Common occupational chemical exposures: General approach and management of selected exposures

INTRODUCTION — Occupational exposures to potentially hazardous chemicals can cause significant morbidity, both acute and chronic, and mortality. Patients who present to an acute care facility may be able to identify their toxic exposure; otherwise, the clinician may have to deduce the probable toxic exposure based on the patient's job description, workplace, and clinical manifestations.

This topic is an overview of the approach to exposures to common occupational chemicals. The following are discussed in separate topics:

●Overview of occupational health (see "Overview of occupational and environmental health")

●Occupational rhinitis and lower airway conditions (see "Occupational rhinitis" and "Occupational asthma: Definitions, epidemiology, causes, and risk factors" and "Irritant-induced asthma" and "Hypersensitivity pneumonitis (extrinsic allergic alveolitis): Epidemiology, causes, and pathogenesis" and "Imaging of occupational lung diseases")

●Occupational risks to reproduction (see "Occupational and environmental risks to reproduction in females: Specific exposures and impact")

●Topical chemical burns and inhalational chemical injury (see "Topical chemical burns: Initial evaluation and management" and "Inhalation injury from heat, smoke, or chemical irritants")

EPIDEMIOLOGY — In 2021, there were 37,441 occupational exposures reported to United States poison control centers, accounting for nearly 2 percent of all calls [1]. There were eight deaths attributed to unintentional occupational exposures. However, these data only include exposures that were called into a poison center and underestimates the actual number of workplace exposures in the United States. The US Department of Labor Bureau of Labor Statistics reported 50 deaths due to occupational inhalational exposures and five deaths due to ingestions in 2020 [2]. In that same year, 405,550 nonfatal exposures to harmful substances (including 3460 chemical burns and 9530 exposures to chemical products) resulted in missed workdays.

In the US from 2008 to 2018, patients with clinically significant occupational poisoning (CSOP; defined as moderate or severe clinical effects) were likely to be male and adults aged 18 to 59 [3]. The most common substances associated with CSOP (in order of decreasing frequency) were caustics, chlorines/hypochlorites, carbon monoxide, hydrocarbons, cleansers/detergents, ammonia, cement, hydrofluoric acid, chlorofluorocarbons, hydrochloric acid, disinfectants, hydrogen sulfide, simple asphyxiants, pyrethrins/pyrethroids, and toluene/xylene. The most common substances associated with fatal occupational poisonings (in order of decreasing frequency) were hydrogen sulfide, ammonia, carbon monoxide, simple asphyxiants, chlorines/hypochlorites, alkalis, pyrethrins/pyrethroids, toluene/xylene, methane, methylene chloride, chlorofluorocarbons, and hydrochloric acid. The most common routes of exposure were inhalational, dermal, and ocular.

INITIAL EVALUATION AND MANAGEMENT

Prearrival preparation — If the treating facility receives advance notice (eg, from emergency medical personnel or an employer), clinicians should prepare by:

●Searching the internet for the exposure product's Safety Data Sheet (SDS), which may provide information on the component substances, pH, expected toxicity, and patient management. If an SDS is not available, the nature of the workplace or industry may yield clues to the exposure. A medical toxicologist or poison control center can also provide advice regarding potential hazardous substances and management priorities. (See 'Regional poison centers' below.)

●Setting up decontamination equipment and a treatment room appropriate for the reported exposure. Decontamination areas should have supplies and medications necessary to provide stabilization of a critically ill patient.

●Donning necessary personal protective equipment (PPE). The level of PPE depends on the exposure and location of care. If the exposure is unknown, the Occupational Safety and Health Administration (OSHA) recommends a level of PPE that includes a powered air-purifying respirator, which is discussed separately. (See "Topical chemical burns: Initial evaluation and management", section on 'Protection of clinicians'.)

Assess and stabilize ABCs — The initial evaluation and management begin with assessing and stabilizing airway, breathing, and circulation (ABCs). In patients with caustic oropharynx exposure, we perform early tracheal intubation before progressive edema leads to complete obstruction and an airway crisis. (See "Airway management in the adult with direct airway trauma for emergency medicine and critical care", section on 'Guiding principle: Secure the airway early'.)

Trauma resuscitation principles (eg, cervical spine immobilization) should be applied if there is concern for significant concomitant injury (eg, blast injury). (See "Initial management of trauma in adults".)

Decontamination

●Dermal – Skin decontamination typically occurs after the ABCs are assessed but may need to be performed during the initial resuscitation in the critically ill patient. For most dermal exposures, removal of all clothing and copious washing or irrigation with soap and water is sufficient. Notable exceptions to water irrigation are dry lime and elemental metals, which must be removed manually since irrigation may cause caustic or exothermic injury. While some chemicals have specific preferred decontamination products (table 1), decontaminate with soap and water until the preferred product is available. (See "Topical chemical burns: Initial evaluation and management", section on 'Chemicals NOT treated with immediate water irrigation'.)

Contaminated clothing should be placed in plastic bags to avoid secondary exposure to health care personnel from off-gassing or caustic contamination. (See "Topical chemical burns: Initial evaluation and management", section on 'Water irrigation'.)

●Ocular – Decontamination of an ocular exposures (table 2) requires copious irrigation to remove solid particulates and minimize caustic injury and is discussed separately. (See "Topical chemical burns: Initial evaluation and management", section on 'Patient with eye exposure'.)

●Gastrointestinal – Decontamination of the gastrointestinal tract is typically not indicated for workplace ingestions since most occupational hazards do not absorb to activated charcoal or are contraindications for gastric lavage or whole bowel irrigation (eg, toxic alcohols, caustics, hydrocarbons, metals).

Notable exceptions that may benefit from gastrointestinal decontamination include organophosphates, paraquat, diquat, thallium, sodium monofluoroacetate, barium carbonate, vacor, and alpha-chloralose (table 3). (See "Gastrointestinal decontamination of the poisoned patient" and "Organophosphate and carbamate poisoning", section on 'Decontamination' and "Paraquat poisoning", section on 'Gastrointestinal decontamination' and "Overview of rodenticide poisoning", section on 'Known poison'.)

