightly heavier than air, water soluble, and widely reactive. The characteristic odor is detectable at concentrations below those causing all adverse effects except allergic reactions. Biologic toxicity results from this reactivity including metabolism to formic acid. Exposure results in profound mucosal irritation that can involve the lower respiratory tract and can continue to worsen over 12 hours. This evolution may be confounded by immediate or delayed allergic manifestations that may have both cutaneous and hematologic components. Ingestion of this caustic agent can produce gastrointestinal distress, setting the stage for ulceration, perforation, and significant absorption. Metabolism of absorbed formaldehyde to formic acid results in metabolic acidosis.6,23
Evacuation personnel must have Level A protection and should provide decontamination as detailed for aromatic organic species. If any significant ingestion is suspected, arrange early endoscopy, treat acidosis with bicarbonate, assess for methanol co-ingestion, and arrange for treatment with alcohol infusion or hemodialysis as guided by toxicologic consultation. Asymptomatic patients are observed for six hours, and those with initial respiratory complaints monitored for 12 hours, and those with any systemic toxicity or ingestion admitted to an intensive care unit for monitoring. Aspiration pneumonitis and renal failure are potential late sequelae. Care and follow-up for eye injuries is the same as that for other organic toxin exposure.6
Phosgene. Phosgene, used as a war gas, plays an important role in the creation of a number of polymers, such as isocyanates, polyurethane, and polycarbonates, it is used for dye, pesticides, and pharmaceutical production. Importantly, as a combustion or decomposition product of most volatile chlorinated compounds, potential exposure may occur whenever even some household solvent or paint removal products are exposed to heat. This nonflammable gas is heavier than air, detectable by odor, and only slightly water soluble. Its slow decomposition in water to form hydrochloric acid is responsible for its toxicity.6
Exposure produces symptoms after 30 minutes to a few hours, with initial minor airway irritation evolving insidiously and inexorably to lower airway, parenchymal, and pulmonary and circulatory destruction over a period of 24 hours. Pulmonary edema and right heart failure from pulmonary capillary stasis ensue. Hypovolemia from fluid translocation can complicate the clinical picture. Skin and corneal burns occur concurrently but pale in severity by comparison.6
Evacuation requires Level A protection. Decontamination measures standard for aromatic organic materials and hydrogen chloride are adequate to limit ongoing eye and skin damage and to prevent secondary risk to rescuers. ED care beyond standard measures includes early intravenous administration of 2 g of methylprednisolone. Admit all phosgene exposures for close observation for at least 24 hours; those individuals with respiratory compromise warrant intensive care unit therapy. Standard skin and eye care recommendations apply.6
Acids. Acids, both inorganic (such as sulfuric, hydrochloric, nitric, phosphoric, chromic, and hydrofluoric) and organic (such as phenol, formic, and acetic) are widely used in manufacturing. Toxic effects are predominantly due to local reactivity but may be compounded by exothermic reaction, release of toxic moieties with decontamination, and systemic absorption of agents. Release of halogen gas, absorption of cyanide, formic acid, or fluoride ions are specific examples of these confounding effects.23,25 The local effects are determined by acid strength, water solubility, and, for organic acids, molecular weight.
Hydrofluoric acid will be discussed as an example of an agent with direct as well a remote effects, hydrochloric acid and phenol as more general examples of toxic effects.6,24
Hydrogen fluoride. Hydrogen fluoride is a colorless gas that is easily detected by odor and is less dense than air. It readily dissolves in water to form hydrofluoric acid. Although a weaker acid than its counterpart halogen acids, it creates major toxic effects due to the deep tissue penetration and resultant local and systemic effects of fluoride. Inhalation, mucous membrane, and cutaneous contact quickly produce local irritation, with extent of exposure being the chief determinant of systemic effects. Ingestion of much smaller amounts can rapidly lead to systemic effects. The basis of both local and systemic toxicity is the formation of calcium and magnesium fluoride salts, which can reduce the effective concentration of these essential cations. Locally, deep chemical burns occur, with the initial clinical signs and symptoms depending upon the concentration, but insidious evolution over the ensuing 24 hours. Corneal destruction and resultant opacification can easily result from eye contact, with deeper damage a likely complication. Direct inhalation of mist or vapor can cause upper and lower airway swelling, massive increase in upper and lower airway secretions, and immediate or delayed lung parenchymal reaction. Ingestion causes local corrosive injury with severe burns, with considerable potential for bleeding and perforation. Systemic effects of hypocalcemia and hypomagnesemiaas well as hyperkalemiamay manifest as lethal hypotension, dysrhythmias, tetany, and seizures. Long-term sequelae in survivors may include local scarring and bone loss, particularly of the finger and toenail areas, pulmonary dysfunction, and blindness.2,22
Evacuation procedures may require Level A protection. Initial decontamination including clothes removal may need to be conducted at this level of protection as well, due to potential splash and vapor contact. Clothing should be double-bagged for appropriate disposal. Concurrent with emergency airway and breathing support, flush exposed skin and eyes for at least 15 minutes with water. This decontamination is followed by transfer of care to a support zone team with level D gear for application of magnesium antacid or, if available, a 2.5% calcium gluconate/water soluble gel slurry to the exposed skin. In the absence of any of these solutions, an additional 10 minutes of water flushing should be performed. Initiate cardiac monitoring for QT and QRS abnormalities and obtain intravenous access. Invasive airway management may be required for obstruction, respiratory distress, or seizures. Nebulized bronchodilators may also be required.
