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GLUTARALDEHYDE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Glutaraldehyde is a low molecular weight aliphatic, mildly acidic (pH 3 to 4) dialdehyde liquid, with two active carbonyl groups. It is used as a tissue fixative, cold sterilant for medical instruments and equipment, disinfectant, as a pharmaceutical, and in x-ray solutions. It is also used in water treatment, a preservative in cosmetics, and a tissue fixative in pathology labs.

Specific Substances

    1) 1,3 Diformylpropane (synonym)
    2) 1,5-Pentanedial (synonym)
    3) 1,5-Pentanedione (synonym)
    4) Glutaral (synonym)
    5) Glutaric dialdehyde (synonym)
    6) GTA (synonym)
    7) Pentane-1,5-dial (synonym)
    8) Pentanedial (synonym)
    9) CAS 111-30-8 (synonym)
    1.2.1) MOLECULAR FORMULA
    1) C5-H8-O2
    2) OCH(CH2)3CHO

Available Forms Sources

    A) FORMS
    1) Glutaraldehyde is a liquid aliphatic dialdehyde which is soluble in water and alcohol (Budavari, 1996). At room temperature, it is a colorless liquid with a pungent odor. It is miscible in water and organic solvents. Glutaraldehyde is not a naturally occurring compound. It is commonly the active ingredient in 2% buffered solutions, requiring sodium bicarbonate to activate the solutions (alkalinization to a pH of 7.5 to 8.5) (Harbison, 1998).
    2) Glutaraldehyde is available in 99%, 50%, 25%, 10% and 2% solutions or a 50% biological solution (S Sweetman , 2001; Ellenhorn et al, 1997; Lewis, 1993).
    B) USES
    1) Glutaraldehyde is an effective biocide, killing bacteria, viruses, fungi, and spores. It is commonly used as a cold sterilant and disinfectant for hospital instruments and equipment that cannot be sterilized by heat. This compound may also be used as a biocide for water treatment and oil field applications. Aqueous solutions are used as embalming fluids and for tanning leather. Glutaraldehyde may also be used as a tissue fixative. It is used as a cross-linking agent for proteins, enzymes, and polyhydroxy compounds. This compound is also used in film emulsions, x-ray processing solutions, as a preservative for cosmetics, a gelatine hardening agent, and as chemical intermediates for sealants and adhesives (Bingham et al, 2001; HSDB , 2001; S Sweetman , 2001; Fukunaga & Khatibi, 2000; Budavari, 1996; Hathaway et al, 1996; Ashford, 1994; Sittig, 1991).
    2) A 5% to 10% buffered glutaraldehyde solution has been recommended for the treatment of plantar hyperhidrosis and recurrent bullous eruption of the hands and feet, and warts (S Sweetman , 2001; DesGroseilliers & Brisson, 1974). Therapeutically, 2% to 10% topical solutions have been used to treat hyperhidrosis, onychomycosis, and verruca vulgaris. Glutaraldehyde solutions have been used prophylactically to prevent friction blisters in athletes and ballet dancers (Comaish, 1973).
    3) Its primary use is as disinfectant, being most effective in a pH of 7.5 to 8.5 as a 2% aqueous solution. Brands containing glutaraldehyde include Cidex, Glutarol, Glutarex, Sporicidin, and Verucasep. The use of glutaraldehyde solutions in simulated cold sterilization procedures resulted in air concentrations of greater than the TLV in the operator's breathing zone in one report. Levels were 0.38 ppm compared to the TLV of 0.2 ppm (Schneider & Blejer, 1973).

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) USES: Glutaraldehyde, an aliphatic dialdehyde, is a colorless liquid with a pungent odor, It is widely used in industrial, scientific and biomedical applications including biocidal treatment of water and paper, controlling bacterial growth in oil fields, cold sterilization of medical instruments and use as a histological fixative. It is commonly used as a disinfectant in endoscopy and bronchoscopy laboratories. It has also be used to treat hyperhidrosis (in low concentrations of 1% to 10%), the treatment of warts, an adhesive in dentistry, and a component in the manufacture of tissue transplants. It is available in aqueous solutions of various concentrations that can range from 1% to 50% (w/w).
    B) TOXICOKINETICS: Glutaraldehyde can act as an eye, skin and respiratory tract irritant. It is also a skin and respiratory tract sensitizer. Clinical events can vary depending on the concentration. It has also been reported to produce dark room disease among radiographers defined as various symptoms of indefinite complaints, sometimes described as similar to sick building syndrome. Symptoms reported in human exposures appear to be dose-dependent.
    C) WITH POISONING/EXPOSURE
    1) COMMON: Glutaraldehyde can be a strong irritant to the eyes, skin, and mucous membranes.
    2) DERMAL: Glutaraldehyde can cause allergic contact dermatitis, skin discoloration and ulceration.
    3) INHALATION: Vapor exposure in humans has been associated with coryza, epistaxis, headache, asthma, chest pain, palpitations, tachycardia, nausea and vomiting. Among health care workers (eg, nurses, medical radiation technologists) peak concentrations of glutaraldehyde have been correlated with chronic bronchitis and nasal symptoms in some exposed individuals. Additional symptoms from exposure may include cough, rhinitis, respiratory difficulty, and lacrimation.
    4) INGESTION: Limited data. In one young adult, a patient developed pain with swallowing and mild abdominal pain following the intentional ingestion of 75 mL of a glutaraldehyde 15% w/v and coco benzyl dimethyl ammonium chloride 10% w/v solution. She recovered completely.
    5) ANIMAL DATA: CNS depression has occurred in experimental animals given intravenous injections.
    0.2.3) VITAL SIGNS
    A) WITH POISONING/EXPOSURE
    1) Fever was observed in a child who developed chemical pneumonia after being inadvertently splashed on the face with a glutaraldehyde solution.
    0.2.4) HEENT
    A) Topical glutaraldehyde has caused severe eye injury in rabbits. A 2% solution may cause severe inflammation, lacrimation, and edema.
    B) Glutaraldehyde is particularly irritating to the nose and throat.
    0.2.6) RESPIRATORY
    A) Occupational asthma has been reported following inhalation. It is delayed in onset.
    B) Hemorrhagic pulmonary congestion and pneumonitis were common effects reported in animals regardless of whether glutaraldehyde was administered IV, orally, or by inhalation.
    0.2.7) NEUROLOGIC
    A) Seizures and CNS depression were noted in animals given intravenous glutaraldehyde.
    0.2.21) CARCINOGENICITY
    A) At the time of this review, no studies were found on the possible carcinogenic activity of glutaraldehyde in humans.

Laboratory Monitoring

    A) Monitor fluid and electrolytes in patients that develop significant diarrhea and/or vomiting following exposure.
    B) Monitor vital signs following an oral exposure.
    C) In rare cases, monitor CBC for evidence of bleeding in patients that develop gastrointestinal bleeding. If respiratory tract irritation or respiratory insufficiency are clinically evident, consider monitoring pulse oximetry, arterial blood gases, chest x-ray, and pulmonary function tests.
    D) Obtain blood gases and/or bicarbonate levels in patients at risk to develop acidosis.
    E) Monitor renal function and liver enzymes as indicated in symptomatic patients.
    F) Pulmonary function tests may be indicated in patients that develop respiratory symptoms following chronic occupational exposure.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Treatment is symptomatic and supportive. INGESTION: There have been rare reports of glutaraldehyde oral exposure. The patient may be at risk to develop pain, difficulty swallowing, irritation or potentially more severe gastrointestinal injury. Assess oral mucosa and consider esophagoscopy if the patient appears symptomatic (ie, pain, difficulty swallowing, drooling). Monitor fluid status and electrolytes in patients that develop significant vomiting. ENDOSCOPIC PROCEDURES: Infrequent reports of exposure to glutaraldehyde solution following endoscopic procedures (ie, sigmoidoscopy, colonoscopy) have occurred resulting in colitis in some patients. Gastrointestinal symptoms (eg, abdominal pain, watery diarrhea) are usually self-limited and resolve within a few days. Monitor fluid and electrolytes in patients with persistent symptoms. Replace fluids and electrolytes as indicated. Gastrointestinal bleeding is a rare finding. INHALATION: Treatment is symptomatic and supportive. Remove patient from glutaraldehyde vapors as needed. Assess respiratory effort and function. Patients with chronic occupational exposure may require ongoing evaluation of respiratory function (ie, pulmonary function studies), a combination of drug therapies (eg, corticosteroids, sympathomimetics) and permanent removal from the chemical as needed. DERMAL: Decontaminate skin with soap and water following exposure. Monitor for ongoing symptoms. OCULAR: Irrigate eyes with copious amounts of water. An ophthalmic exam may be necessary if symptoms persist.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Treatment is symptomatic and supportive. ACUTE: Monitor gastrointestinal and respiratory effort following ingestion. CHRONIC: Glutaraldehyde-induced occupational asthma has been reported in some healthcare workers with a chronic exposure. Ongoing respiratory evaluation and support may be necessary in patients that develop persistent symptoms despite removal from the chemical.
    C) DECONTAMINATION
    1) PREHOSPITAL: INGESTION: Because of the potential for further gastrointestinal injury, do NOT induce emesis. Activated charcoal is generally not recommended due to the risk of producing emesis and/or obscuring endoscopic findings, if endoscopy is needed. DERMAL: Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists. OCULAR: Exposed eyes should be irrigated copiously with water for at least 15 minutes. An ophthalmic examination should be considered if irritation or pain persists thereafter. Glutaraldehyde in concentrations as low as 2% may cause ocular damage (severe inflammation, lacrimation, and edema).
    2) HOSPITAL: INGESTION: Activated charcoal is not recommended as it may interfere with endoscopy, if needed. Consider insertion of a small, flexible nasogastric or orogastric tube to aspirate gastric contents after a recent significant ingestion of glutaraldehyde. The risk of worsening mucosal injury must be weighed against the potential benefit. DERMAL: Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists. OCULAR: Exposed eyes should be irrigated copiously with water for at least 15 minutes. An ophthalmic examination should be considered if irritation or pain persists thereafter. Glutaraldehyde in concentrations as low as 2% may cause ocular damage (severe inflammation, lacrimation, and edema).
    D) AIRWAY MANAGEMENT
    1) Move patient to fresh air following an acute exposure to glutaraldehyde vapor. Monitor respiratory effort and function. Obtain a baseline pulse oximetry or ABGs in patients that develop evidence of respiratory symptoms. Although infrequently reported, ingestion of glutaraldehyde solution produced laryngeal edema in a young adult requiring intubation and mechanical ventilation.
    E) ANTIDOTE
    1) There is no known antidote.
    F) ENHANCED ELIMINATION
    1) It is unknown if glutaraldehyde would be removed by enhanced elimination procedures.
    G) PATIENT DISPOSITION
    1) HOME CRITERIA: Patients with mild eye or skin irritation can be managed at home with decontamination. Persistent symptoms following decontamination may require further evaluation by a healthcare provider. Patients with an intentional ingestion of glutaraldehyde should be evaluated in a healthcare setting to assess for gastrointestinal injury or systemic toxicity.
    2) OBSERVATION CRITERIA: Patients with significant eye irritation, or more than mild pulmonary or skin irritation should be sent to a healthcare facility for evaluation and treatment as indicated.
    3) ADMISSION CRITERIA: Patients with evidence of ongoing (eg, pulmonary injury following an acute exposure) symptoms should be admitted to a monitored setting.
    4) CONSULT CRITERIA: Consult a poison center or medical toxicologist for assistance in managing a severe poisoning.
    0.4.3) INHALATION EXPOSURE
    A) Move patient to fresh air following an acute exposure to glutaraldehyde vapor and monitor for respiratory distress.
    0.4.4) EYE EXPOSURE
    A) Exposed eyes should be irrigated copiously with water for at least 15 minutes. An ophthalmic examination should be considered if irritation or pain persists thereafter. Glutaraldehyde in concentrations as low as 2% may cause ocular damage (severe inflammation, lacrimation, and edema).
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists.

Range Of Toxicity

    A) TOXICITY: A toxic dose has not been established in man. Ten percent solutions have caused dermatitis when applied therapeutically. Two percent solutions have caused ocular damage. One young adult intentionally ingested 75 mL of a glutaraldehyde 15% w/v and coco benzyl dimethyl ammonium chloride 10% w/v solution and developed metabolic acidosis and laryngeal edema. She required intubation and mechanical ventilation but recovered completely.
    B) OCCUPATIONAL EXPOSURE: Glutaraldehyde has been used in the healthcare setting for high level disinfection and it is a known irritant of the skin, eyes, nose and lungs in some individuals. Healthcare personnel have developed allergic dermatitis, rhinitis and occupational asthma after chronic exposure.