DIFFERENTIAL DIAGNOSIS BASED ON CLINICAL MANIFESTATIONS

General approach — If an exposure is unknown, the toxin class may be suspected based on the following (see "General approach to drug poisoning in adults", section on 'Overview of approach' and "Initial management of the critically ill adult with an unknown overdose", section on 'Rapid first look: Examination, monitoring, and testing'):

●Toxidrome (table 4)

●Characteristic odor (table 5)

●Hyperthermia or hypothermia (table 6)

●Changes in heart rate and blood pressure (table 7)

●Changes in respiration (table 8)

Most occupational exposures produce immediate symptoms. Notable exceptions that may present with delayed onset of symptoms include the following:

●Tracheobronchial and lung parenchymal injury due to inhalational exposure of a caustic with low water solubility (eg, chlorine, oxides of nitrogen, phosgene) may take hours to manifest. (See 'Chlorines/hypochlorites' below and 'Phosgene' below and "Inhalation injury from heat, smoke, or chemical irritants".)

●Ethylene glycol or methanol ingestion can take hours to manifest a metabolic acidosis. (See "Methanol and ethylene glycol poisoning: Pharmacology, clinical manifestations, and diagnosis".)

●Inhaled or ingested methylene chloride. (See "Carbon monoxide poisoning".)

●A dilute hydrofluoric acid dermal exposure may result in delayed-onset soft tissue injury. Fingertip pain with mild erythema or whitish skin discoloration that starts several hours after cleaning product exposure should raise suspicion for hydrofluoric acid exposure. (See "Topical chemical burns: Initial evaluation and management", section on 'Hydrofluoric (HF) acid' and 'Hydrofluoric acid' below.)

Specific clinical manifestations — The presence and onset of clinical manifestations can also provide clues to the nature and extent of an exposure, such as the following:

Altered mental status — Occupational exposure to carbon monoxide, cyanide, hydrogen sulfide, hydrocarbons (eg, toluene, xylene), toxic alcohols, methylene chloride, arsenic, and simple asphyxiants can cause altered mental status. The specific exposure may be suspected based on the patient's job duties, workplace environment, and additional clinical manifestations, such as the following:

●Immediate onset of a metabolic acidosis and sudden loss of consciousness suggest poisoning with a cellular asphyxiant (eg, carbon monoxide, cyanide, hydrogen sulfide). (See "Carbon monoxide poisoning" and "Cyanide poisoning" and 'Hydrogen sulfide' below.)

●Delayed onset of a metabolic acidosis suggests poisoning with a toxic alcohol or methylene chloride (an industrial solvent and a component of paint remover that is hepatically metabolized to carbon monoxide). (See "Methanol and ethylene glycol poisoning: Pharmacology, clinical manifestations, and diagnosis" and "Carbon monoxide poisoning".)

●Slurred speech, ataxia, or diplopia suggests a hydrocarbon ingestion. (See "Acute hydrocarbon exposure: Clinical toxicity, evaluation, and diagnosis", section on 'Hydrocarbon ingestion'.)

●Vomiting and diarrhea suggest inorganic arsenic poisoning. Massive hemolysis suggests arsine gas poisoning.

●A history of working in an enclosed space suggests simple asphyxia from accumulation of gasses. (See 'Methane, propane, butane' below.)

Altered mental status can also be related to nonoccupational etiologies, such as alcohol or drug intoxication (table 9), hypoglycemia, or central nervous system lesions (eg, stroke, hemorrhage). (See "Stupor and coma in adults", section on 'Evaluation' and "Diagnosis of delirium and confusional states", section on 'Evaluation'.)

Dyspnea, cough, or wheezing — Inhalational exposures can cause dyspnea, cough, or wheezing as a result of lower respiratory tract irritation/injury, bronchospasm, or immunologic (ie, sensitization) and nonimmunologic mechanisms. Inhaled chemicals with low water solubility predominantly cause lower respiratory tract injury.

●Caustic agents that can cause an inhalational injury include hydrofluoric acid, hydrochloric acid, chlorine, hypochlorites, sodium hydroxide, chloramine, oxides of nitrogen, and other volatile acids and bases. The general evaluation and management of irritant inhalational injuries are discussed separately. (See "Inhalation injury from heat, smoke, or chemical irritants".)

●Many agents (eg, diisocyanates, chloramine) (table 10) have been associated with occupational asthma. (See "Occupational asthma: Definitions, epidemiology, causes, and risk factors".)

●Hypersensitivity pneumonitis can be caused by chemicals (table 11) or organic antigens. (See "Hypersensitivity pneumonitis (extrinsic allergic alveolitis): Epidemiology, causes, and pathogenesis", section on 'Etiologic agents'.)

●"Metal fume fever" typically occurs in welders. Symptoms include cough, dyspnea, chest tightness, fevers, chills, malaise, headaches, and myalgias without significant radiographic pulmonary findings. (See 'Zinc oxide fumes' below.)

●Chronic or repeated exposure to many industrial substances can cause pneumoconioses (ie, interstitial lung diseases) or granulomatous disease. (See "Approach to the adult with interstitial lung disease: Clinical evaluation" and "Asbestos-related pleuropulmonary disease" and "Silicosis" and "Chronic beryllium disease (berylliosis)" and "Flock worker's lung".)

Irritation of eyes, nose, or throat — Many of the same chemicals that cause dyspnea, cough, and wheezing also can irritate the eyes, nose, and throat. Routes of exposure include contact with vapor, splash injury, and ingestion. (See 'Dyspnea, cough, or wheezing' above.)

Chemicals with high water solubility preferentially cause upper respiratory tract (ie, nose and throat) irritation and injury and do not affect the lower respiratory tract unless exposure is massive or occurs in an enclosed space from which the patient cannot escape.

Exposure to ammonia, chlorine, hypochlorites, hydrochloric acid, hydrofluoric acid, sulfuric acid, hydroxides, formaldehyde, isocyanates, and chromium is discussed below. The general evaluation and management of occupational rhinitis (including irritant-induced rhinitis) are discussed separately. (See "Occupational rhinitis".)

Skin burn — Occupational causes include splash injury with hydrochloric acid, hydrofluoric acid, sulfuric acid, hydroxides, ammonia, and other acids and bases. These are discussed below. (See 'Selected caustics and irritants' below.)

Signs and symptoms of common chemicals that cause burns are reviewed in the table (table 12). The general evaluation and management of topical chemical burns are discussed separately. (See "Topical chemical burns: Initial evaluation and management".)

Rash — Rashes from occupational exposures generally include:

●Irritant contact dermatitis – This is the most common form of occupational contact dermatitis occurring in many high-risk occupations (table 13). The general evaluation and management are discussed separately. (See "Irritant contact dermatitis in adults".)