ED management focuses on continuation of measures started in the field and monitoring for systemic toxicity, especially for inhalations, ingestions, or burns greater than 1% of body surface area. Burned skin must be debrided and one of the protective solutions mentioned above applied and massaged until any pain abates. Treat deep wounds and potential subungual burns with local injections of 5% calcium gluconate at a dose of 0.5 mL/cm2 of surface burn. Burns to digital areas require intra-arterial infusion of 10% calcium chloride in 50 mL D5W over four hours in a regional vessel, or 10 mL of calcium gluconate in 20 mL normal saline intravenously. Toxicologic consultants may recommend that inhalation victims receive an inhalation treatment of 100 mL of 2.5% calcium gluconate. Irrigate eyes with 500 mL of 1% calcium gluconate, complete an examination, and arrange emergent ophthalmologic consultation or follow-up depending upon findings and extent of exposure.
Give all patients with potential ingestion 8 ounces of water, an equal volume of magnesium-based antacid, and arrange gastroenterologic consultation. Determine serum calcium levels and begin calcium gluconate infusion for hypocalcemia. Admit any patients with systemic symptoms or with fingertip, eye, or burns to more than 10% body surface area; also admit patients with early pain, any ingestion, or symptomatic inhalation injury. Others may be discharged after six hours of observation with appropriate follow-up.6,25
Hydrogen chloride. Hydrogen chloride is extensively used in metallurgy for processing of natural products, and in the manufacture of plastics, rubber, fertilizer, and dye stuffs. It is a colorless or slightly yellow gas with an easily noted odor that is denser than air and dissolves readily in water to form hydrochloric acid. It is not flammable, but is highly reactive with most metals, hydroxides, amines, and alkalis, and exhibits biological toxicity primarily by this mechanism.6,25
Exposure results in a concentration- and duration-dependent irritation of involved skin and mucous membranes, manifested at the extreme by deep cutaneous burns, and laryngeal, bronchial, and pulmonary parenchymal edema. Ingestion creates similar problems with resultant necrosis and potential for bleeding and perforation. Fluid shifts associated with these responses can cause hypovolemic shock. Evacuation personnel must have Level A protection. Initial decontamination and subsequent management is similar to that for hydrogen fluoride, with the exception of application or injection of calcium preparations, since chloride ion does not exhibit the same degree of penetration and cationic binding as fluoride and systemic chloridism is rare enough that anticipatory treatment is not indicated. Admit patients with significant eye or cutaneous burns, with inhalation injury, or with ingestion. Toxicologic consultants may advise nebulized bicarbonate solution and pentoxifylline to limit lung injury. Other patients may be observed for six hours and discharged if no evolution of symptoms is noted. Patients with ingestion should have endoscopic evaluation within 6-18 hours of injury, or urgently if symptoms develop. Arrange for eye injuries to be re-evaluated in 24 hours.6,25,26
Phenol. Phenol, a white powder, clear crystal, or liquid, is an organic acid widely used in disinfectants, adhesives, and in synthetic processes. Its low volatility usually limits inhalation exposure, but both respiratory and gastrointestinal routes are efficient conduits. It is rapidly absorbed through skin, enhancing its own uptake through the burn it creates.