Clinical Effects

Summary Of Exposure

    A) USES: Glutaraldehyde, an aliphatic dialdehyde, is a colorless liquid with a pungent odor, It is widely used in industrial, scientific and biomedical applications including biocidal treatment of water and paper, controlling bacterial growth in oil fields, cold sterilization of medical instruments and use as a histological fixative. It is commonly used as a disinfectant in endoscopy and bronchoscopy laboratories. It has also be used to treat hyperhidrosis (in low concentrations of 1% to 10%), the treatment of warts, an adhesive in dentistry, and a component in the manufacture of tissue transplants. It is available in aqueous solutions of various concentrations that can range from 1% to 50% (w/w).
    B) TOXICOKINETICS: Glutaraldehyde can act as an eye, skin and respiratory tract irritant. It is also a skin and respiratory tract sensitizer. Clinical events can vary depending on the concentration. It has also been reported to produce dark room disease among radiographers defined as various symptoms of indefinite complaints, sometimes described as similar to sick building syndrome. Symptoms reported in human exposures appear to be dose-dependent.
    C) WITH POISONING/EXPOSURE
    1) COMMON: Glutaraldehyde can be a strong irritant to the eyes, skin, and mucous membranes.
    2) DERMAL: Glutaraldehyde can cause allergic contact dermatitis, skin discoloration and ulceration.
    3) INHALATION: Vapor exposure in humans has been associated with coryza, epistaxis, headache, asthma, chest pain, palpitations, tachycardia, nausea and vomiting. Among health care workers (eg, nurses, medical radiation technologists) peak concentrations of glutaraldehyde have been correlated with chronic bronchitis and nasal symptoms in some exposed individuals. Additional symptoms from exposure may include cough, rhinitis, respiratory difficulty, and lacrimation.
    4) INGESTION: Limited data. In one young adult, a patient developed pain with swallowing and mild abdominal pain following the intentional ingestion of 75 mL of a glutaraldehyde 15% w/v and coco benzyl dimethyl ammonium chloride 10% w/v solution. She recovered completely.
    5) ANIMAL DATA: CNS depression has occurred in experimental animals given intravenous injections.

Vital Signs

    3.3.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Fever was observed in a child who developed chemical pneumonia after being inadvertently splashed on the face with a glutaraldehyde solution.
    3.3.3) TEMPERATURE
    A) WITH POISONING/EXPOSURE
    1) DERMAL
    a) CASE REPORT: A 6-year-old child was inadvertently splashed on the face during surgery with approximately 100 mL of glutaraldehyde (Cidex(R)) and developed vomiting, fever, tachypnea and tachycardia for 6 hours after exposure. Chemical pneumonia also developed. The child recovered completely without permanent sequelae (Takigawa & Endo, 2006).

Heent

    3.4.1) SUMMARY
    A) Topical glutaraldehyde has caused severe eye injury in rabbits. A 2% solution may cause severe inflammation, lacrimation, and edema.
    B) Glutaraldehyde is particularly irritating to the nose and throat.
    3.4.2) HEAD
    A) ANIMAL DATA/TEETH: In animal studies, it was found that glutaraldehyde would not be toxic when used as a pulpotomy agent (Ranly et al, 1989).
    3.4.3) EYES
    A) SUMMARY: Glutaraldehyde is an eye irritant; the degree of irritation is dependent on the concentration of the solution (Ballantyne & Myers, 2001). Cases of keratopathy and conjunctivitis have been reported in hospital workers exposed to a 2% solution of glutaraldehyde (Takigawa & Endo, 2006).
    B) LACRIMATION has been seen following exposure in hospital workers (Waldron, 1992).
    C) CONJUNCTIVITIS: A case of moderate conjunctivitis is reported with conjunctival inflammation accompanied by tearing, swelling of the eyelids, burning pain, and photophobia following leakage of glutaraldehyde from an Ohio conductive mask into the eyes (Murray & Ruddy, 1985). Water solutions of glutaraldehyde are relatively strong eye irritants (HSDB , 2001).
    D) KERATOPATHY: Diffuse conjunctival injection, corneal opacification and edema, and a large epithelial defect and fold in Descemet's membrane occurred in a woman following placement of a Hoskin lens that had been soaked in glutaraldehyde and inadequately rinsed (Dailey et al, 1993).
    1) Courtright et al (1995) described postoperative corneal edema following cataract surgery in a number of patients due to significant levels of glutaraldehyde left on instruments with small lumens after disinfecting.
    E) INFLAMMATION: Glutaraldehyde has caused severe eye injury in rabbits (Grant & Schuman, 1993). A 2% solution caused severe inflammation, lacrimation, and edema. Recovery took 7 to 8 days (Stonehill et al, 1963). A 25% aqueous solution in rabbit eyes resulted in severe injury (Grant & Schuman, 1993).
    1) Human exposure to concentrations above the TLV has caused eye irritation (CDC, 1987).
    3.4.5) NOSE
    A) NASAL IRRITATION: Glutaraldehyde is a strong irritant of the nasal mucosa (Nicewicz et al, 1986). Nasal catarrh and obstruction were reported in about 27% of hospital workers exposed to glutaraldehyde in the workplace, compared to about 11% of unexposed workers (Norback, 1988).
    1) Animal studies have demonstrated respiratory tract lesions, essentially confined to the nasal passages and occurring specifically in the most anterior sections (Gross et al, 1994).
    B) EPISTAXIS: Recurrent twice weekly episodes of epistaxis, headaches, eye and throat irritation, chest tightness, and a skin rash were reported in a technician sterilizing gastroenterology equipment (Wiggins et al, 1989).
    3.4.6) THROAT
    A) PHARYNGITIS: Human exposure to levels greater than the TLV has caused throat discomfort (CDC, 1987). Throat irritation was more common in hospital workers exposed to glutaraldehyde in low concentrations (maximum 0.57 mg/m(3)), compared to unexposed workers (Norback, 1988).
    B) CHEILITIS: A chemical burn of the lower lip was reported after use of orthodontic band seater that had been cleaned with sodium hydroxide and glutaraldehyde. Leakage of clear fluid was noted from a tarnished area of the instrument (Moore & Igel, 1988).
    C) COUGH and an unpleasant taste in the mouth may occur (Waldron, 1992).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) TACHYARRHYTHMIA
    1) WITH POISONING/EXPOSURE
    a) OCCUPATIONAL EXPOSURE
    1) CASE SERIES: Connaughton (1993) reported 7 patients with occupational exposures to glutaraldehyde (dermal and inhalation) all presenting with palpitations or tachycardia. Pulse oximeter showed a heart rate of 224 and 166 beats/min in 2 patients, respectively. In the first, ECG revealed supraventricular tachycardia at a rate of 180 beats/min. In the second, ECG revealed either a sinus tachycardia or a supraventricular tachycardia. When exposure to glutaraldehyde ceased, the symptoms resolved (Connaughton, 1993).
    b) DERMAL
    1) CASE REPORT: A 6-year-old child was inadvertently splashed on the face during surgery with approximately 100 mL of glutaraldehyde (Cidex(R)) and developed vomiting, fever, tachypnea and tachycardia for 6 hours after exposure. Chemical pneumonia also developed. The child recovered completely without permanent sequelae (Takigawa & Endo, 2006).

Respiratory

    3.6.1) SUMMARY
    A) Occupational asthma has been reported following inhalation. It is delayed in onset.
    B) Hemorrhagic pulmonary congestion and pneumonitis were common effects reported in animals regardless of whether glutaraldehyde was administered IV, orally, or by inhalation.
    3.6.2) CLINICAL EFFECTS
    A) IRRITATION SYMPTOM
    1) WITH POISONING/EXPOSURE
    a) Respiratory irritation has been reported in workers who have used glutaraldehyde. Other related symptoms have included nasal irritation, pharyngeal irritation, and sore throat (Takigawa & Endo, 2006).
    B) EDEMA OF LARYNX
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT/INGESTION: A 19-year-old woman presented to the ED about 1.5 hours after intentionally ingesting 75 mL of Omnicide(R) (glutaraldehyde 15% w/v and coco benzyl dimethyl ammonium chloride 10% w/v). She developed spontaneous vomiting and complained of pain with swallowing and mild abdominal pain. Initially her physical exam was normal. However, 10 hours after admission she developed dyspnea and tachypnea with audible stridor and basal crepitations. During intubation, laryngeal edema was observed. Therapy included IV antibiotics and hydrocortisone therapy. The patient also developed metabolic acidosis within the first 24 hours which resolved with supportive care only; no sodium bicarbonate. She was successfully extubated on day 6. An endoscopy was not performed because the patient rapidly improved. The patient was discharged to home on day 9 and then lost to follow-up (Perera et al, 2008).
    C) BRONCHOSPASM
    1) WITH POISONING/EXPOSURE
    a) OCCUPATIONAL
    1) Many cases of asthma due to occupational glutaraldehyde exposure have been reported (Takigawa & Endo, 2006; Copeland & Nugent, 2015; Ong et al, 2004; Nicewicz et al, 1986; Corrado et al, 1986; Gannon et al, 1995).
    a) CASE REPORT: A 55-year-old woman, previously employed at an endoscopy lab where she cleaned scopes with 2.5% glutaraldehyde solution with no special protective equipment for approximately one year, was referred for evaluation of a chronic cough. Her initial physical exam was normal. However, spirometry showed a decreased peak expiratory flow and a reduced peak inspiratory flow and was started on fluticasone and albuterol inhalers as needed. Upon follow-up, she felt better but continued to have upper and lower respiratory symptoms especially if exposed to fumes or chemicals. At 6-months, the patient was started on salmeterol with fluticasone and albuterol as needed. Overall, the patient continued to tolerate normal activity with the exception of ongoing episodic (about 2 per week) pulmonary exacerbations. During the evaluation period, multiple spirometric tests showed variable results including restrictive patterns with a response to bronchodilators, obstructive pattern with a paradoxic bronchoconstrictive response to bronchodilators, and obstructive pattern with a partial response to bronchodilators in this patient with glutaraldehyde-induced occupational asthma (Copeland & Nugent, 2015).
    b) CASE REPORT: A 32-year-old laboratory technician developed glutaraldehyde-induced rhinitis and asthma following occupational exposure. She came in contact with glutaraldehyde vapor during sterilization of mouthpieces being cleaned for spirometry studies. Her symptoms improved when she was away from work and recurred when she returned and was then placed on medical leave. Diagnostic studies were positive for a 25% drop in FEV1 after exposure to glutaraldehyde but not other substances used as a control. The patient was able to return to work once the sterilization process was changed and her asthma symptoms improved. She was maintained on a low dose of inhaled corticosteroid therapy (Ong et al, 2004).
    c) CASE REPORT: A delayed onset of asthma, 2 hours after returning home from work, was described in a respiratory technician who used a 2% alkaline glutaraldehyde solution to sterilize equipment for one year. The attacks increased in frequency and severity, and seemed to be related to the duration of glutaraldehyde exposure. Inhalation challenge with normal use of the 2% solution for 1 hour showed a delayed response after 2 hours. Air concentrations were not measured. Subsequently, when making frequent visits to a room where the solution was stored, she developed status asthmaticus. An immunologic mechanism was ruled out (Nicewicz et al, 1986).
    d) CASE SERIES: Corrado et al (1986) reported a series of 4 nurses complaining of occupational rhinitis and asthma related to the use of 2% alkaline glutaraldehyde disinfectants. Three of the 4 had prior histories of atopy and asthma. One of these 3 had a positive immediate and delayed increase in nasal airway resistance after controlled rechallenge, but no evidence of pulmonary function deterioration. Another patient developed a 22% fall in FEV1 80 minutes following exposure. Symptoms in the other 2 patients were not confirmed by challenge (Corrado et al, 1986).
    e) CASE SERIES: Gannon et al (1995) diagnosed occupational asthma in 7 workers, all of whom demonstrated positive specific bronchial challenge tests to glutaraldehyde. Peak expiratory flow (PEF) records in all 7 were suggestive of occupational asthma. Mean level of glutaraldehyde in air during the challenge tests was 0.068 mg/m(3), a level below current occupational exposure standards (Gannon et al, 1995).
    D) PNEUMONIA
    1) WITH POISONING/EXPOSURE
    a) CHEMICAL PNEUMONIA
    1) DERMAL
    a) CASE REPORT: A 6-year-old child was inadvertently splashed on the face during surgery with approximately 100 mL of glutaraldehyde (Cidex(R)) and developed vomiting, fever, tachypnea and tachycardia for 6 hours after exposure. Chemical pneumonia also developed. The child recovered completely without permanent sequelae (Takigawa & Endo, 2006).
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) NASAL ULCER
    a) Mice and rats exposed to high levels of inhalational glutaraldehyde all died due to occlusion of the external nares. Glutaraldehyde induced lesions, including epithelial erosions, inflammation, and squamous metaplasia which were confined to the anterior third of the nose (Gross et al, 1994).
    2) PNEUMONITIS
    a) Congestion and pneumonitis were common effects in exposed animals regardless of whether glutaraldehyde was administered intravenously, orally, or by inhalation (Stonehill et al, 1963).