●Allergic contact dermatitis – Many industrial chemicals are sensitizing agents that can cause allergic dermatitis. Common causes include hexavalent chromium; para-phenylenediamine (black dye); natural latex; and proteins present in various plants, animals, and food ingredients handled by workers. The general evaluation and management are discussed separately. (See "Clinical features and diagnosis of allergic contact dermatitis" and "Management of allergic contact dermatitis in adults".)

●Both allergic and irritant contact dermatitis – Wet cement is unique because it can cause both allergic and irritant contact dermatitis since it contains a sensitizing agent (hexavalent chromium) and has a caustic pH (10 to 12). (See "Topical chemical burns: Initial evaluation and management", section on 'Cement burns'.)

Signs of metabolic acidosis — Occupational causes of an elevated anion-gap metabolic acidosis include carbon monoxide, cyanide, hydrogen sulfide, methylene chloride, and toxic alcohols. Lactate concentrations >10 mmol/L are highly suggestive of poisoning with a cellular asphyxiant (eg, cyanide, hydrogen sulfide). (See "Approach to the adult with metabolic acidosis", section on 'Diagnosis and evaluation'.)

EVALUATION AND MANAGEMENT BASED ON SELECTED, KNOWN EXPOSURES

All caustics/irritants: general evaluation and management — All caustics and irritants share similar initial evaluation and management, which are outlined below and discussed in detail separately:

●Decontaminate dermal burns immediately with copious soap and water. Ocular exposure should be decontaminated with flushing of the eye with sterile water or normal saline (ophthalmic anesthetic application may be helpful). (See "Topical chemical burns: Initial evaluation and management", section on 'Water irrigation'.)

●Following decontamination, assess skin burn depth and evaluate ocular exposures for corneal burns and open globe injury. (See "Open globe injuries: Emergency evaluation and initial management", section on 'Physical examination' and "Topical chemical burns: Initial evaluation and management", section on 'Burn assessment'.)

●Provide fluid resuscitation for large burns, similar to thermal burns. (See "Emergency care of moderate and severe thermal burns in adults", section on 'Fluid resuscitation'.)

●Evaluate and manage respiratory tract signs and symptoms:

•Suspect upper respiratory tract edema or injury based on clinical findings (eg, stridor, hoarseness) and confirm the diagnosis by visual inspection of the airway. (See "Inhalation injury from heat, smoke, or chemical irritants", section on 'Diagnosis'.)

•Obtain a chest radiograph (CXR) in a patient with possible lower respiratory tract injury. Clinical manifestations include tachypnea, hypoxia, retractions, decreased breath sounds, wheezing, rales, rhonchi, and respiratory fatigue and failure. Some exposures (eg, chlorine, oxides of nitrogen) can cause delayed lung injury and require prolonged observation. (See "Inhalation injury from heat, smoke, or chemical irritants", section on 'Chest imaging'.)

•Provide supportive treatment for upper and lower respiratory tract edema/injury. In a patient with stridor, administer nebulized racemic epinephrine (2.25% solution diluted in 2 to 3 mL normal saline; 0.05 to 0.1 mL/kg; maximum dose 0.5 mL). Perform early tracheal intubation since airway injury or edema may progress. Treat bronchospasm with inhaled bronchodilators (eg, albuterol). (See "Inhalation injury from heat, smoke, or chemical irritants", section on 'Pulmonary care'.)

•Severe acute lung injury or acute respiratory distress syndrome (ARDS) may require mechanical ventilation. (See "Inhalation injury from heat, smoke, or chemical irritants", section on 'Ventilator management' and "Mechanical ventilation of adults in the emergency department".)

●Do not routinely decontaminate a caustic ingestion. Symptomatic patients should undergo endoscopy within 12 to 24 hours of the exposure for grading, and may need antibiotics or surgery. (See "Caustic esophageal injury in adults".)

Selected caustics and irritants

Ammonia

●Occupational uses and chemical properties – Aqueous ammonia (a dilute 5 to 10 percent solution of ammonia in water) is used for cleaning and disinfecting. Anhydrous ammonia is pure ammonia and is used in industrial refrigeration systems, in agriculture as a source of nitrogen, and in the illicit manufacture of methamphetamine in clandestine drug laboratories.

Ammonia has a distinctive acrid odor detectable at low concentrations (5 parts-per-million [ppm]) that can alert workers of its presence. As such, most clinically significant occupational exposures to anhydrous ammonia occur when it is suddenly released into an enclosed space and the worker is unable to escape.

●Clinical manifestations of exposure [4]

•Topical aqueous ammonia: conjunctivitis and irritant dermatitis

•Ammonia vapor: conjunctivitis

•Inhalation: upper respiratory tract irritation at low concentrations (50 to 100 ppm) and bronchospasm and pulmonary injury (ie, diffuse alveolar damage and/or ARDS) at higher concentrations (approximately 500 ppm)

•Anhydrous ammonia splash: freeze-dry burn similar to frostbite due to the cooling effect of rapid evaporation; clothing may be frozen to the skin

Long-term sequelae can include reactive airways dysfunction syndrome (RADS) and reactive upper airways dysfunction syndrome (RUDS) [5]. (See "Topical chemical burns: Initial evaluation and management" and "Irritant-induced asthma".)

●Evaluation and management – Ophthalmic mast cell stabilizers (eg, azelastine, ketotifen) may be used for irritant conjunctivitis from aqueous ammonia.

Frozen clothing from anhydrous ammonia should be removed only after flushing and warming to prevent inadvertent removal of adherent skin [6,7]. For anhydrous ammonia exposure, repeat irrigation should be performed every four to six hours for the first 24 hours. (See "Topical chemical burns: Initial evaluation and management", section on 'Anhydrous ammonia'.)

The general evaluation and management are described above. (See 'All caustics/irritants: general evaluation and management' above.)

Hydrochloric acid

●Occupational uses and chemical properties – Hydrochloric acid and muriatic acid (hydrochloric acid with impurities) are used in laboratories, cleaning or etching concrete, metal cleaning, jewelry manufacture and cleaning, removal of scale from toilets and swimming pools, and in the illicit production of methamphetamine.

Muriatic acid is faintly yellow with a sharp, pungent odor that limits inhalational exposure. Muriatic acid fumes are denser than air and may accumulate in low-lying areas. These are strong acids with a pH of 1 to 2.

●Clinical manifestations of exposure – Exposure immediately causes tissue injury (coagulative necrosis) with eschar formation that limits the depth of injury [8].