Systemic effects include arrhythmias, vomiting, seizures or CNS depression, with the possibility of delayed renal and hepatic damage. Severe skin, eye, and mucosal burns are characteristic of the compound. Rescuers require level B protection only if unsafe levels of vapor are present. Clothing removal and copious water irrigation are essential. However, vegetable oil or polyethylene glycol are preferable as solvents for all exposed areas other than the eyes, since they more effectively limit the characteristic sequestration of the compound under burn eschar. Do not induce emesis in cases of ingestion, but give activated charcoal if available. Hospital care requires a continuation of field care, including the use of specific solvents, if available, and standard eye care. Arrhythmias are best treated with beta blockers. Laboratory evaluation includes assessment for hemolyis, renal, and hepatic injury. Admit patients with suspected serious exposure since toxicity may be delayed; discharge others if asymptomatic after six hours.6
Herbicides. The vast number of compounds in common use pose a risk predominantly to individuals engaged in their synthesis and application. Exposure is usually by cutaneous contact, although serious toxicity can occur by the less common inhalation or ingestion routes. The chlorphenoxy agents, the bipyridyls, glyphosate, and acrolein will be discussed as representative of common agents from herbicide groups; each has a distinct mechanism of action.22
Chlorphenoxy Agents. Chlorphenoxy agents are photosynthesis inhibitors. They are solids with a faint phenolic odor. Exposed patients may present with lethargy, vomiting and diarrhea, cardiac dysrhythmias, myotonia, peripheral neuropathy, and myoglobinuria.
Evacuation personnel must wear skin, face, and eye protection. Decontamination staff should be similarly protected and should use standard measures. Field care should include electrocardiographic monitoring and, in consultation with medical control, consideration of forced alkaline diuresis. ED treatment consists of forced alkaline diuresis, keeping urine pH in the 7.6-8.8 range, standard supportive care, and sustained cardiac and metabolic monitoring.25,27 Admission is indicated to monitor for evolution of metabolic acidosis, seizures, hyperthermia, hyperkalemia, renal failure, and hepatic dysfunction.
Bipyridyl Agents. The bipyridyl agents, paraquat and diquat, are photobleaching herbicides with a faint ammonia-like odor. Skin and eye exposure can cause insidiously progressive irritation. Dermal absorption and inhalation routes are less likely than accidental or intentional ingestion to cause systemic symptoms. Vomiting and diarrhea and minor respiratory symptoms characterize the early phase, which then progresses to multisystem failure at a rate partly dependent on exposure extent. Oral, esophageal, and gastric burns are common after ingestion exposure. Paraquat causes an alveolitis that progresses to permanent fibrosis in survivors.
Pneumothoraces can further complicate care.28 Diquat toxicity to the lung is minimal, but poisoning with this agent causes brainstem microhemorrhage and infarction instead.
Field treatment consists of removal from exposure and simple skin decontamination. If ingestion is suspected, do not induce emesis; in consultation with medical control, activated charcoal may be given. The field team may wear chemical protective clothing, but respiratory protection is not essential unless the evacuation could entail contact with large concentrations or volumes of free agent.
ED care focuses on initiation or continuation of this gastrointestinal decontamination when indicatedcharcoal lavage followed by serial doses of charcoal and sorbitol given as long as the complications of ileus or perforation do not occur. Oxygen potentiates toxicity, so provide supplementary oxygen only if hypoxemia is demonstrated. Confirmatory testing by blood and urine assay is available if needed. Monitor liver and renal function. Admit patients to an intensive care unit for continued supportive care. Request toxicology consult regarding early dialysis, hemoperfusion, and forced diuresis since late application of these modalities has not been demonstrated to modify the clinical course. A 50% early and late mortality characterizes moderately severe poisoning, while rapid death within 24 hours is the usual outcome with severe exposures.25
Glyphosate is a commonly encountered amino acid synthesis inhibitor which is poorly absorbed from either the skin or gastrointestinal tract. Its local irritative effects account for the cutaneous burning and gastroenteritis symptoms which occur with topical and ingestion exposure. Fluid shifts and relative intravascular volume depletion may result in associated renal and hepatic dysfunction. Field and ED care are similar to that for the bipyridyl agents although the clinical course should be much more benign.25,29
Acrolein, or acrylaldehyde, is a potent agent which acts as a general cell poison. Its use is regulated but is particularly popular in waterway and drainage algae and weed control. It is volatile with a pungent odor and profoundly irritating to skin and mucous membranes, so that apparently limited contact or inhalation may produce disproportionate toxicity. Signs and symptoms of irritation predominate with cutaneous, inhalation, or ingestion exposure. Evacuation should be effected with Level A protection. Standard decontamination procedures should be applied for 15 minutes.25,30
Insecticides. Organophosphate and carbamate insecticides are a constant in agricultural and home settings. Although the many preparations vary in volatility, any agent spread by aerosol may have the potential for respiratory, as well as cutaneous and gastrointestinal absorption. All inhibit acetylcholinesterase, allowing acetylcholine to accumulate at synapses and myoneural junctions. The resulting effects can be a variable constellation of symptoms. Poisoning of CNS receptors causes confusion, dysarthria, and ataxia. Effects at nicotinic receptors are fatigue and weakness, then fasciculations progressing to paralysis, while at muscarinic receptors stimulation produces miosis, excessive secretions, abdominal cramping, urinary and fecal incontinence, and bradycardia.6 Rescuers should wear skin protective equipment with extent of respiratory protection determined by the anticipated levels.