Neurologic

    3.7.1) SUMMARY
    A) Seizures and CNS depression were noted in animals given intravenous glutaraldehyde.
    3.7.2) CLINICAL EFFECTS
    A) CENTRAL NERVOUS SYSTEM DEFICIT
    1) WITH POISONING/EXPOSURE
    a) Dizziness, lethargy, ataxia, and coma have been reported in FORMALDEHYDE intoxication and might develop in severe glutaraldehyde poisoning (Burkhart et al, 1990)(Kline, 1925).
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) SEIZURES
    a) Seizures were noted in animals given intravenous doses of glutaraldehyde (Stonehill et al, 1963).
    2) CNS DEPRESSION
    a) CNS depression was noted with intravenous glutaraldehyde administration to animals (Stonehill et al, 1963).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) WITH POISONING/EXPOSURE
    a) INGESTION
    1) CASE REPORT: A 19-year-old woman presented to the ED about 1.5 hours after intentionally ingesting 75 mL of Omnicide(R) (glutaraldehyde 15% w/v and coco benzyl dimethyl ammonium chloride 10% w/v). She developed spontaneous vomiting and complained of pain with swallowing and mild abdominal pain. Initially, her physical exam was normal. However, 10 hours after admission she developed dyspnea and tachypnea with audible stridor and basal crepitations. During intubation, laryngeal edema was observed. Therapy included IV antibiotics and hydrocortisone therapy. The patient also developed metabolic acidosis within the first 24 hours which resolved with supportive care only; no sodium bicarbonate. She was successfully extubated on day 6. An endoscopy was not performed because the patient rapidly improved. The patient was discharged to home on day 9 and then lost to follow-up (Perera et al, 2008).
    b) DERMAL
    1) CASE REPORT: A 6-year-old child was inadvertently splashed on the face during surgery with approximately 100 mL of glutaraldehyde (Cidex(R)) and developed vomiting, fever, tachypnea and tachycardia for 6 hours after exposure. Chemical pneumonia also developed. The child recovered completely without permanent sequelae (Takigawa & Endo, 2006).
    c) INHALATION
    1) Low levels of occupational exposure (mean 0.05 mg/m(3)) were associated with an increased incidence of headache and nausea in hospital workers (Norback, 1988).
    B) GASTRITIS
    1) WITH POISONING/EXPOSURE
    a) IRRITATION: When ingested, glutaraldehyde has caused irritation of the gastrointestinal tract (CDC, 1987).
    C) GASTROINTESTINAL HEMORRHAGE
    1) WITH POISONING/EXPOSURE
    a) Hemorrhage may occur at higher ingested doses (Stonehill et al, 1963).
    D) COLITIS
    1) WITH THERAPEUTIC USE
    a) SUMMARY: In rare cases, glutaraldehyde-induced colitis has occurred in patients following endoscopic procedures (eg, colonoscopy, sigmoidoscopy) resulting in self-limited symptoms of abdominal pain, watery diarrhea and rectal bleeding. Symptoms usually occur within hours and up to 2 days later and usually resolve in a few days (Mohamad et al, 2014; Babb & Paaso, 1995; Birnbaum et al, 1995; Fukunaga & Khatibi, 2000).
    b) An outbreak of bloody diarrhea occurred in patients undergoing flexible sigmoidoscopy with instruments soaked in 2% glutaraldehyde and not adequately rinsed (Durante et al, 1992).
    c) Acute proctitis with bloody diarrhea and ulcerations was diagnosed in 3 patients following flexible sigmoidoscopy with instruments disinfected with glutaraldehyde, but not adequately rinsed (Babb & Paaso, 1995).
    d) Glutaraldehyde-induced hemorrhagic colitis is described in 4 patients who developed a self-limited syndrome of abdominal pain and cramps, tenesmus, and rectal bleeding within 48 hours of sigmoidoscopy or colonoscopy. CT demonstrated circumferential thickening of the colonic wall in all of the patients. All patients recovered following conservative management (Birnbaum et al, 1995).
    e) West et al (1995) described 3 patients with glutaraldehyde-induced proctocolitis following sigmoidoscopy with tubing connecting water bottles to the endoscopes which were disinfected with glutaraldehyde.
    f) Two cases are reported of glutaraldehyde-induced colitis after normal screening with flexible sigmoidoscopes that had been disinfected with glutaraldehyde. Rectal bleeding and abdominal pain within 24 hours of sigmoidoscopy with associated with fever and leukocytosis were described in both cases. Uneventful recovery occurred within 4 days (Fukunaga & Khatibi, 2000).
    g) A woman developed abdominal pain and bloody diarrhea
    3.8.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) BLOODY DIARRHEA
    a) Colonic instillation of 2% glutaraldehyde into 33 rats resulted in bloody diarrhea and necrotic mucosal damage. Three of the rats that died also had hydrothorax with congested lungs (Durante et al, 1992).

Hepatic

    3.9.2) CLINICAL EFFECTS
    A) LIVER ENZYMES ABNORMAL
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: Increased hepatic transaminase levels were reported in one human exposure (RMPCF, 1984).

Acid-Base

    3.11.2) CLINICAL EFFECTS
    A) ACIDOSIS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT/INGESTION: A 19-year-old woman presented to the ED about 1.5 hours after intentionally ingesting 75 mL of Omnicide(R) (glutaraldehyde 15% w/v and coco benzyl dimethyl ammonium chloride 10% w/v). She developed spontaneous vomiting and complained of pain with swallowing and mild abdominal pain. Initially her physical exam was normal. However, 10 hours after admission she developed dyspnea and tachypnea with audible stridor and basal crepitations. During intubation, laryngeal edema was observed. Therapy included IV antibiotics and hydrocortisone therapy. The patient also developed metabolic acidosis within the first 24 hours which resolved with supportive care only; no sodium bicarbonate. She was successfully extubated on day 6. An endoscopy was not performed because the patient rapidly improved. The patient was discharged to home on day 9 and then lost to follow-up (Perera et al, 2008).

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) VASCULAR DISORDER
    1) WITH THERAPEUTIC USE
    a) A 5% solution is an effective hemostatic agent (Hannah, 1972).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) ALLERGIC CONTACT DERMATITIS
    1) WITH THERAPEUTIC USE
    a) Glutaraldehyde has been used therapeutically to treat several skin disorders, including epidermolysis bullosa, hyperhidrosis, herpes zoster, onychomycosis and warts. In some cases, it has produced adverse clinical effects including contact dermatitis, ulceration and skin discoloration (Beauchamp et al, 1992).
    2) WITH POISONING/EXPOSURE
    a) SUMMARY: Allergic contact dermatitis has been reported many times following exposure to glutaraldehyde (Takigawa & Endo, 2006; Sanderson & Cronin, 1968; Fisher, 1981; Hansen, 1983; Goncalo et al, 1984; Bardazzi et al, 1986; Jaworsky et al, 1987; Fowler, 1989; Bingham et al, 2001; HSDB , 2001).
    b) CASE SERIES: Allergic contact hypersensitivity, as determined by patch testing, was found in 7% of exposed funeral service workers (Nethercott & Holness, 1988).
    c) CASE SERIES: The concentration of glutaraldehyde in water necessary to induce dermal sensitization was 0.5% in a study of 109 human volunteers. Mild to moderate local erythema was reported in 6.4% of the subjects (Ballantyne & Berman, 1984).
    B) DERMATITIS
    1) WITH THERAPEUTIC USE
    a) A 1% solution of pure nonactivated glutaraldehyde is not irritating to skin. Primary irritant effects were suspected in dermatitis seen in hospital workers exposed to a 2% activated solution (Norback, 1988).
    b) CASE SERIES: The use of a 0.13% hand dip of activated glutaraldehyde was reported to cause xerosis in 10 of 11 subjects and erythema in 1 subject (Halderman et al, 1986).
    c) CASE REPORT: A painless white lesion developed on the finger of a surgeon handling a Hoskin lens soaked in glutaraldehyde and inadequately rinsed (Dailey et al, 1993).
    d) A 10% solution has caused pruritus, even with therapeutic use (S Sweetman , 2001).
    C) DISCOLORATION OF SKIN
    1) WITH THERAPEUTIC USE
    a) Glutaraldehyde has been used therapeutically to treat several skin disorders, including epidermolysis bullosa, hyperhidrosis, herpes zoster, onychomycosis and warts. In some cases, it has produced adverse clinical effects including contact dermatitis, ulceration and skin discoloration (Beauchamp et al, 1992).
    b) SKIN DISCOLORATION: Dermally applied solutions of 2% to 10% are used therapeutically. These may cause staining of the skin and nails to a brown or a golden brown color (Suringa, 1970).
    D) SKIN ULCER
    1) WITH THERAPEUTIC USE
    a) Glutaraldehyde has been used therapeutically to treat several skin disorders, including epidermolysis bullosa, hyperhidrosis, herpes zoster, onychomycosis and warts. In some cases, it has produced adverse clinical effects including contact dermatitis, ulceration and skin discoloration (Beauchamp et al, 1992).
    E) ALOPECIA
    1) WITH THERAPEUTIC USE
    a) CASE REPORT: Hair loss secondary to allergic contact dermatitis was reported in a 22-year-old woman who used a hair conditioner containing glutaraldehyde (Jaworsky et al, 1987).
    3.14.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) DERMATITIS CONTACT
    a) Guinea pigs and mice have demonstrated a dose-dependent contact hypersensitivity response to glutaraldehyde (Stern et al, 1989).
    2) OTHER NONSPECIFIC
    a) Glutaraldehyde applied to the skin of mice produced marked tissue destruction. Evidence of epithelial edema, acanthosis, hyperkeratosis, and parakeratosis was apparent. Epithelial degeneration was widespread (Hess et al, 1991).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) SPASMODIC MOVEMENT
    1) WITH POISONING/EXPOSURE
    a) Muscle twitching was seen after a dermal and oral exposure to glutaraldehyde (RMPCF, 1984).

Immunologic

    3.19.2) CLINICAL EFFECTS
    A) ACUTE ALLERGIC REACTION
    1) WITH POISONING/EXPOSURE
    a) Contact dermatitis has been reported in patients exposed to glutaraldehyde (Bingham et al, 2001; Jordan et al, 1972). The sensitivity of these dermal reactions can vary depending on the site to which the glutaraldehyde is applied (Maibach & Prystowsky, 1977). Glutaraldehyde sensitive patients do NOT appear to be cross-reactive to formaldehyde (Maibach, 1975). The mechanism was nonimmunologic in one case (Jaworsky et al, 1987).

Reproductive

    3.20.2) TERATOGENICITY
    A) ANIMAL STUDIES
    1) When given to pregnant mice by gavage during the period of organogenesis, only the highest dose (5 mL/kg of a 2% acidic solution) produced increased malformations (eg; stunted fetuses). At this dose significant maternal and fetal toxicity was seen. Because of clustering of the malformations within one litter, it was concluded that glutaraldehyde was not teratogenic (Marks et al, 1980).
    2) Glutaraldehyde, given by gastric intubation at doses of 0, 25, 50, or 100 mg/kg on days 6 to 15 of gestation, was not teratogenic in rats, even at the highest dose when maternal toxicity was observed (Ema et al, 1992).
    3.20.3) EFFECTS IN PREGNANCY
    A) HUMANS
    1) LACK OF EFFECT
    a) Two studies (not totally independent) have evaluated the incidence of miscarriages in women exposed to hospital sterilization agents. Although an increased incidence of spontaneous abortion was seen with exposure to ethylene oxide, none was apparent with exposure to either formaldehyde or glutaraldehyde (Hemminnki et al, 1982).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS111-30-8 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) Not Listed
    3.21.2) SUMMARY/HUMAN
    A) At the time of this review, no studies were found on the possible carcinogenic activity of glutaraldehyde in humans.
    3.21.4) ANIMAL STUDIES
    A) CARCINOMA
    1) Female rats had increased large granular lymphocytic leukemias after receiving glutaraldehyde in the drinking water at levels up to 1,000 ppm for 2 years (Andersen, 1996).
    2) NASAL CANCERS - Glutaraldehyde was tested against the known rat nasal carcinogen, formaldehyde, and found to be 5 times as potent as formaldehyde. Preliminary data suggest that a chronic inhalation study is needed to assess the carcinogenic potential of glutaraldehyde (St Clair et al, 1989).
    B) LACK OF EFFECT
    1) No evidence of carcinogenicity was seen in 2 year inhalation studies in rats exposed to 250, 500 or 750 ppb. No evidence of carcinogenic activity was seen in mice exposed to 62.5, 125 or 250 ppb (HSDB , 2001).
    2) Male and female F344 rats and B6C3F1 mice were exposed to glutaraldehyde at levels up to 1000 ppb for up to 13 weeks. No evidence of pre-neoplastic lesions was seen in the respiratory tract (Gross et al, 1994).