•Dermal or ophthalmic: chemical burns

•Acute inhalational: predominantly upper airway injury with burning pain, tissue edema, cough, laryngospasm, and asphyxia; more intense exposures may result in lower airway injury with pulmonary edema, bronchospasm, and ARDS

•Chronic low-level inhalational/vapor: chronic respiratory tract irritation, nasal septal ulceration or perforation, conjunctivitis, and dental enamel erosion and discoloration [9]

●Evaluation and management – The general evaluation and management are described above. (See 'All caustics/irritants: general evaluation and management' above.)

Chlorines/hypochlorites

●Occupational uses and chemical properties – Chlorine is a green-yellow gas with intermediate water solubility. Chlorine gas has an irritating, pungent odor ("odor of bleach"). It reacts with water to form toxic products: hydrochloric acid (a caustic) and hypochlorous acid (forms free radicals).

Individuals maintaining swimming pools can be exposed to chlorine gas if chlorine tablets are handled improperly. Aqueous chlorine gas is used for pool chlorination by commercial services. Individuals using cleaning agents can be exposed when chlorine gas is generated from mixing chlorine acids with bases (eg, muriatic acid mixed with bleach). Firefighters may be exposed to chlorine gas generated during the combustion of chlorinated hydrocarbons (eg, polyvinyl chloride).

Hypochlorites are used as cleaning or disinfecting agents. Household bleach is sodium hypochlorite.

Chloramine gas forms when hypochlorites are mixed with a nitrogen donor such as ammonia. Chloramine gas has high water solubility and is a potent respiratory irritant, which typically forces the individual to leave the hazardous environment. Chloramine gas is also a sensitizer. Lifeguards at commercial pools may experience chronic low-dose chloramine exposure from pool chlorine mixing with human nitrogenous wastes [10].

●Clinical manifestations of exposure – Chlorine gas exposure can affect both the upper and lower respiratory tracts. Hydrochloric and hypochlorous acid are produced in the lower respiratory tract, causing a potentially slow-onset caustic injury.

•Acute chlorine gas inhalation: mucous membrane irritation/injury and parenchymal injury; airway compromise, pulmonary edema, and ARDS can develop and may be delayed up to six hours after exposure [11]

•Low-intensity repeated chlorine gas: may cause chronic respiratory complaints and flu-like symptoms; long term sequelae can include RADS and RUDS (see "Irritant-induced asthma")

•Dermal hypochlorite: allergic and irritant contact dermatitis [12]

•Ophthalmic liquid or aerosolized hypochlorite: irritant conjunctivitis and chemosis

•Ingestion of industrial-strength hypochlorite solution: esophageal and stomach injury and perforation; such injury is rare with accidental ingestion of household (approximately 5 percent) bleach (see "Caustic esophageal injury in adults")

•Acute chloramine gas: rapid-onset nasopharyngeal irritation; pulmonary edema and ARDS if exposure to high concentration or in enclosed spaces [13]

•Chronic low-level chloramine gas: occupational asthma (see "Irritant-induced asthma" and "Occupational asthma: Definitions, epidemiology, causes, and risk factors")

●Evaluation and management – In a patient with an inhalational exposure, we monitor for at least six hours with serial pulmonary examinations and pulse oximetry because of concern for delayed-onset lung injury. The CXR on presentation may be normal in a patient with a potentially toxic exposure. We obtain a CXR in any patient with hypoxia or signs of lung injury (eg, tachypnea, abnormal lung auscultation). We also obtain a CXR in a patient with mild to moderate symptoms (eg, cough, mucous membrane irritation) that have not improved after six hours. A patient who is asymptomatic (or minimally symptomatic and improving) with normal vital signs after six hours can be discharged. Any patient with hypoxia or infiltrates on CXR should be admitted for monitoring for respiratory decompensation.

Management of inhalational exposure is mostly supportive. We provide humidified supplemental oxygen for hypoxia, dyspnea, and/or upper airway irritation and inhaled beta-adrenergic agonists (eg, albuterol) for bronchospasm and/or cough [14,15]. We administer nebulized sodium bicarbonate solution (eg, 4 mL of 3.75% solution) to help control symptoms such as chest pain and throat irritation. However, evidence is mostly observational and/or does not routinely demonstrate a benefit [16-21]. A patient with severe lung injury may require mechanical ventilation. (See "Inhalation injury from heat, smoke, or chemical irritants", section on 'Ventilator management' and "Mechanical ventilation of adults in the emergency department".)

In a patient with a severe inhalational injury (eg, bilateral pulmonary infiltrates, respiratory failure), we suggest administering a glucocorticoid. A reasonable approach is to administer similar doses used to treat a severe asthma exacerbation (eg, methylprednisolone 60 to 80 mg every 6 to 12 hours), but a routinely accepted protocol does not exist. Some experts may administer inhaled glucocorticoids (eg, budesonide) in addition or as an alternative. The evidence for benefit is not conclusive and mostly based on animal models and observational studies [22-29]. Glucocorticoids may inhibit neutrophilic response and release of inflammatory mediators that cause mismatch of ventilation and perfusion, thus limiting progression of lung injury.

The general evaluation and management are described above. (See 'All caustics/irritants: general evaluation and management' above.)

Phosgene

●Occupational uses and chemical properties – Phosgene has been used as a chemical warfare agent and in various industrial processes, including the polyurethane industry, chemical (eg, dye, pesticide, pharmaceutical) manufacturing, ore processing, and welding [30]. Phosgene is a liquid at cold temperatures (<0°C [32°F]) and is otherwise a colorless gas or white cloud that is heavier than air. The gas is described to have an odor of newly mown or musty hay, grass, or corn. The odor threshold is between 0.5 and 1.5 ppm [31]. Its use in chemical warfare is discussed separately. (See "Chemical terrorism: Rapid recognition and initial medical management".)

Phosgene (COCl₂) has low water solubility. It minimally reacts with water in the upper respiratory tract but hydrolyzes to hydrochloric acid (caustic) and carbon dioxide in the lower airways [31]. It also reacts with functional groups (eg, amino, hydrazino, sulfhydryl), causing protein acylation, lipid and protein denaturation, membrane damage, and disruption of enzymes.

●Clinical manifestations of exposure – Exposure to phosgene gas can cause mucous membrane irritation, choking-like sensation, cough, vomiting, and delayed-onset pulmonary edema or ARDS [31,32]. Significant mucous membrane irritation may not occur resulting in prolonged exposure. Moderate concentration exposure characteristically produces a symptom-free latent period of 2 to 24 hours, followed by chest pain and progressive dyspnea that can worsen in severity over two to three days. High-concentration exposure can produce a shorter latent period. Hypotension has been reported in patients who develop ARDS [32].