Victims are initially decontaminated by flushing for five minutes with cool water, then washed twice with mild soap and warm water. Irrigate the eyes for five minutes. Subsequent care of patients with significant symptoms may require intubation until respiratory secretions can be managed. Medical control can authorize atropine dosing titrated to secretion control. Hospital care includes continued decontamination with special attention to skin folds, and nails. Green soap is recommended for all areas except the eyes. Titrate atropine administration to secretion control, using 0.015-0.05 mg/kg as an initial guide. Large initial doses and repeated doses every 15 minutes, or a continuous infusion, may be needed over the first 24 hours. For organophosphate poisoning with CNS toxicity, praladoxime is indicated; give 1-2 g intravenously at 200 mg/min (25-50 mg/kg at 4 mg/kg/min in children). The drug may also have to be repeated at half the initial dose to be effective, and dosing every four hours, or a continuous infusion may be required. All patients should have red blood cell cholinesterase determinations. Admit symptomatic patients to a closely monitored setting. Observe asymptomatic patients for six hours.6
Summary
An informed, carefully considered preparation for hazardous materials incidents in concert with LEPC activity is vital to safe and successful emergency care in these all too likely events. Attention to equipment, staff training, communication, information, and health surveillance needs is crucial to mitigating, rather than magnifying, the incident impact. Use of available online consultant services is a vital part of the emergency response, especially for implementing toxin-specific management protocols.
References
1. Borak, J. Hazardous Materials Exposure: Emergency Response and Patient Care. Englewood Cliffs, NJ: Brady; 1991.
2. Hall IH, Dhara VR, Kaye WE, et al. Surveillance of hazardous substance releases and related health effects. Arch Environ Health 1994;49:45-48.
3. Hall IH, Dhara VR, Price-Green PA, et al. Surveillance of emergency events involving hazardous substances-United States, 1990 - 1992. Morb Mortal Wkly Rep MMWR 1994;43:1-6.
4. Cox RD. Decontamination and management of hazardous materials exposure victims in the ED. Ann Emerg Med 1994;23:761-770.
5. Kirk MA, Cisek J, Rose SR. Emergency department response to hazardous materials incidents. Emerg Med Clin North Am 1994;12;461-481.
6. Agency for Toxic Substances and Disease Registry. Managing Hazardous Materials Incidents. Volumes I, ll, lll U. S. Department of Health and Human Services. Public Health Service.
7. Schultz, M. et al. Simulated exposure of hospital emergency personnel to solvent vapors and respirable dust during decontamination of chemically exposed patients. Ann Emerg Med 1995;26:324-329.
8. McQuiston, TH et al. Hazardous waste worker education: Long-term effects. J Occup Med 1994;36(12):1310-1323.
9. Graber DR, et al. Working with community organizations to evaluate potential disease clusters. Soc Sci Med 1993; 37(8):1079-1085.
10. Leonard RB, Calabro JJ, Noji EK, et al. SARA (Superfund Amendments and Reauthorization Act) Title III: implications for emergency physicians. Ann Emerg Med 1989;18:1212-1216.
11. Rekus JF. Disaster drills identify potential for problems in real emergencies. Occup Health Saf 1989;58:126-130.
12. Occupational safety and health guidelines for chemical hazards. Morb Mortal Wkly Rep MMWR 1990;39:367-368.
13. Phillips BG, Browner D. Responders: levels and logic of respirators. Occup Health Saf 1992;61;96, 99-102.
14. Stull JO. Chemical protective clothing. Occup Health Saf 1992;61:49-52.
15. Arad M, Berkenstadt H, Zelingher J, et al. The effects of continuous operation in a chemical protective ensemble on the performance of medical tasks in trauma management. J Trauma 1993;35:800-804.
16. Leonard RB. Hazardous materials accidents: initial scene assessment and patient care. Aviat Space Environ Med 1993;64:546-551.
17. El Sanadi, N, Grove C, Takacs M, et al. A hospital-based, hazardous materials decontamination and treatment unit: Utilization patterns over a nine-month period. Prehosp Dis Med 1993;8:337-340.
18. Leduc D, Gris P, Lheureux P, et al. Acute and long term respiratory damage following inhalation of ammonia. Thorax 1992;47:755-777.