Genotoxicity

    A) Glutaraldehyde, in a dentin bonding agent, has been shown to be mutagenic in an Ames assay using Salmonella typhimurium strains as well as in sister chromatid exchange and mutations in mouse lymphocyte cells and cytogenetic changes in hamster ovary cells.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor fluid and electrolytes in patients that develop significant diarrhea and/or vomiting following exposure.
    B) Monitor vital signs following an oral exposure.
    C) In rare cases, monitor CBC for evidence of bleeding in patients that develop gastrointestinal bleeding. If respiratory tract irritation or respiratory insufficiency are clinically evident, consider monitoring pulse oximetry, arterial blood gases, chest x-ray, and pulmonary function tests.
    D) Obtain blood gases and/or bicarbonate levels in patients at risk to develop acidosis.
    E) Monitor renal function and liver enzymes as indicated in symptomatic patients.
    F) Pulmonary function tests may be indicated in patients that develop respiratory symptoms following chronic occupational exposure.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Monitor fluid and electrolytes in patients that develop significant diarrhea and/or vomiting following exposure.
    2) Monitor renal function and liver enzymes as indicated in symptomatic patients.
    B) ACID/BASE
    1) Obtain blood gases and/or bicarbonate levels in patients at risk to develop acidosis.
    4.1.4) OTHER
    A) OTHER
    1) PULMONARY FUNCTION TESTS
    a) If respiratory tract irritation or respiratory insufficiency are clinically evident, consider monitoring pulse oximetry, arterial blood gases, chest x-ray, and pulmonary function tests.
    b) Pulmonary function tests may be indicated in patients that develop respiratory symptoms following chronic occupational exposure.

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) A chest x-ray may be helpful to look for evidence of infiltrate or pneumonitis, if suspected clinically.

Methods

    A) CHROMATOGRAPHY
    1) High-performance liquid chromatography (HPLC) has been used for the determination of glutaraldehyde in samples (Ellenhorn et al, 1997).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Patients with evidence of ongoing (eg, pulmonary injury following an acute exposure) symptoms should be admitted to a monitored setting.
    6.3.1.2) HOME CRITERIA/ORAL
    A) Patients with mild eye or skin irritation can be managed at home with decontamination. Persistent symptoms following decontamination may require further evaluation by a healthcare provider. Patients with an intentional ingestion of glutaraldehyde should be evaluated in a healthcare setting to assess for gastrointestinal injury or systemic toxicity.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Consult a poison center or medical toxicologist for assistance in managing a severe poisoning.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients with significant eye irritation, or more than mild pulmonary or skin irritation should be sent to a healthcare facility for evaluation and treatment as indicated.

Monitoring

    A) Monitor fluid and electrolytes in patients that develop significant diarrhea and/or vomiting following exposure.
    B) Monitor vital signs following an oral exposure.
    C) In rare cases, monitor CBC for evidence of bleeding in patients that develop gastrointestinal bleeding. If respiratory tract irritation or respiratory insufficiency are clinically evident, consider monitoring pulse oximetry, arterial blood gases, chest x-ray, and pulmonary function tests.
    D) Obtain blood gases and/or bicarbonate levels in patients at risk to develop acidosis.
    E) Monitor renal function and liver enzymes as indicated in symptomatic patients.
    F) Pulmonary function tests may be indicated in patients that develop respiratory symptoms following chronic occupational exposure.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) SUMMARY
    1) Because of the potential for further gastrointestinal injury, do NOT induce emesis.
    B) ACTIVATED CHARCOAL
    1) Activated charcoal is generally not recommended due to the risk of producing emesis and/or obscuring endoscopic findings if endoscopy is needed.
    6.5.2) PREVENTION OF ABSORPTION
    A) SUMMARY
    1) Spontaneous vomiting is likely to develop following ingestion of glutaraldehyde. Because of the potential for further gastrointestinal injury, do NOT induce emesis.
    B) NASOGASTRIC SUCTION
    1) Consider insertion of a small, flexible nasogastric tube to aspirate gastric contents after a recent significant ingestion of glutaraldehyde. The risk of worsening mucosal injury (including perforation) must be weighed against the potential benefit.
    C) ACTIVATED CHARCOAL
    1) NOT RECOMMENDED: Activated charcoal is generally not recommended due to the risk of producing emesis, producing further mucosal injury, as well as the potential to obscure endoscopic findings, if endoscopy is needed.
    6.5.3) TREATMENT
    A) SUPPORT
    1) MANAGEMENT OF MILD TO MODERATE TOXICITY
    a) Treatment is symptomatic and supportive. INGESTION: There have been rare reports of glutaraldehyde oral exposure. The patient may be at risk to develop pain, difficulty swallowing, irritation or potentially more severe gastrointestinal injury. Assess oral mucosa and consider esophagoscopy if the patient appears symptomatic (ie, pain, difficulty swallowing, drooling). Monitor fluid status and electrolytes in patients that develop significant vomiting. ENDOSCOPIC PROCEDURES: Infrequent reports of exposure to glutaraldehyde solution following endoscopic procedures (ie, sigmoidoscopy, colonoscopy) have occurred resulting in colitis in some patients. Gastrointestinal symptoms (eg, abdominal pain, watery diarrhea) are usually self-limited and resolve within a few days. Monitor fluid and electrolytes in patients with persistent symptoms. Replace fluids and electrolytes as indicated. Gastrointestinal bleeding is a rare finding. INHALATION: Treatment is symptomatic and supportive. Remove patient from glutaraldehyde vapors as needed. Assess respiratory effort and function. Patients with chronic occupational exposure may require ongoing evaluation of respiratory function (ie, pulmonary function studies), a combination of drug therapies (eg, corticosteroids, sympathomimetics) and permanent removal from the chemical as needed. DERMAL: Decontaminate skin with soap and water following exposure. Monitor for ongoing symptoms. OCULAR: Irrigate eyes with copious amounts of water. An ophthalmic exam may be necessary if symptoms persist.
    2) MANAGEMENT OF SEVERE TOXICITY
    a) Treatment is symptomatic and supportive. ACUTE: Monitor gastrointestinal and respiratory effort following ingestion. CHRONIC: Glutaraldehyde-induced occupational asthma has been reported in some healthcare workers with a chronic exposure. Ongoing respiratory evaluation and support may be necessary in patients that develop persistent symptoms despite removal from the chemical.
    B) MONITORING OF PATIENT
    1) Monitor fluid and electrolytes in patients that develop significant watery diarrhea and/or vomiting following an exposure to a glutaraldehyde solution.
    2) Monitor vital signs following an oral exposure.
    3) In rare cases, monitor CBC for evidence of bleeding in patients that develop gastrointestinal bleeding. If respiratory tract irritation or respiratory insufficiency are clinically evident, consider monitoring pulse oximetry, arterial blood gases, chest x-ray, and pulmonary function tests.
    4) Obtain blood gases or bicarbonate levels in patients at risk to develop acidosis.
    5) Monitor renal function and liver enzymes as indicated in symptomatic patients.
    6) Pulmonary function tests may be indicated in patients that develop respiratory symptoms following chronic occupational exposure.
    C) ENDOSCOPIC PROCEDURE
    1) Esophagoscopy should be considered following oral ingestion of concentrated glutaraldehyde solutions (if esophageal or gastric injury is suspected) to assess the severity of the injury (Allen et al, 1970).
    D) ACIDOSIS
    1) Limited exposure information.
    2) CASE REPORT: Metabolic acidosis and laryngeal edema were reported following the intentional ingestion of a glutaraldehyde (15% w/v) solution in a young adult. With supportive care, acidosis resolved without sodium bicarbonate (Perera et al, 2008).
    3) METABOLIC ACIDOSIS: Treat severe metabolic acidosis (pH less than 7.1) with sodium bicarbonate, 1 to 2 mEq/kg is a reasonable starting dose(Kraut & Madias, 2010). Monitor serum electrolytes and arterial or venous blood gases to guide further therapy.

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
    B) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.
    6.7.2) TREATMENT
    A) BRONCHOSPASM
    1) BRONCHOSPASM SUMMARY
    a) Administer beta2 adrenergic agonists. Consider use of inhaled ipratropium and systemic corticosteroids. Monitor peak expiratory flow rate, monitor for hypoxia and respiratory failure, and administer oxygen as necessary.
    2) ALBUTEROL/ADULT DOSE
    a) 2.5 to 5 milligrams diluted with 4 milliliters of 0.9% saline by nebulizer every 20 minutes for three doses. If incomplete response, administer 2.5 to 10 milligrams every 1 to 4 hours as needed OR administer 10 to 15 milligrams every hour by continuous nebulizer as needed. Consider adding ipratropium to the nebulized albuterol; DOSE: 0.5 milligram by nebulizer every 30 minutes for three doses then every 2 to 4 hours as needed, NOT administered as a single agent (National Heart,Lung,and Blood Institute, 2007).
    3) ALBUTEROL/PEDIATRIC DOSE
    a) 0.15 milligram/kilogram (minimum 2.5 milligrams) diluted with 4 milliliters of 0.9% saline by nebulizer every 20 minutes for three doses. If incomplete response administer 0.15 to 0.3 milligram/kilogram (maximum 10 milligrams) every 1 to 4 hours as needed OR administer 0.5 mg/kg/hr by continuous nebulizer as needed. Consider adding ipratropium to the nebulized albuterol; DOSE: 0.25 to 0.5 milligram by nebulizer every 20 minutes for three doses then every 2 to 4 hours as needed, NOT administered as a single agent (National Heart,Lung,and Blood Institute, 2007).
    4) ALBUTEROL/CAUTIONS
    a) The incidence of adverse effects of beta2-agonists may be increased in older patients, particularly those with pre-existing ischemic heart disease (National Asthma Education and Prevention Program, 2007). Monitor for tachycardia, tremors.
    5) CORTICOSTEROIDS
    a) Consider systemic corticosteroids in patients with significant bronchospasm. PREDNISONE: ADULT: 40 to 80 milligrams/day in 1 or 2 divided doses. CHILD: 1 to 2 milligrams/kilogram/day (maximum 60 mg) in 1 or 2 divided doses (National Heart,Lung,and Blood Institute, 2007).
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) SUMMARY: Glutaraldehyde in concentrations as low as 2% can cause ocular damage (ie, severe inflammation, lacrimation, and edema).
    B) EYE IRRIGATION, ROUTINE: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
    6.9.2) TREATMENT
    A) SKIN ABSORPTION
    1) SUMMARY
    a) There is limited information regarding systemic absorption in animals or humans following dermal exposure.
    b) CASE REPORT: A 6-year-old child was inadvertently splashed on the face during surgery with approximately 100 mL of glutaraldehyde (Cidex(R)) and developed vomiting, fever, tachypnea and tachycardia for 6 hours after exposure. Chemical pneumonia also developed. The child recovered completely without permanent sequelae (Takigawa & Endo, 2006).
    c) ANIMAL DATA: Systemic toxicity from dermal exposure to glutaraldehyde does not appear likely based on animal studies (Stonehill et al, 1963). However, concentrations of 15% glutaraldehyde or higher have produced severe localized irritation and injury including erythema, edema, necrosis and scab formation (Ballantyne & Myers, 2001).
    B) IRRITATION SYMPTOM
    1) Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.
    C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Enhanced Elimination

    A) SUMMARY
    1) It is unknown if glutaraldehyde would be removed by enhanced elimination procedures.