Following a phosgene exposure, most patients fully recover within one to three weeks, but reported long-term sequelae include chronic bronchitis, emphysema, and RADS [32]. (See "Irritant-induced asthma".)

Contact with the liquid form can cause erythema, severe burns (ie, frostbite), or conjunctivitis.

●Evaluation and management – In a patient with an inhalational exposure, we monitor for at least 24 hours with serial pulmonary examinations and pulse oximetry because of concern for delayed-onset lung injury. The CXR may shows pulmonary edema; early findings (four to eight hours after exposure) can include hilar enlargement or ill-defined patchy infiltrates that can ultimately progress to ARDS [32].

Management of inhalational exposure is mostly supportive and similar to chlorine gas (discussed immediately above). Vasopressors may be needed for hypotension that does not improve with intravenous crystalloid. Use of intravenous glucocorticoids and nebulized N-acetylcysteine has been described, but evidence is limited to small observational studies [32]. A patient with severe lung injury may require mechanical ventilation. (See "Inhalation injury from heat, smoke, or chemical irritants", section on 'Ventilator management' and "Mechanical ventilation of adults in the emergency department".)

The general evaluation and management are described above. (See 'All caustics/irritants: general evaluation and management' above.)

Sulfurous/sulfuric acid

●Occupational uses and chemical properties – Sulfuric acid is used in the production of lead-acid (eg, automobile, boat) batteries, cleaning products (eg, drain cleaner), wastewater treatment, textile manufacturing, chemical manufacturing, jewelry manufacturing, agriculture, fertilizer production (ammonium sulfate), clandestine drug manufacture, and mineral extraction. Sulfur dioxide is used in smelting and oil refinery industries and is converted to sulfurous acid (H₂SO₃) when dissolved in water.

●Clinical manifestations of exposure – Caustic injury causes coagulative necrosis with eschar formation, which limits the depth of tissue injury.

•Gastrointestinal, dermal, or ophthalmic: chemical burns

•Dilute sulfuric acid: irritant contact dermatitis that may manifest after exposure cessation

•Sulfuric acid mist or vapor: highly irritating to the upper and lower respiratory tracts with upper airway burning pain, cough, or dyspnea and laryngeal edema and ARDS if intense exposure; long-term sequelae include RADS [33,34] (see "Irritant-induced asthma")

●Evaluation and management – Laboratory testing, although not required, may demonstrate an elevated anion gap due to the unmeasured bisulfate ion. (See "Serum anion gap in conditions other than metabolic acidosis".)

The general evaluation and management are described above. (See 'All caustics/irritants: general evaluation and management' above.)

Formaldehyde

●Occupational uses and chemical properties – Formaldehyde is a small organic compound commonly stored as formalin, a saturated aqueous solution (approximately 40 percent formaldehyde) that typically also contains methanol as a stabilizing agent. It is used as a fumigant, disinfectant, histologic fixative, embalming agent, precursor chemical; in textile production, fertilizer production, paper production, foundry work; as a binding agent for particle board and plywood; and in the production of resins. It is also a thermal decomposition product and may be present in smoke.

Formaldehyde is a gas under ambient conditions with a strong, pungent odor.

●Clinical manifestations of exposure

•Acute formaldehyde inhalation/vapor: eye and nasopharyngeal irritation (potentially severe); bronchospasm, pulmonary edema, and ARDS with higher concentration exposure

•Splash ophthalmic exposure: corneal opacity formation [35]

•Dermal: irritant contact dermatitis; workers with repeated exposure may develop an allergic contact dermatitis [36]

•Formalin ingestion: even small amounts can cause gastrointestinal injury, metabolic acidosis, and may be fatal [37]

•Chronic formaldehyde exposure: known human carcinogen [38]; associated with reversible decrements in pulmonary function testing

●Evaluation and management – A patient with dermatitis from minimal or only airborne exposure should be referred for allergy patch testing to determine if they are sensitized to formaldehyde. (See "Clinical features and diagnosis of allergic contact dermatitis".)

In a patient with formalin ingestion and metabolic acidosis, we recommend intravenous sodium bicarbonate and hemodialysis. Sodium bicarbonate administration attenuates the severe metabolic acidosis from formaldehyde metabolism to formic acid, may improve the effectiveness of vasopressors, and may increase renal excretion of formate. Hemodialysis can correct a metabolic acidosis and effectively eliminate formaldehyde, formic acid, and methanol [37,39,40]. (See "Approach to the adult with metabolic acidosis", section on 'Acute metabolic acidosis' and "Methanol and ethylene glycol poisoning: Management".)

The general evaluation and management are described above. (See 'All caustics/irritants: general evaluation and management' above.)

Hydroxides

●Occupational uses and chemical properties – Hydroxides (eg, sodium hydroxide, potassium hydroxide, calcium hydroxide, others) are found in cleaning products (eg, drain and oven cleaner, degreasers), cement/mortar, mining applications, paint removers, cosmetics, clandestine drug manufacturing, semiconductor manufacturing, pulp and paper manufacturing, roadbuilding, and jewelry manufacturing. They are strong bases and used for pH adjustment.

●Clinical manifestations of exposure – Hydroxides cause liquefactive necrosis and saponify cell membranes and fats, resulting in deeper tissue injury compared with acids.

•Dermal or ophthalmic: chemical burns; dilute (<2 percent) liquid hydroxides or hydroxide dust can causes irritant contact dermatitis [41] (see "Irritant contact dermatitis in adults")

•Inhalation of hydroxide aerosols or cement dust: upper airway injury with burning pain, edema, and cough; more intense exposures may cause lower respiratory tract injury and ARDS [42]

•Ingestion: esophageal and/or gastric perforation and mediastinitis; concentrated hydroxide (eg, lye) ingestion poses high risk of transmural necrosis and perforation (see "Caustic esophageal injury in adults")

●Evaluation and management – The general evaluation and management are described above. (See 'All caustics/irritants: general evaluation and management' above.)

Isocyanates

●Occupational uses and chemical properties – Isocyanates are used in the manufacture of polyurethane products such as paints, surface coatings, furniture, foams, insulation materials, and adhesives. Exposures can occur during polyurethane product manufacturing or during the application of polyurethane paint, surface coatings, or spraying of polyurethane foams. Pyrolysis and thermal decomposition of polyurethane products may release isocyanates.

Isocyanates are water soluble, highly reactive, low molecular weight chemicals.