19. Snyder JW, Safir EF, Summerville GP, et al. Occupational fatality and persistent neurological sequelae following exposure to hydrogen sulfide. Am J Emerg Med 1995;13:199-203.
20. Erickson T, Amed V, Leibach SJ, et al. Acute bone marrow toxicity and pancytopenia following exposure to lead chromate, xylene, and ethylbenzene in a degloving injury. Am J of Hematol 1994;47:257-261.
21. Ellenhorn’s Medical Toxicology: Diagnosis and Treatment of Human Poisoning. Baltimore:Williams and Wilkins; 1997:100-101.
22. Jerca L, Busuioc A, Serban F, et.al. Glutathione and the redox index in different types of cellular oxidative states: Acrylonitrile poisoning. Rev Med Chir Soc Med Iasi 1992;96:219-222.
23. Chan TC, Williams SR, Clark RF, et al. Formic acid burns resulting in systemic toxicity. Ann Emerg Med 1995;26:383-386.
24. Leung HW, Paustenbach DJ. Organic acids and bases: review of toxicologic studies. Am J Ind Med 1990;18:717-735.
25. Sullivan JB, Kreiger GR. Hazardous Materials Toxicology: Clinical Principles of Environmental Health. Baltimore: Williams and Wilkins; 1992:762-778,1063-1075.
26. Nebulized bicarbonate in the treatment of chlorine gas inhalation. J Toxicol 1994;32:233-241.
27. Flanagan RJ, Meredith JJ, Ruprah M, et al. Alkaline diuresis for acute poisoning with chlorphenoxy herbicides and ioxynil. Lancet 1990;335:454-458.
28. Chen KW, Wu H, Huang JJ, et al. Bilateral spontaneous pneumothoraces, pneumopericardium, pneumomediastinum, and subcutaneous emphysema: a rare presentation of paraquat intoxication. Ann Emerg Med 1994;23:1132-1134.
29. Mack RB. The night the light went off in Sestos. Roundup (glyphosate) poisoning. N C Med J 1993;54: 35-36.
30. Critchley JA, Beeley JM, Clark RJ, et al. Evaluation of N-acetylcysteine and methylprednisolone as therapy for oxygen and acrolein induced lung damage. Environ Health Perspect 1990; 85:89-94.
Physicians CME Questions
17. Sources of information about potentially hazardous materials of use to emergency physicians include:
A. shipping manifests.
B MSDS sheets.
C. poison control centers.
D. online computer and 800 access telephone consultation services.
E. All of the above
18. Safe entry into an area with an ill-defined chemical hazard requires:
A. assessment of flammability risk.
B. use of Level A protective gear.
C. participation in post-exposure decontamination.
D. participation in a post-exposure health surveillance program.
E. All of the above
19. The first stage of decontamination on exit from the hot zone:
A. is carried out immediately by the evacuation team unless multiple casualties are still inside.
B. includes victim clothing removal and wash down.
C. is ideally followed by immediate transport with further decontamination en route to definitive care.
D. takes precedence over all other emergency procedures except CPR.
E. All of the above
20. ED care of victims of a hazardous materials exposure includes:
A. further decontamination unless adequate field secondary decontamination can be assured.
B. further decontamination of symptomatic external surfaces.
C. use of Level C or chemical protective gear by staff unless a higher level is indicated.
D. continued communication in order to fully define victim, rescue personnel, and staff risks.
E. All of the above
21. Ammonia exposure:
A. can pose a secondary hazard to rescuers even after hot-zone exit.
B. evokes profound mucosal reaction that can lead to upper and lower airway dysfunction.
C. requires hospital emergency department evaluation for inhalation injury and eye injury.
D. All of the above
22. Which of the following is not considered a volatile organic agent?
A. Benzene
B. Tolulene
C. Acrylonitrile
D. Nitrous oxide
23. Which of the following is false regarding acrylonitrile?
A. Mechanism of toxicity includes release of cyanide.
B. Unpleasant odor usually serves as an adequate warning of exposure.
C. Significant absorption is possible via the skin and respiratory tract.
D. Arrhythmias and cardiovascular collapse are possible.
24. According to the article, which of the following is not a sign of toxic exposure that would be easily evaluated by EMS personnel in that respond to the scene in protective gear?
A. Altered consciousness
B. Airway compromise or distress
C. Cardiovascular instability
D. Pulmonary edema
You have reached your article limit for the month. Subscribe now to access this article plus other member-only content.
- Award-winning Medical Content
- Latest Advances & Development in Medicine
- Unbiased Content