Range Of Toxicity

Maximum Tolerated Exposure

    A) SUMMARY
    1) A maximum tolerated dose has not been established.
    B) INGESTION
    1) CASE REPORT: A 19-year-old woman presented to the ED about 1.5 hours after intentionally ingesting 75 mL of Omnicide(R) (glutaraldehyde 15% w/v and coco benzyl dimethyl ammonium chloride 10% w/v). She developed spontaneous vomiting and complained of pain with swallowing and mild abdominal pain. Initially her physical exam was normal. However, 10 hours after admission she developed dyspnea and tachypnea with audible stridor and basal crepitations. During intubation, laryngeal edema was observed. Therapy included IV antibiotics and hydrocortisone therapy. The patient also developed metabolic acidosis within the first 24 hours which resolved with supportive care only; no sodium bicarbonate. She was successfully extubated on day 6. An endoscopy was not performed because the patient rapidly improved. The patient was discharged to home on day 9 and then lost to follow-up (Perera et al, 2008).
    C) DERMAL
    1) CASE REPORT: A 6-year-old child was inadvertently splashed on the face during surgery with approximately 100 mL of glutaraldehyde (Cidex(R)) and developed vomiting, fever, tachypnea and tachycardia for 6 hours after exposure. Chemical pneumonia also developed. The child recovered completely without permanent sequelae (Takigawa & Endo, 2006).
    D) OCCUPATIONAL EXPOSURE
    1) Glutaraldehyde has been used in the healthcare setting for high level disinfection including endoscopes, it is a known irritant of the skin, eyes, nose and lungs in some individuals. Healthcare personnel have developed allergic dermatitis, rhinitis and occupational asthma after ongoing exposure (Copeland & Nugent, 2015; Rosenman & Beckett, 2015; Gutterman et al, 2013; Rideout et al, 2005).
    2) PEL: The permissible exposure limit has been set at 0.05 to 0.2 part per million for vapor contamination from glutaraldehyde has been set by the American Conference of Governmental Industrial Hygienists (ACGIH) (Gutterman et al, 2013; Ballantyne & Myers, 2001).
    3) In the United Kingdom, glutaraldehyde has been withdrawn from use (Gutterman et al, 2013).
    4) CASE REPORT: A 32-year-old pulmonary technician developed glutaraldehyde-induced rhinitis and asthma following occupational exposure. She came in contact with glutaraldehyde vapor during sterilization of mouthpieces being cleaned for spirometry studies. Her symptoms improved when she was away from work and recurred when working and was then placed on medical leave. Diagnostic studies were positive for a 25% drop in FEV1 after exposure to glutaraldehyde but not other substances used as a control. The patient was able to return to work once the sterilization process was changed and her asthma symptoms improved. She was maintained on a low dose of inhaled corticosteroid therapy (Ong et al, 2004).
    5) CASE SERIES: Gannon et al (1995) diagnosed occupational asthma in 7 workers, all of whom demonstrated positive specific bronchial challenge tests to glutaraldehyde. Peak expiratory flow (PEF) records in all 7 were suggestive of occupational asthma. Mean level of glutaraldehyde in air during the challenge tests was 0.068 mg/m(3), a level below current occupational exposure standards (Gannon et al, 1995).
    E) ANIMAL DATA
    1) INGESTION
    a) ACUTE TOXICITY: In animal studies, the effects of ingestion of glutaraldehyde were followed in the rat. When mortality was expressed as mL solution dosed/kg of body weight, a dose response relationship for lethality was found with solutions of 5% and greater producing moderate acute oral toxicity and those of 2% and lower causing slight toxicity. Of note, when LD50s are expressed as mL of solution, toxicity decreases with decreasing glutaraldehyde concentration (ie, dilution). However, when toxicity is expressed as the absolute amount of glutaraldehyde doses (ie, milligrams glutaraldehyde/kilogram) there is a reciprocal relationship between LD50 and dosage (Ballantyne & Myers, 2001).
    1) Signs of oral toxicity in both rats and mice given 2% solutions included a decrease of spontaneous behavior, piloerection and abdominal swelling (Takigawa & Endo, 2006).
    2) In mice, similar acute oral toxicity was found. In addition, the findings confirmed the inverse relationship between toxicity and dose when expressed as milligram glutaraldehyde per kilogram. The reasons are somewhat unclear, but the findings suggest that at higher concentrations there is severe irritancy and corrosivity to the upper gastrointestinal tract and death may occur, while at lower concentrations a lesser degree of gastrointestinal irritancy may occur which might allow a greater amount of glutaraldehyde to be absorbed and result in systemic toxicity (Ballantyne & Myers, 2001).
    2) DERMAL
    a) ACUTE TOXICITY: In animal studies, the percutaneous effects of glutaraldehyde were as follows (Ballantyne & Myers, 2001):
    1) Concentrations of 15% glutaraldehyde or higher: Severe skin irritation and injury included erythema, edema, necrosis and scab formation.
    2) Concentrations of 10% glutaraldehyde: Less marked skin irritation, but erythema, edema, necrosis and scab formation occurred.
    3) Concentrations of 5% glutaraldehyde: Mild to moderate skin irritation, but necrosis did not develop.
    b) A 2% glutaraldehyde solution produced no systemic effects, whether applied as a single dose or in multiple applications. In this study where rabbits had a 2% glutaraldehyde solution and an 8% formaldehyde solution applied, the glutaraldehyde produced some yellow and brown skin stainings, but was not nearly as severe an irritant as formaldehyde (Stonehill et al, 1963).
    3) OCULAR
    a) ACUTE TOXICITY: In animal studies, eye irritation studies showed a dose-dependent response for the development of periocular injury and/or inflammation (Ballantyne & Myers, 2001):
    1) Concentrations of 45% glutaraldehyde: Severe conjunctival and marked diffuse corneal injury occurred and were persistent.
    2) Concentrations of 5% glutaraldehyde: Marked corneal injury developed.
    3) Concentrations of 2% glutaraldehyde: Produced mild corneal injury.
    4) Concentrations of 1% glutaraldehyde: The lowest concentration that produced corneal injury in rabbits; it also produced conjunctival hyperemia and chemosis of mild to moderate effects.
    5) Lowest no effect level (absence of corneal injury): 0.5% concentration.
    4) INHALATION
    a) INHALATION: When equicidal concentrations of solutions were allowed to evaporate in a closed system, a 2% glutaraldehyde produced no symptoms in 4 hours, while an 8% formaldehyde produced respiratory tract irritation and pulmonary damage. When the concentration of both compounds were increased, the clinical effects became equally severe. When the concentration of both compounds were increased, the clinical effects became equally severe (Stonehill et al, 1963).

Workplace Standards

    A) ACGIH TLV Values for CAS111-30-8 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.
    a) Adopted Value
    1) Glutaraldehyde, activated and inactivated
    a) TLV:
    1) TLV-TWA:
    2) TLV-STEL:
    3) TLV-Ceiling: 0.05 ppm
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A4
    2) Codes: SEN
    3) Definitions:
    a) A4: Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    b) SEN: The designation SEN refers to the potential for an agent to produce sensitization, as confirmed by human or animal data. The notation does not imply that this is the critical effect or that this is the sole basis for the TLV. Although, for those TLVs that are based on sensitization, the TLV is meant to protect workers from induction of this effect, but cannot protect workers who have already become sensitized. The notation should be used to assist in identifying sensitization hazards and reducing respiratory, dermal, and conjunctival exposures to sensitizing agents in the workplace. Please see "Definitions and Notations" (in TLV booklet) for full definition.
    c) TLV Basis - Critical Effect(s): URT, skin, and eye irr; CNS impair
    d) Molecular Weight: 100.11
    1) For gases and vapors, to convert the TLV from ppm to mg/m(3):
    a) [(TLV in ppm)(gram molecular weight of substance)]/24.45
    2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:
    a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance
    e) Additional information:

    B) NIOSH REL and IDLH Values for CAS111-30-8 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Glutaraldehyde
    2) REL:
    a) TWA:
    b) STEL:
    c) Ceiling: 0.2 ppm (0.8 mg/m(3))
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s): See Appendix C (Aldehydes)
    3) IDLH: Not Listed

    C) Carcinogenicity Ratings for CAS111-30-8 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Glutaraldehyde, activated and inactivated
    a) A4 :Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    3) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Glutaraldehyde
    5) MAK (DFG, 2002): Category 3B ; Listed as: Glutaraldehyde
    a) Category 3B : Substances for which in vitro or animal studies have yielded evidence of carcinogenic effects that is not sufficient for classification of the substance in one of the other categories. Further studies are required before a final decision can be made. A MAK value can be established provided no genotoxic effects have been detected. (Footnote: In the past, when a substance was classified as Category 3 it was given a MAK value provided that it had no detectable genotoxic effects. When all such substances have been examined for whether or not they may be classified in Category 4, this sentence may be omitted.)
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS111-30-8 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: ACGIH, 1991 Lewis, 1996 HSDB, 2001 RTECS, 2001
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 13,900 mcg/kg
    2) LD50- (ORAL)MOUSE:
    a) 100 mg/kg
    3) LD50- (SKIN)MOUSE:
    a) >5840 mg/kg
    4) LD50- (SUBCUTANEOUS)MOUSE:
    a) 1430 mg/kg
    5) LD50- (INTRAPERITONEAL)RAT:
    a) 17,900 mcg/kg
    6) LD50- (ORAL)RAT:
    a) 252 mg/kg
    b) 2380 mg/kg
    c) 134 mg/kg
    d) 600 mg/kg
    e) 0.82 g/kg
    f) 2.38 mL/kg -- Of a 25% solution (Smyth et al, 1962)
    7) LD50- (SKIN)RAT:
    a) >2500 mg/kg
    8) LD50- (SUBCUTANEOUS)RAT:
    a) 2390 mg/kg

Summary

    A) TOXICITY: A toxic dose has not been established in man. Ten percent solutions have caused dermatitis when applied therapeutically. Two percent solutions have caused ocular damage. One young adult intentionally ingested 75 mL of a glutaraldehyde 15% w/v and coco benzyl dimethyl ammonium chloride 10% w/v solution and developed metabolic acidosis and laryngeal edema. She required intubation and mechanical ventilation but recovered completely.
    B) OCCUPATIONAL EXPOSURE: Glutaraldehyde has been used in the healthcare setting for high level disinfection and it is a known irritant of the skin, eyes, nose and lungs in some individuals. Healthcare personnel have developed allergic dermatitis, rhinitis and occupational asthma after chronic exposure.

Therapeutic Dose

    7.2.1) ADULT
    A) GENERAL
    1) Solutions of 5 percent to 10 percent have been used to treat hyperhidrosis and onychomycoses (S Sweetman , 2001).

Minimum Lethal Exposure

    A) ROUTE OF EXPOSURE
    1) The probable oral lethal dose of glutaraldehyde for humans ranges from 50 mg/kg to 5 g/kg, or between 1 teaspoon and 1 pint, for a 70 kg (150 lb) person (HSDB , 2001). Ten percent solutions have caused dermatitis when applied therapeutically.
    2) Glutaraldehyde is a moderate sensitizer of human skin (Beauchamp et al, 1992).
    3) WORKPLACE: In the workplace, glutaraldehyde and formaldehyde are frequently used together; however, there was no evidence of sensitization to glutaraldehyde due to formaldehyde exposure or vice versa (Beauchamp et al, 1992).
    B) ABSORPTION
    1) Glutaraldehyde can be absorbed through the skin and pulp chamber of the teeth when used as a dental adhesive (Beauchamp et al, 1992).

Pharmacology Toxicology

Pharmacologic Mechanism

    A) Glutaraldehyde is a saturated dialdehyde with 2 active carbonyl groups. During proper conditions, these carbonyl groups undergo either together or singly, aldehyde reactions to form acetals, cyanohydrins, oximes and hydrazones. Cross-linking of the peptidoglycan in the bacterial cell wall with intermolecular bonding between teichoic acid chains and glutaraldehyde may result in partial sealing and contraction of the outer cell envelope. Protein reacts with the carbonyl groups in a cross linking reaction. Glutaraldehyde polymerizes relatively rapidly at a pH above 9 (Stonehill et al, 1963).

Toxicologic Mechanism

    A) Glutaraldehyde is a saturated dialdehyde with 2 active carbonyl groups. During proper conditions, these carbonyl groups undergo aldehyde reactions, either singly or together, to form acetals, cyanohydrins, oximes and hydrazones. Protein reacts with the carbonyl groups in a cross linking reaction. Glutaraldehyde polymerizes relatively rapidly at a pH above 9 (Stonehill et al, 1963).

Physicochemical

Physical Characteristics

    A) Glutaraldehyde exists as a colorless to pale yellow, oily liquid with a pungent odor like rotten apples. This compound will polymerize in water to a glassy form (CHRIS, 2005; Budavari, 1996) . ACGIH (1991) reports that glutaraldehyde forms colorless crystals.

Ph

    A) Solutions in water are slightly acidic. When buffered to a pH of 7.5-8.5, solutions are only stable for 1 to 2 weeks. Alkaline solutions tend to polymerize and precipitate (S Sweetman , 2001).