●Clinical manifestations of exposure – Isocyanates cause upper airway mucous membrane irritation, conjunctivitis, cough, and shortness of breath. High-concentration exposures can cause pulmonary edema, hypersensitivity pneumonitis ("bathtub refinisher's lung"), RADS, bronchiolitis obliterans, and hypoxic respiratory failure [43]. (See "Hypersensitivity pneumonitis (extrinsic allergic alveolitis): Clinical manifestations and diagnosis" and "Irritant-induced asthma" and "Overview of bronchiolar disorders in adults", section on 'Bronchiolitis obliterans'.)

Diisocyanates (eg, toluene diisocyanate) are potent sensitizing agents and one of the most common causes of occupational asthma, which occurs in 5 to 15 percent of exposed workers [44]. (See "Occupational asthma: Definitions, epidemiology, causes, and risk factors".)

●Evaluation and management – The general evaluation and management are described above. (See 'All caustics/irritants: general evaluation and management' above.)

Sensitization to isocyanates mandates removal from exposure. Even a low-level exposure can precipitate life-threatening bronchospasm in a sensitized individual [45]. (See "Occupational asthma: Management, prognosis, and prevention".)

Hydrofluoric acid — Hydrofluoric acid is used as a rust remover; wheel or car wash cleaner; cleaning agent for metal, brick, and stone; glass and silicon etching (eg, in semiconductor wafer manufacture); and in petrochemical refining. Concentrated hydrofluoric acid solutions cause immediate caustic injury, whereas dilute solutions cause delayed toxicity from local or systemic hypocalcemia. Inhalational, ocular, oral, or dermal exposures, as well as systemic toxicity from hypocalcemia and hyperkalemia, can occur. Chronic inhalational exposure may result in sensitization and occupational asthma ("potroom worker's asthma"). The evaluation and management of hydrofluoric acid exposure are discussed separately. (See "Topical chemical burns: Initial evaluation and management", section on 'Hydrofluoric (HF) acid'.)

Cellular asphyxiants

Hydrogen sulfide

●Occupational uses and chemical properties – Hydrogen sulfide is a byproduct of microbial decomposition of organic matter (eg, rotting fish in the hull of boat) and various industrial processes in oil, coal, and natural gas extraction and refining, sewage treatment, paper mills, leather manufacturing, roofing asphalt, construction, agriculture (eg, manure pits), and clandestine drug manufacturing.

Hydrogen sulfide is a colorless gas that is heavier than air. It has a "rotten egg" odor that may alert workers, but the odor is not universally protective since paralysis of the olfactory nerve occurs with exposures >100 ppm [46]. Hydrogen sulfide poses significant risk to rescuers with inadequate or without personal protective equipment (PPE). In a study of fatal occupational hydrogen sulfide poisonings, 21 percent of incidents also resulted in the death of a coworker or rescuer [47].

Hydrogen sulfide is a potent inhibitor of mitochondrial cytochrome oxidase and interferes with oxidative phosphorylation. It reacts with water to form sodium sulfide, which is a local irritant. It reacts with copper and silver producing a black tarnish on coins and jewelry.

●Clinical manifestations of exposure

•Ophthalmic: keratitis, photophobia, and blepharospasm at low hydrogen sulfide concentrations (50 ppm); corneal ulceration at higher concentrations

•Pulmonary: dyspnea and cough that can progress to hemorrhagic pulmonary edema and ARDS; the onset of pulmonary edema may be immediate or delayed (in patients surviving immediate poisoning)

•Systemic/metabolic: confusion, headache, dizziness, seizure, sudden loss of consciousness ("knockdown agents"), severe elevated anion-gap metabolic acidosis (blood pH <7.0, lactate concentrations >10 mmol/L), and cardiovascular collapse at concentrations >250 ppm

•Low-dose chronic exposure: mucous membrane irritation, eye irritation, fatigue, headache, dizziness, and memory impairment

●Evaluation and management – Hydrogen sulfide poisoning is a clinical diagnosis and is suspected in patients with an occupational exposure who rapidly develop severe lactic acidosis, altered mental status, and cardiovascular collapse. The presence of a black tarnish on coins or jewelry is a clue. Testing includes serum chemistries, lactate, complete blood count, arterial blood gas, electrocardiogram, and CXR.

The only necessary decontamination is removal of clothing. Initial care is supportive. Patients are often critically ill and require tracheal intubation and circulatory support (eg, intravenous fluids, vasopressors). A patient with clinically significant poisoning (symptoms other than just local irritation) should receive high-flow oxygen (eg, nonrebreather mask, high-flow nasal cannula). A patient with lactic acidosis and severe acidemia (pH less than 7.1) should be treated with sodium bicarbonate infusion. (See "Bicarbonate therapy in lactic acidosis", section on 'Approach'.)

In a patient with neurologic or cardiovascular toxicity that does not improve quickly (within one to two hours), we suggest sodium nitrite 300 mg intravenously and hyperbaric oxygen (if available and the patient is stable for transfer to a chamber). Sodium nitrite may help reestablish aerobic metabolism by facilitating binding of hydrogen sulfide to ferric iron in methemoglobin, but evidence is limited to case reports [48,49]. Hyperbaric oxygen may increase the availability of oxygen to competitively inhibit sulfide-cytochrome binding, enhance detoxification of hydrogen sulfide, and minimize tissue injury, but evidence is also limited to case reports [50,51]. (See "Hyperbaric oxygen therapy".)

Carbon monoxide — Carbon monoxide poisoning, a common cause of occupational injury and death, is frequently associated with the operation of internal combustion engines (eg, generators, forklifts) in enclosed spaces. Occupational exposure can also occur from inhalation or ingestion of methylene chloride (dichloromethane), a solvent used in industrial processes, adhesives, paints, stains, chemical processing, and metal cleaning, which is hepatically metabolized to carbon monoxide. The evaluation and management of carbon monoxide poisoning are discussed separately. (See "Carbon monoxide poisoning".)

Hydrocarbons

N-hexane, methyl-n-butyl ketone

●Occupational uses and chemical properties – N-hexane and methyl-N-butyl ketone are used as solvents, most commonly for adhesives. Inhalational exposures can occur in industries such as textile manufacturing, furniture manufacture, shoemaking, roofing, printing facilities, and laminating. Both are metabolized to 2,5-hexanedione, which causes an axonal polyneuropathy ("shoemakers' polyneuropathy") [52]. The neuropathy can also occur with recreational misuse of solvents (eg, glue sniffing). (See "Overview of polyneuropathy" and "Overview of acquired peripheral neuropathies in children", section on 'Toxins'.)