Molecular Weight

    A) 100.12

Other

    A) ODOR THRESHOLD
    1) 0.04 ppm (ACGIH, 1991)

References

General Bibliography

    1) 40 CFR 372.28: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Lower thresholds for chemicals of special concern. National Archives and Records Administration (NARA) and the Government Printing Office (GPO). Washington, DC. Final rules current as of Apr 3, 2006.
    2) 40 CFR 372.65: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Chemicals and Chemical Categories to which this part applies. National Archives and Records Association (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Apr 3, 2006.
    3) 49 CFR 172.101 - App. B: Department of Transportation - Table of Hazardous Materials, Appendix B: List of Marine Pollutants. National Archives and Records Administration (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Aug 29, 2005.
    4) 49 CFR 172.101: Department of Transportation - Table of Hazardous Materials. National Archives and Records Administration (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Aug 11, 2005.
    5) 62 FR 58840: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 1997.
    6) 65 FR 14186: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
    7) 65 FR 39264: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
    8) 65 FR 77866: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
    9) 66 FR 21940: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2001.
    10) 67 FR 7164: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2002.
    11) 68 FR 42710: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2003.
    12) 69 FR 54144: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2004.
    13) ACGIH: Documentation of the Threshold Limit Values and Biological Exposure Indices, 6th ed, Am Conference of Govt Ind Hyg, Inc, Cincinnati, OH, 1991.
    14) AIHA: 2006 Emergency Response Planning Guidelines and Workplace Environmental Exposure Level Guides Handbook, American Industrial Hygiene Association, Fairfax, VA, 2006.
    15) Allen RE, Moshinsky MJ, & Stallone RJ: Corrosive injuries of the stomach. Arch Surg 1970; 100:409-413.
    16) American Conference of Governmental Industrial Hygienists : ACGIH 2010 Threshold Limit Values (TLVs(R)) for Chemical Substances and Physical Agents and Biological Exposure Indices (BEIs(R)), American Conference of Governmental Industrial Hygienists, Cincinnati, OH, 2010.
    17) Andersen FA: Final report on the safety assessment of glutaral. J Am Coll Toxicol 1996; 15:98-139.
    18) Ansell-Edmont: SpecWare Chemical Application and Recommendation Guide. Ansell-Edmont. Coshocton, OH. 2001. Available from URL: http://www.ansellpro.com/specware. As accessed 10/31/2001.
    19) Ashford R: Ashford's Dictionary of Industrial Chemicals, Wavelength Publications Ltd, London, England, 1994.
    20) Babb RR & Paaso BT: Glutaraldehyde proctitis. West J Med 1995; 163:477-478.
    21) Ballantyne B & Berman B: Dermal sensitizing potential of glutaraldehyde: a review and recent observations. J Toxicol Cutan Ocular Toxicol 1984; 3:251-262.
    22) Ballantyne B & Myers RC: The acute toxicity and primary irritancy of glutaraldehyde solutions. Vet HumToxicol 2001; 43(4):193-202.
    23) Bardazzi F, Melino M, & Alagna G: Glutaraldehyde dermatitis in nurses. Contact Dermatitis 1986; 14:319-320.
    24) Bata Shoe Company: Industrial Footwear Catalog, Bata Shoe Company, Belcamp, MD, 1995.
    25) Beauchamp RO Jr, St Clair MB, Fennell TR, et al: A critical review of the toxicology of glutaraldehyde. Crit Rev Toxicol 1992; 22(3-4):143-174.
    26) Benson WG: J Soc Occup Med 1984; 34:63-64.
    27) Best Manufacturing: ChemRest Chemical Resistance Guide. Best Manufacturing. Menlo, GA. 2002. Available from URL: http://www.chemrest.com. As accessed 10/8/2002.
    28) Best Manufacturing: Degradation and Permeation Data. Best Manufacturing. Menlo, GA. 2004. Available from URL: http://www.chemrest.com/DomesticPrep2/. As accessed 04/09/2004.
    29) Bingham E, Cohrssen B, & Powell CH: Patty's Toxicology, 5th ed, John Wiley & Sons, Inc, New York, NY, 2001.
    30) Birnbaum BA, Gordon RB, & Jacobs JE: Glutaraldehyde colitis: radiologic findings. Radiology 1995; 195:131-134.
    31) Boss Manufacturing Company: Work Gloves, Boss Manufacturing Company, Kewanee, IL, 1998.
    32) Budavari S: The Merck Index, 12th ed, Merck & Co, Inc, Whitehouse Station, NJ, 1996, pp 761.
    33) Burgess JL, Kirk M, Borron SW, et al: Emergency department hazardous materials protocol for contaminated patients. Ann Emerg Med 1999; 34(2):205-212.
    34) CDC: Symptoms of irritation associated with exposure to glutaraldehyde -- Colorado. CDC: MMWR 1987; 36:190-191.
    35) CHRIS : CHRIS Hazardous Chemical Data. US Department of Transportation, US Coast Guard. Washington, DC (Internet Version). Edition expires 1998; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    36) CHRIS: CHRIS Hazardous Chemical Data. US Department of Transportation, US Coast Guard. Washington, DC (Internet Version). Edition expires 2004; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    37) CHRIS: CHRIS Hazardous Chemical Data. US Department of Transportation, US Coast Guard. Washington, DC (Internet Version). Edition expires 2005; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    38) ChemFab Corporation: Chemical Permeation Guide Challenge Protective Clothing Fabrics, ChemFab Corporation, Merrimack, NH, 1993.
    39) Clayton GD & Clayton FE: Patty's Industrial Hygiene and Toxicology, Vol 2A, Toxicology, 4th ed, John Wiley & Sons, New York, NY, 1993.
    40) Comaish S: Glutaraldehyde lowers skin friction and enhances skin resistance to acute friction injury. ACTA Derm Venereol 1973; 53:455-460.
    41) Comasec Safety, Inc.: Chemical Resistance to Permeation Chart. Comasec Safety, Inc.. Enfield, CT. 2003. Available from URL: http://www.comasec.com/webcomasec/english/catalogue/mtabgb.html. As accessed 4/28/2003.
    42) Comasec Safety, Inc.: Product Literature, Comasec Safety, Inc., Enfield, CT, 2003a.
    43) Connaughton P: Occupational exposure to glutaraldehyde associated with tachycardia and palpitations. Med J Aust 1993; 159:567.
    44) Copeland S & Nugent K: Persistent and Unusual Respiratory Findings after Prolonged Glutaraldehyde Exposure. Int J Occup Environ Med 2015; 6(3):177-183.
    45) Corrado OJ, Osman J, & Davies RJ: Asthma and rhinitis after exposure to glutaraldehyde in endoscopy units. Human Toxicol 1986; 5:325-327.
    46) DFG: List of MAK and BAT Values 2002, Report No. 38, Deutsche Forschungsgemeinschaft, Commission for the Investigation of Health Hazards of Chemical Compounds in the Work Area, Wiley-VCH, Weinheim, Federal Republic of Germany, 2002.
    47) Dailey JR, Parnes RE, & Aminlari A: Glutaraldehyde keratopathy. Am J Ophthalmol 1993; 115:256-258.
    48) DesGroseilliers JP & Brisson P: Localized epidermolysis bullosa. Report of two cases and evaluation of therapy with glutaraldehyde. Arch Dermatol 1974; 109:70-72.
    49) DuPont: DuPont Suit Smart: Interactive Tool for the Selection of Protective Apparel. DuPont. Wilmington, DE. 2002. Available from URL: http://personalprotection.dupont.com/protectiveapparel/suitsmart/smartsuit2/na_english.asp. As accessed 10/31/2002.
    50) DuPont: Permeation Guide for DuPont Tychem Protective Fabrics. DuPont. Wilmington, DE. 2003. Available from URL: http://personalprotection.dupont.com/en/pdf/tyvektychem/pgcomplete20030128.pdf. As accessed 4/26/2004.
    51) DuPont: Permeation Test Results. DuPont. Wilmington, DE. 2002a. Available from URL: http://www.tyvekprotectiveapprl.com/databases/default.htm. As accessed 7/31/2002.
    52) Durante L, Zulty J, & Israel E: Investigation of an outbreak of bloody diarrhea: association with endoscopic cleaning solution and demonstration of lesions in an animal model. Am J Med 1992; 92:476-480.
    53) EPA: Search results for Toxic Substances Control Act (TSCA) Inventory Chemicals. US Environmental Protection Agency, Substance Registry System, U.S. EPA's Office of Pollution Prevention and Toxics. Washington, DC. 2005. Available from URL: http://www.epa.gov/srs/.
    54) ERG: Emergency Response Guidebook. A Guidebook for First Responders During the Initial Phase of a Dangerous Goods/Hazardous Materials Incident, U.S. Department of Transportation, Research and Special Programs Administration, Washington, DC, 2004.
    55) Ellenhorn MJ, Schonwald S, & Ordog G: Ellenhorn's Medical Toxicology: Diagnosis and Treatment of Human Poisoning, 2nd ed, Williams & Wilkins, Baltimore, MD, 1997.
    56) Ema M, Itami T, & Kawasaki H: Teratological assessment of glutaraldehyde in rats by gastric intubation. Toxicol Lett 1992; 63:147-153.
    57) Fisher AA: Reactions to glutaraldehyde with particular reference to radiologists and x-ray technicians. Cutis 1981; 28:113-120.
    58) Foussereau J: Doc Med Trav 1985; 23:13-14.
    59) Fowler JF: Allergic contact dermatitis from glutaraldehyde exposure. J Occup Med 1989; 31:852-853.
    60) Fukunaga K & Khatibi A: Glutaraldehyde colitis: a complication of screening flexible sigmoidoscopy in the primary care setting (letter). Ann Intern Med 2000; 133:315.
    61) Gannon PFG, Bright P, & Campbell M: Occupational asthma due to glutaraldehyde and formaldehyde in endoscopy and x ray departments. Thorax 1995; 50:156-159.
    62) Goncalo S, Menetes Brandao F, & Pecy Ueiro M: Occupational contact dermatitis to glutaraldehyde. Contact Dermatitis 1984; 10:183-184.
    63) Grant WM & Schuman JS: Toxicology of the Eye 4th edition, Charles C Thomas, Springfield, IL, 1993.
    64) Gross EA, Mellick PW, & Kari FW: Histopathology and cell replication responses in the respiratory tract of rats and mice exposed by inhalation to glutaraldehyde for up to 13 weeks. Fundam Appl Toxicol 1994; 23:348-362.
    65) Guardian Manufacturing Group: Guardian Gloves Test Results. Guardian Manufacturing Group. Willard, OH. 2001. Available from URL: http://www.guardian-mfg.com/guardianmfg.html. As accessed 12/11/2001.
    66) Gutterman E, Jorgensen L, Mitchell A, et al: Adverse staff health outcomes associated with endoscope reprocessing. Biomed Instrum Technol 2013; 47(2):172-179.
    67) HSDB : Hazardous Substances Data Bank. National Library of Medicine. Bethesda, MD (Internet Version). Edition expires 2001; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    68) HSDB : Hazardous Substances Data Bank. National Library of Medicine. Bethesda, MD (Internet Version). Edition expires 2004; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    69) HSDB : Hazardous Substances Data Bank. National Library of Medicine. Bethesda, MD (Internet Version). Edition expires 2005; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    70) Hannah DR: Glutaraldehyde and calcium hydroxide. A pulp dressing material. Br Dent J 1972; 132:227-231.
    71) Hansen KS: Contact Dermatitis 1983; 9:343-351.
    72) Harbison RD: Glutaraldehyde. In Harbison RD (ed): Hamilton & Hardy's Industrial Toxicology, 5th ed, Mosby, St. Louis, MO, 1998.
    73) Hathaway GJ, Proctor NH, & Hughes JP: Chemical Hazards of the Workplace, 3rd ed, Van Nostrand Reinhold Company, New York, NY, 1991, pp 312-313.
    74) Hathaway GJ, Proctor NH, & Hughes JP: Chemical Hazards of the Workplace, 4th ed, Van Nostrand Reinhold Company, New York, NY, 1996.
    75) Hess JA, Molinari JA, & Gleason MJ: Epidermal toxicity of disinfectants. Am J Dentistry 1991; 4:51-56.
    76) Hurd HK: Mutat Res 1985; 148:25-34.
    77) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: 1,3-Butadiene, Ethylene Oxide and Vinyl Halides (Vinyl Fluoride, Vinyl Chloride and Vinyl Bromide), 97, International Agency for Research on Cancer, Lyon, France, 2008.
    78) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Formaldehyde, 2-Butoxyethanol and 1-tert-Butoxypropan-2-ol, 88, International Agency for Research on Cancer, Lyon, France, 2006.
    79) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Household Use of Solid Fuels and High-temperature Frying, 95, International Agency for Research on Cancer, Lyon, France, 2010a.
    80) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Smokeless Tobacco and Some Tobacco-specific N-Nitrosamines, 89, International Agency for Research on Cancer, Lyon, France, 2007.
    81) IARC Working Group on the Evaluation of Carcinogenic Risks to Humans : IARC Monographs on the Evaluation of Carcinogenic Risks to Humans: Some Non-heterocyclic Polycyclic Aromatic Hydrocarbons and Some Related Exposures, 92, International Agency for Research on Cancer, Lyon, France, 2010.
    82) IARC: List of all agents, mixtures and exposures evaluated to date - IARC Monographs: Overall Evaluations of Carcinogenicity to Humans, Volumes 1-88, 1972-PRESENT. World Health Organization, International Agency for Research on Cancer. Lyon, FranceAvailable from URL: http://monographs.iarc.fr/monoeval/crthall.html. As accessed Oct 07, 2004.
    83) ICAO: Technical Instructions for the Safe Transport of Dangerous Goods by Air, 2003-2004. International Civil Aviation Organization, Montreal, Quebec, Canada, 2002.
    84) ILC Dover, Inc.: Ready 1 The Chemturion Limited Use Chemical Protective Suit, ILC Dover, Inc., Frederica, DE, 1998.
    85) International Agency for Research on Cancer (IARC): IARC monographs on the evaluation of carcinogenic risks to humans: list of classifications, volumes 1-116. International Agency for Research on Cancer (IARC). Lyon, France. 2016. Available from URL: http://monographs.iarc.fr/ENG/Classification/latest_classif.php. As accessed 2016-08-24.
    86) International Agency for Research on Cancer: IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. World Health Organization. Geneva, Switzerland. 2015. Available from URL: http://monographs.iarc.fr/ENG/Classification/. As accessed 2015-08-06.
    87) Jaworsky C, Taylor JS, & Evey P: Allergic contact dermatitis to glutaraldehyde in a hair conditioner. Cleve Clin J Med 1987; 54:443-444.
    88) Jordan WP, Dahl MV, & Albert HL: Contact dermatitis from glutaraldehyde. Arch Dermatol 1972; 105:94-95.
    89) Kappler, Inc.: Suit Smart. Kappler, Inc.. Guntersville, AL. 2001. Available from URL: http://www.kappler.com/suitsmart/smartsuit2/na_english.asp?select=1. As accessed 7/10/2001.
    90) Kimberly-Clark, Inc.: Chemical Test Results. Kimberly-Clark, Inc.. Atlanta, GA. 2002. Available from URL: http://www.kc-safety.com/tech_cres.html. As accessed 10/4/2002.
    91) Kline BS: Formaldehyde poisoning with a report of a fatal case. Arch Intern Med 1925; 36:220-228.
    92) Kraut JA & Madias NE: Metabolic acidosis: pathophysiology, diagnosis and management. Nat Rev Nephrol 2010; 6(5):274-285.
    93) LaCrosse-Rainfair: Safety Products, LaCrosse-Rainfair, Racine, WI, 1997.
    94) Lewis RJ: Hawley's Condensed Chemical Dictionary, 12th ed, John Wiley & Sons, Inc, New York, NY, 1993.
    95) Lewis RJ: Sax's Dangerous Properties of Industrial Materials, 9th ed, Van Nostrand Reinhold Company, New York, NY, 1996.
    96) MAPA Professional: Chemical Resistance Guide. MAPA North America. Columbia, TN. 2003. Available from URL: http://www.mapaglove.com/pro/ChemicalSearch.asp. As accessed 4/21/2003.
    97) MAPA Professional: Chemical Resistance Guide. MAPA North America. Columbia, TN. 2004. Available from URL: http://www.mapaglove.com/ProductSearch.cfm?id=1. As accessed 6/10/2004.
    98) Maibach H: Glutaraldehyde: cross-reactions to formaldehyde?. Contact Dermatitis 1975; 1:326-327.
    99) Maibach HI & Prystowsky: Glutaraldehyde (Pentanedial) allergic contact dermatitis. Arch Dermatol 1977; 113:170-171.
    100) Mar-Mac Manufacturing, Inc: Product Literature, Protective Apparel, Mar-Mac Manufacturing, Inc., McBee, SC, 1995.
    101) Marigold Industrial: US Chemical Resistance Chart, on-line version. Marigold Industrial. Norcross, GA. 2003. Available from URL: www.marigoldindustrial.com/charts/uschart/uschart.html. As accessed 4/14/2003.
    102) Marks TA, Worthy WC, & Staples RE: Influence of formaldehyde and Sonacide(R) (potentiated acid glutaraldehyde) on embryo and fetal development in mice. Teratology 1980; 22:51-58.
    103) Memphis Glove Company: Permeation Guide. Memphis Glove Company. Memphis, TN. 2001. Available from URL: http://www.memphisglove.com/permeation.html. As accessed 7/2/2001.
    104) Mohamad MZ, Koh KS, & Chong VH: Gluteraldehyde-induced colitis: a rare cause of lower gastrointestinal bleeding. Am J Emerg Med 2014; 32(6):685.e1-685.e2.
    105) Montgomery Safety Products: Montgomery Safety Products Chemical Resistant Glove Guide, Montgomery Safety Products, Canton, OH, 1995.
    106) Moore Rn & Igel KA: Lip burn from band seater. Am J Orthod Dentofac Orthop 1988; 93:183-185.
    107) Murray WJ & Ruddy MP: Toxic eye injury during induction of anesthesia. South Med J 1985; 79:1012-1013.
    108) NFPA: Fire Protection Guide to Hazardous Materials, 13th ed., National Fire Protection Association, Quincy, MA, 2002.
    109) NIOSH : Pocket Guide to Chemical Hazards. National Institute for Occupational Safety and Health. Cincinnati, OH (Internet Version). Edition expires 1998; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    110) NIOSH: Pocket Guide to Chemical Hazards. National Institute for Occupational Safety and Health. Cincinnati, OH (Internet Version). Edition expires 2005; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    111) NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 1, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2001.
    112) NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 2, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2002.
    113) NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 3, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2003.
    114) NRC: Acute Exposure Guideline Levels for Selected Airborne Chemicals - Volume 4, Subcommittee on Acute Exposure Guideline Levels, Committee on Toxicology, Board on Environmental Studies and Toxicology, Commission of Life Sciences, National Research Council. National Academy Press, Washington, DC, 2004.
    115) Naradzay J & Barish RA: Approach to ophthalmologic emergencies. Med Clin North Am 2006; 90(2):305-328.
    116) Nat-Wear: Protective Clothing, Hazards Chart. Nat-Wear. Miora, NY. 2001. Available from URL: http://www.natwear.com/hazchart1.htm. As accessed 7/12/2001.
    117) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2,3-Trimethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d68a&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    118) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2,4-Trimethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006m. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d68a&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    119) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2-Butylene Oxide (Proposed). United States Environmental Protection Agency. Washington, DC. 2008d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648083cdbb&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    120) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,2-Dibromoethane (Proposed). United States Environmental Protection Agency. Washington, DC. 2007g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064802796db&disposition=attachment&contentType=pdf. As accessed 2010-08-18.
    121) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 1,3,5-Trimethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d68a&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    122) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for 2-Ethylhexyl Chloroformate (Proposed). United States Environmental Protection Agency. Washington, DC. 2007b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648037904e&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    123) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Acrylonitrile (Proposed). United States Environmental Protection Agency. Washington, DC. 2007c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648028e6a3&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    124) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Adamsite (Proposed). United States Environmental Protection Agency. Washington, DC. 2007h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    125) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Agent BZ (3-quinuclidinyl benzilate) (Proposed). United States Environmental Protection Agency. Washington, DC. 2007f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803ad507&disposition=attachment&contentType=pdf. As accessed 2010-08-18.
    126) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Allyl Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2008. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648039d9ee&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    127) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Aluminum Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    128) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Arsenic Trioxide (Proposed). United States Environmental Protection Agency. Washington, DC. 2007m. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480220305&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    129) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Automotive Gasoline Unleaded (Proposed). United States Environmental Protection Agency. Washington, DC. 2009a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cc17&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    130) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Biphenyl (Proposed). United States Environmental Protection Agency. Washington, DC. 2005j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064801ea1b7&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    131) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Bis-Chloromethyl Ether (BCME) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006n. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648022db11&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    132) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Boron Tribromide (Proposed). United States Environmental Protection Agency. Washington, DC. 2008a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803ae1d3&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    133) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Bromine Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2007d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648039732a&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    134) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Bromoacetone (Proposed). United States Environmental Protection Agency. Washington, DC. 2008e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809187bf&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    135) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Calcium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    136) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Carbonyl Fluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2008b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803ae328&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    137) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Carbonyl Sulfide (Proposed). United States Environmental Protection Agency. Washington, DC. 2007e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648037ff26&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    138) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Chlorobenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2008c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064803a52bb&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    139) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Cyanogen (Proposed). United States Environmental Protection Agency. Washington, DC. 2008f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809187fe&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    140) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Dimethyl Phosphite (Proposed). United States Environmental Protection Agency. Washington, DC. 2009. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cbf3&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    141) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Diphenylchloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    142) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethyl Isocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648091884e&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    143) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethyl Phosphorodichloridate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480920347&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    144) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethylbenzene (Proposed). United States Environmental Protection Agency. Washington, DC. 2008g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809203e7&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    145) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ethyldichloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    146) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Germane (Proposed). United States Environmental Protection Agency. Washington, DC. 2008j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963906&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    147) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Hexafluoropropylene (Proposed). United States Environmental Protection Agency. Washington, DC. 2006. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064801ea1f5&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    148) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Ketene (Proposed). United States Environmental Protection Agency. Washington, DC. 2007. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ee7c&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    149) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Magnesium Aluminum Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    150) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Magnesium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    151) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Malathion (Proposed). United States Environmental Protection Agency. Washington, DC. 2009k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064809639df&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    152) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Mercury Vapor (Proposed). United States Environmental Protection Agency. Washington, DC. 2009b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a8a087&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    153) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyl Isothiocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963a03&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    154) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyl Parathion (Proposed). United States Environmental Protection Agency. Washington, DC. 2008l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963a57&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    155) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyl tertiary-butyl ether (Proposed). United States Environmental Protection Agency. Washington, DC. 2007a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064802a4985&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    156) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methylchlorosilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2005. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5f4&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    157) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyldichloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    158) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Methyldichlorosilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2005a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c646&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    159) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Mustard (HN1 CAS Reg. No. 538-07-8) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006a. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6cb&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    160) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Mustard (HN2 CAS Reg. No. 51-75-2) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006b. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6cb&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    161) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Mustard (HN3 CAS Reg. No. 555-77-1) (Proposed). United States Environmental Protection Agency. Washington, DC. 2006c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6cb&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    162) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Tetroxide (Proposed). United States Environmental Protection Agency. Washington, DC. 2008n. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648091855b&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    163) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Nitrogen Trifluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2009l. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963e0c&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    164) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Parathion (Proposed). United States Environmental Protection Agency. Washington, DC. 2008o. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480963e32&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    165) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Perchloryl Fluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2009c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e268&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    166) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Perfluoroisobutylene (Proposed). United States Environmental Protection Agency. Washington, DC. 2009d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e26a&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    167) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phenyl Isocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008p. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096dd58&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    168) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phenyl Mercaptan (Proposed). United States Environmental Protection Agency. Washington, DC. 2006d. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020cc0c&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    169) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phenyldichloroarsine (Proposed). United States Environmental Protection Agency. Washington, DC. 2007k. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020fd29&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    170) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phorate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008q. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096dcc8&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    171) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phosgene (Draft-Revised). United States Environmental Protection Agency. Washington, DC. 2009e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a8a08a&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    172) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Phosgene Oxime (Proposed). United States Environmental Protection Agency. Washington, DC. 2009f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e26d&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    173) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Potassium Cyanide (Proposed). United States Environmental Protection Agency. Washington, DC. 2009g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cbb9&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    174) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Potassium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005c. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    175) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Propargyl Alcohol (Proposed). United States Environmental Protection Agency. Washington, DC. 2006e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ec91&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    176) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Selenium Hexafluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2006f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ec55&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    177) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Silane (Proposed). United States Environmental Protection Agency. Washington, DC. 2006g. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d523&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    178) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Sodium Cyanide (Proposed). United States Environmental Protection Agency. Washington, DC. 2009h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7cbb9&disposition=attachment&contentType=pdf. As accessed 2010-08-15.