●Clinical manifestations of exposure – Manifestations of the polyneuropathy include distal numbness, tingling, sensory loss, and symmetric, ascending weakness. The distal axonal degeneration produces a dying-back neuropathy affecting both motor and sensory nerves. Upper motor neuron damage has also been reported, resulting in spasticity and increased deep tendon reflexes [53].

●Evaluation and management – Nerve conduction studies may demonstrate slowing of both motor and sensory conduction velocities. (See "Overview of nerve conduction studies".)

Management is cessation of exposure. Recovery is slow and may be incomplete.

Toluene

●Occupational uses and chemical properties – Toluene is an aromatic hydrocarbon used as an organic solvent for spray paint, stains, oil paints, inks, paint thinners, leather tanning, degreasing agents, nail polish, and in numerous other industrial and commercial products.

●Clinical manifestations of exposure – Acute exposure mimics alcohol intoxication (eg, sedation, ataxia, confusion) and can sensitize the myocardium to catecholamine-induced dysrhythmias.

Chronic toluene exposure is associated with prolonged or permanent neuropsychiatric sequelae ("painter's syndrome") that include deficits in memory, attention, executive function, and processing speed. Physical examination findings can include dysarthria, increased deep tendon reflexes, ataxia, and impaired vision and hearing.

●Evaluation and management – The evaluation and management of acute aromatic hydrocarbon exposure are discussed separately. (See "Acute hydrocarbon exposure: Clinical toxicity, evaluation, and diagnosis".)

In a patient with chronic toluene exposure, magnetic resonance imaging may demonstrate white matter degeneration (ie, leukoencephalopathy) with cortical and cerebellar atrophy [54]. Electroencephalography may demonstrate diffuse slowing [55]. A postshift urine hippuric acid, o-cresol, or benzylmercapturic acid concentration can be obtained as a marker of exposure [56,57]. (See "Inhalant misuse in children and adolescents", section on 'Hydrocarbons'.)

Methane, propane, butane — Propane and butane are components of liquefied petroleum gas (LPG, or autogas). Methane is the main component of compressed natural gas (CNG). Exposures can occur from working with equipment that uses LPG/CNG as fuel (eg, trash trucks, ice resurfacers, forklifts, generators) or in the LPG/CNG storage and transportation industry. A leak in an enclosed area from an LPG/CNG tank, storage, or transportation container can result in accumulation of methane, propane, and butane gas and cause asphyxiation by displacing oxygen from the air. Both propane and butane are used in torches, as fuels, and as propellants for aerosols in various applications such as oil-based cooking sprays, insecticide-fogging mixtures, and cosmetic/personal care aerosols. The evaluation and management of acute aliphatic hydrocarbon exposure are discussed separately. (See "Acute hydrocarbon exposure: Clinical toxicity, evaluation, and diagnosis".)

Chronic exposure to LPG/CNG has been associated with respiratory complaints and decreased pulmonary function indices on spirometry, likely from nitrogen dioxide in the combustion products [58]. (See "Irritant-induced asthma".)

Metals

Chromium

●Occupational uses – Chromium is used for pigment production, leather tanning, electroplating, as a wood preservative, as an anti-corrosive agent, and in galvanizing solutions. Cement workers and leather tanners are at high risk for sensitization [59]. Exposure is typically dermal.

Inhalational exposure can occur if chromium fumes are liberated during welding of stainless steel.

●Clinical manifestations of exposure

•Dermal: inflammation (hand dermatitis, "blackjack disease") and ulceration ("chrome holes"); sensitization to chromium causes allergic contact dermatitis (see "Clinical features and diagnosis of allergic contact dermatitis")

•Acute inhalation: respiratory tract irritation, cough, and shortness of breath

•Repeated inhalational exposures: respiratory tract ulcerations, including nasal septal perforation; pulmonary sensitization may occur, causing bronchospasm and occupational asthma (see "Irritant-induced asthma" and "Occupational asthma: Definitions, epidemiology, causes, and risk factors")

●Management – Management includes dermal decontamination and removal from exposure, which may necessitate job change. Management of allergic contact dermatitis and occupational asthma is discussed elsewhere. (See "Management of allergic contact dermatitis in adults" and "Occupational asthma: Management, prognosis, and prevention".)

Zinc oxide fumes — Inhalation of zinc oxide fumes, which typically occurs in welders, can cause "metal fume fever" (also called "Monday morning syndrome," "foundry fever," "smelter shakes," and "welder's ague") [60,61]. Inhalation of other metal oxides, such as copper, magnesium, tin, or cadmium, may also be contributory or causative.

●Clinical manifestations – Symptoms of metal fume fever include cough, dyspnea, chest tightness, fevers, chills, malaise, headaches, and myalgias. Symptoms start abruptly four to eight hours after fume exposure and resolve spontaneously within 24 to 48 hours. Short-term tolerance (ie, tachyphylaxis) develops and repeated exposure towards the end of the workweek does not cause symptoms, but symptoms recur on Monday following absence of exposure during the weekend.

●Evaluation and management – CXR is typically normal, but may demonstrate diffuse patchy infiltrates in severe cases. Treatment is supportive; supplemental oxygen or bronchodilators are rarely needed. Patients require a careful workplace exposure assessment and adherence to using PPE while welding.

Lead — Occupations associated with lead exposure include firing range workers, commercial painters (eg, bridges), welders, crystal glass makers, lead-storage battery manufacturing, lead smelters, and renovators of older residential buildings (lead was banned from residential paint in 1978 in the United States). Lead exposure is typically chronic and occurs from inhalation of lead dust or fumes. Manifestations range in severity and can include somnolence, anhedonia, hypertension, headaches, memory loss, kidney injury, anemia, peripheral neuropathy, encephalopathy, and seizures. The evaluation and management of lead poisoning are discussed separately. (See "Lead exposure, toxicity, and poisoning in adults".)

Cadmium — Cadmium is used as an anticorrosive metal surface coating in welding. Acute exposure to cadmium oxide fumes causes a severe pneumonitis. Chronic exposure is associated with kidney interstitial injury, osteomalacia, pathologic fractures, obstructive lung disease, and lung cancer. The evaluation and management of cadmium toxicity are discussed separately. (See "Epidemiology and toxicity of cadmium".)

FOLLOW-UP CARE — Patients with injury or disease caused by an occupational exposure should be instructed to arrange follow-up with an occupational health specialist. In many cases, occupational exposures, injury, or disease are considered reportable to the Occupational Safety and Health Administration (OSHA) and should be reported by the employer. (See 'Occupational/environmental medicine clinicians' below and "Overview of occupational and environmental health", section on 'Follow-up'.)

ADDITIONAL RESOURCES

Regional poison centers — Regional poison control centers in the United States are available at all times for consultation on patients with known or suspected poisoning, and who may be critically ill, require admission, or have clinical pictures that are unclear (1-800-222-1222). In addition, some hospitals have medical toxicologists available for bedside consultation. Whenever available, these are invaluable resources to help in the diagnosis and management of ingestions or overdoses. Contact information for poison centers around the world is provided separately. (See "Society guideline links: Regional poison control centers".)

Occupational/environmental medicine clinicians — Clinicians specializing in Occupational and Environmental Medicine can be located by contacting the Association of Occupational and Environmental Clinics (AOEC), a group of occupational medicine clinics (frequently academically affiliated) with board-certified occupational medicine physicians (phone: 202-347-4976; website: www.aoec.org), or the American College of Occupational and Environmental Medicine Physicians (www.acoem.org).

Society guideline links — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: General measures for acute poisoning treatment" and "Society guideline links: Treatment of acute poisoning caused by specific agents other than drugs of abuse" and "Society guideline links: Lead and other heavy metal poisoning".)

SUMMARY AND RECOMMENDATIONS

●Initial evaluation and management – Patients may seek care knowing to which substance they were exposed, or the clinician may have to deduce the possible exposure based on job description, workplace environment, and clinical manifestations. The most common substances associated with fatal occupational poisoning in the United States include hydrogen sulfide, ammonia, carbon monoxide, simple asphyxiants, and chlorines. The product's (if known) Safety Data Sheet (SDS) may provide information on the component substances, pH, expected toxicity, and management. (See 'Epidemiology' above and 'Initial evaluation and management' above.)

Decontamination typically occurs after airway, breathing, and circulation (ABCs) are assessed, but may need to be performed during the initial resuscitation in the critically ill patient. Some exposures require specific decontamination (table 1 and table 3). (See 'Assess and stabilize ABCs' above and 'Decontamination' above.)

●Differential diagnosis if exposure is unknown – Identifying a toxidrome (table 4); characteristic odor (table 5); or disturbances in temperature (table 6), heart rate and blood pressure (table 7), and respiration (table 8) can suggest a toxin class and guide initial management. Most occupational exposures produce immediate symptoms but notable exceptions include low water solubility agents (eg, chlorine, oxides of nitrogen, phosgene), ethylene glycol, methanol, methylene chloride, and hydrofluoric acid. The presence and onset of clinical manifestations can also provide clues to the nature and extent, such as the following (see 'General approach' above):

•Altered mental status – Carbon monoxide, cyanide, hydrogen sulfide, hydrocarbons (eg, toluene, xylene), toxic alcohols, methylene chloride, arsenic, simple asphyxiants, and nonoccupational etiologies (see 'Altered mental status' above)

•Dyspnea, cough, or wheezing – Caustics/irritants (eg, hydrofluoric acid, hydrochloric acid, chlorine, hypochlorites, sodium hydroxide, chloramine, oxides of nitrogen), sensitizers (eg, diisocyanates, chloramine) (table 10), agents that cause hypersensitivity pneumonitis (table 11), zinc oxide fumes, and pneumoconioses (see 'Dyspnea, cough, or wheezing' above)

•Irritation of eyes, nose, or throat – Typically agents with high water solubility (eg, ammonia, chlorine, hypochlorites, hydrochloric acid, hydrofluoric acid, sulfuric acid, hydroxides, formaldehyde, isocyanates, chromium, many others) (see 'Irritation of eyes, nose, or throat' above)

•Skin burns and rashes – Includes acids/bases (eg, hydrochloric acid, hydrofluoric acid, sodium hydroxide, ammonia), irritants (table 13), and sensitizers (see 'Skin burn' above and 'Rash' above)

•Signs of metabolic acidosis – Carbon monoxide, cyanide, hydrogen sulfide, methylene chloride, and toxic alcohols (see 'Signs of metabolic acidosis' above)

●Evaluation and management based on known exposure – Common occupational exposures are presented above and some selected exposures are summarized below (see 'Evaluation and management based on selected, known exposures' above):

•Chlorine – Chlorine gas has an irritating, pungent odor (the "odor of bleach") and can injure both the upper and lower respiratory tracts. Signs of lung injury may be delayed up to six hours after exposure. Patients should be monitored for at least six hours with serial pulmonary examination and pulse oximetry for delayed-onset respiratory symptoms. Symptomatic patients are managed with respiratory support, humidified supplemental oxygen, and inhaled beta-adrenergic agonists (eg, albuterol). Nebulized sodium bicarbonate solution (eg, 4 mL of 3.75% solution) may help control symptoms such as chest pain and throat irritation but likely does not provide a therapeutic benefit. In a patient with a severe inhalational injury (eg, bilateral pulmonary infiltrates, respiratory failure), we suggest administering glucocorticoids (Grade 2C). A reasonable dose is methylprednisolone 60 to 80 mg every 6 to 12 hours. These may limit progression of lung injury by inhibiting neutrophilic response and release of inflammatory mediators. (See 'Chlorines/hypochlorites' above.)

•Formaldehyde/formalin – Exposure can cause ocular, skin, and upper and lower respiratory tract irritation. Splash exposure can cause corneal opacity formation. Formalin ingestions can cause gastrointestinal injury, metabolic acidosis, and may be fatal. These require upper endoscopy. In a patient with formalin ingestion and metabolic acidosis, we recommend intravenous sodium bicarbonate and hemodialysis (Grade 1B). Sodium bicarbonate may temporize the acidosis and hemodialysis can effectively eliminate formaldehyde, formic acid, and methanol. (See 'Formaldehyde' above.)

•Hydrogen sulfide – Manifestations include ocular irritation, pulmonary edema, sudden loss of consciousness, cardiovascular collapse, and severe lactic acidosis. Initial management is supportive with high-flow supplemental oxygen, circulatory support, and sodium bicarbonate infusion (if acidosis present). In a patient with neurologic or cardiovascular toxicity that does not improve quickly (within one to two hours), we suggest sodium nitrite and hyperbaric oxygen (Grade 2C). The dose of sodium nitrite is 300 mg intravenously. (See 'Hydrogen sulfide' above.)