    179) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Sodium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    180) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Strontium Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005f. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    181) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Sulfuryl Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2006h. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020ec7a&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    182) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tear Gas (Proposed). United States Environmental Protection Agency. Washington, DC. 2008s. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096e551&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    183) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tellurium Hexafluoride (Proposed). United States Environmental Protection Agency. Washington, DC. 2009i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7e2a1&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    184) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tert-Octyl Mercaptan (Proposed). United States Environmental Protection Agency. Washington, DC. 2008r. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096e5c7&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    185) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Tetramethoxysilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2006j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d632&disposition=attachment&contentType=pdf. As accessed 2010-08-17.
    186) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Trimethoxysilane (Proposed). United States Environmental Protection Agency. Washington, DC. 2006i. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d632&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    187) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Trimethyl Phosphite (Proposed). United States Environmental Protection Agency. Washington, DC. 2009j. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=0900006480a7d608&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    188) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Trimethylacetyl Chloride (Proposed). United States Environmental Protection Agency. Washington, DC. 2008t. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648096e5cc&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    189) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for Zinc Phosphide (Proposed). United States Environmental Protection Agency. Washington, DC. 2005e. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020c5ed&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    190) National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances: Acute Exposure Guideline Levels (AEGLs) for n-Butyl Isocyanate (Proposed). United States Environmental Protection Agency. Washington, DC. 2008m. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=09000064808f9591&disposition=attachment&contentType=pdf. As accessed 2010-08-12.
    191) National Asthma Education and Prevention Program: Expert Panel Report 3 (EPR-3): Guidelines for the Diagnosis and Management of Asthma-Summary Report 2007. J Allergy Clin Immunol 2007; 120(5 Suppl):S94-S138.
    192) National Heart,Lung,and Blood Institute: Expert panel report 3: guidelines for the diagnosis and management of asthma. National Heart,Lung,and Blood Institute. Bethesda, MD. 2007. Available from URL: http://www.nhlbi.nih.gov/guidelines/asthma/asthgdln.pdf.
    193) National Institute for Occupational Safety and Health: NIOSH Pocket Guide to Chemical Hazards, U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, Cincinnati, OH, 2007.
    194) National Research Council : Acute exposure guideline levels for selected airborne chemicals, 5, National Academies Press, Washington, DC, 2007.
    195) National Research Council: Acute exposure guideline levels for selected airborne chemicals, 6, National Academies Press, Washington, DC, 2008.
    196) National Research Council: Acute exposure guideline levels for selected airborne chemicals, 7, National Academies Press, Washington, DC, 2009.
    197) National Research Council: Acute exposure guideline levels for selected airborne chemicals, 8, National Academies Press, Washington, DC, 2010.
    198) Neese Industries, Inc.: Fabric Properties Rating Chart. Neese Industries, Inc.. Gonzales, LA. 2003. Available from URL: http://www.neeseind.com/new/TechGroup.asp?Group=Fabric+Properties&Family=Technical. As accessed 4/15/2003.
    199) Nethercott JR & Holness DL: Contact dermatitis in funeral service workers. Contact Dermatitis 1988; 18:263-267.
    200) Nicewicz JT, Murphy DMF, & Welsh JP: Occupational asthma caused by gluteraldehyde exposure. Immunol Allerg Pract 1986; 8:18-24.
    201) Norback D: Skin and respiratory symptoms from exposure to alkaline glutaraldehyde in medical services. Scand J Work Environ Health 1988; 14:366-371.
    202) North: Chemical Resistance Comparison Chart - Protective Footwear . North Safety. Cranston, RI. 2002. Available from URL: http://www.linkpath.com/index2gisufrm.php?t=N-USA1. As accessed April 30, 2004.
    203) North: eZ Guide Interactive Software. North Safety. Cranston, RI. 2002a. Available from URL: http://www.northsafety.com/feature1.htm. As accessed 8/31/2002.
    204) Ong TH, Tan KL, Lee HS, et al: A case report of occupational asthma due to gluteraldehyde exposure. Ann Acad Med Singapore 2004; 33(2):275-278.
    205) Peate WF: Work-related eye injuries and illnesses. Am Fam Physician 2007; 75(7):1017-1022.
    206) Perera PM, Kularathne K, & Gawarammana IB: Laryngeal edema and metabolic acidosis after Omnicide ingestion. Clin Toxicol (Phila) 2008; 46(9):858-860.
    207) Playtex: Fits Tough Jobs Like a Glove, Playtex, Westport, CT, 1995.
    208) Prigent F, Iborra C, & Meslay C: Glutaraldehyde-induced cutaneous necrosis after topical treatment of a wart. Ann Dermatol Venereol 1996; 123:644-646.
    209) Pryor P: NIOSH Report No HETA-83-074-1525. National Institute for Occupational Safety and Health, 1984.
    210) RTECS : Registry of Toxic Effects of Chemical Substances. National Institute for Occupational Safety and Health. Cincinnati, OH (Internet Version). Edition expires 2001; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    211) Ranly DM, Horn D, & Hubbard GB: Assessment of the systemic distribution and toxicity of glutaraldehyde as a pulpotomy agent. Pediatr Dentistry 1989; 11:8-13.
    212) Rideout K, Teschke K, Dimich-Ward H, et al: Considering risks to healthcare workers from glutaraldehyde alternatives in high-level disinfection. J Hosp Infect 2005; 59(1):4-11.
    213) River City: Protective Wear Product Literature, River City, Memphis, TN, 1995.
    214) Rosenman KD & Beckett WS: Web based listing of agents associated with new onset work-related asthma. Respir Med 2015; 109(5):625-631.
    215) Ruiz-Rubio ME: Mutat Res 1985; 147:153-163.
    216) Ryan CK & Potter GD: Disinfectant colititis. Rinse as well as you wash. J Clin Gastroenterol 1995; 21:6-9.
    217) S Sweetman : Martindale: The Complete Drug Reference. London: Pharmaceutical Press (electronic version). The Pharmaceutical Press. London, UK (Internet Version). Edition expires 2001; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    218) Safety 4: North Safety Products: Chemical Protection Guide. North Safety. Cranston, RI. 2002. Available from URL: http://www.safety4.com/guide/set_guide.htm. As accessed 8/14/2002.
    219) Sanderson KV & Cronin E: Glutaraldehyde and contact dermatitis. Br Med J 1968; 3:802.
    220) Schneider M & Blejer HP: In house report No SU-171, Occupational Health Section, California Department of Health, Los Angeles, CA, 1973.
    221) Schweikl J, Schmalz, & Bey B: Mutagenicity of dentin bonding agents. J Biomed Mat Res 1994; 28:1061-1067.
    222) Servus: Norcross Safety Products, Servus Rubber, Servus, Rock Island, IL, 1995.
    223) Sittig M: Handbook of Toxic and Hazardous Chemicals and Carcinogens, 3rd ed, Noyes Publications, Park Ridge, NJ, 1991.
    224) Slesinski RS: Food Chem Toxicol 1983; 21:621-629.
    225) Spencer PS: Toxicol Appl Pharmacol 1978; 44:17-28.
    226) St Clair MD, Gross EA, & Morgan KT: Interactions of glutaraldehyde with nasal epithelium. Toxicologist 1989; 9:37.
    227) Standard Safety Equipment: Product Literature, Standard Safety Equipment, McHenry, IL, 1995.
    228) Stern ML, Holsapple MP, & McCay JA: Contact hypersensitivity response to glutaraldehyde in guinea pigs and mice. Toxicol Ind Health 1989; 5:31-43.
    229) Stonehill AA, Krop S, & Borick PM: Buffered glutaraldehyde -- a new chemical sterilization solution. Am J Hosp Pharm 1963; 20:458-465.
    230) Suringa DWR: Treatment of superficial onychomycoses with topically applied glutaraldehyde. A preliminary study. Arch Dermatol 1970; 102:163-167.
    231) Takigawa T & Endo Y: Effects of glutaraldehyde exposure on human health. J Occup Health 2006; 48(2):75-87.
    232) Tingley: Chemical Degradation for Footwear and Clothing. Tingley. South Plainfield, NJ. 2002. Available from URL: http://www.tingleyrubber.com/tingley/Guide_ChemDeg.pdf. As accessed 10/16/2002.
    233) Trelleborg-Viking, Inc.: Chemical and Biological Tests (database). Trelleborg-Viking, Inc.. Portsmouth, NH. 2002. Available from URL: http://www.trelleborg.com/protective/. As accessed 10/18/2002.
    234) Trelleborg-Viking, Inc.: Trellchem Chemical Protective Suits, Interactive manual & Chemical Database. Trelleborg-Viking, Inc.. Portsmouth, NH. 2001.
    235) U.S. Department of Energy, Office of Emergency Management: Protective Action Criteria (PAC) with AEGLs, ERPGs, & TEELs: Rev. 26 for chemicals of concern. U.S. Department of Energy, Office of Emergency Management. Washington, DC. 2010. Available from URL: http://www.hss.doe.gov/HealthSafety/WSHP/Chem_Safety/teel.html. As accessed 2011-06-27.
    236) U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project : 11th Report on Carcinogens. U.S. Department of Health and Human Services, Public Health Service, National Toxicology Program. Washington, DC. 2005. Available from URL: http://ntp.niehs.nih.gov/INDEXA5E1.HTM?objectid=32BA9724-F1F6-975E-7FCE50709CB4C932. As accessed 2011-06-27.
    237) U.S. Environmental Protection Agency: Discarded commercial chemical products, off-specification species, container residues, and spill residues thereof. Environmental Protection Agency's (EPA) Resource Conservation and Recovery Act (RCRA); List of hazardous substances and reportable quantities 2010b; 40CFR(261.33, e-f):77-.
    238) U.S. Environmental Protection Agency: Integrated Risk Information System (IRIS). U.S. Environmental Protection Agency. Washington, DC. 2011. Available from URL: http://cfpub.epa.gov/ncea/iris/index.cfm?fuseaction=iris.showSubstanceList&list_type=date. As accessed 2011-06-21.
    239) U.S. Environmental Protection Agency: List of Radionuclides. U.S. Environmental Protection Agency. Washington, DC. 2010a. Available from URL: http://www.gpo.gov/fdsys/pkg/CFR-2010-title40-vol27/pdf/CFR-2010-title40-vol27-sec302-4.pdf. As accessed 2011-06-17.
    240) U.S. Environmental Protection Agency: List of hazardous substances and reportable quantities. U.S. Environmental Protection Agency. Washington, DC. 2010. Available from URL: http://www.gpo.gov/fdsys/pkg/CFR-2010-title40-vol27/pdf/CFR-2010-title40-vol27-sec302-4.pdf. As accessed 2011-06-17.
    241) U.S. Environmental Protection Agency: The list of extremely hazardous substances and their threshold planning quantities (CAS Number Order). U.S. Environmental Protection Agency. Washington, DC. 2010c. Available from URL: http://www.gpo.gov/fdsys/pkg/CFR-2010-title40-vol27/pdf/CFR-2010-title40-vol27-part355.pdf. As accessed 2011-06-17.
    242) U.S. Occupational Safety and Health Administration: Part 1910 - Occupational safety and health standards (continued) Occupational Safety, and Health Administration's (OSHA) list of highly hazardous chemicals, toxics and reactives. Subpart Z - toxic and hazardous substances. CFR 2010 2010; Vol6(SEC1910):7-.
    243) U.S. Occupational Safety, and Health Administration (OSHA): Process safety management of highly hazardous chemicals. 29 CFR 2010 2010; 29(1910.119):348-.
    244) United States Environmental Protection Agency Office of Pollution Prevention and Toxics: Acute Exposure Guideline Levels (AEGLs) for Vinyl Acetate (Proposed). United States Environmental Protection Agency. Washington, DC. 2006. Available from URL: http://www.regulations.gov/search/Regs/contentStreamer?objectId=090000648020d6af&disposition=attachment&contentType=pdf. As accessed 2010-08-16.
    245) Verschueren K: Handbook of Environmental Data on Organic Chemicals. 4th ed. CD-ROM version. Wiley-Interscience. Hoboken, NJ. 2001.
    246) Waldron HA: Glutaraldehyde allergy in hospital workers (Letter). Lancet 1992; 339:880.
    247) Wells Lamont Industrial: Chemical Resistant Glove Application Chart. Wells Lamont Industrial. Morton Grove, IL. 2002. Available from URL: http://www.wellslamontindustry.com. As accessed 10/31/2002.
    248) Wiggins P, McCurdy SA, & Zeidenberg W: Epistaxis due to glutaraldehyde exposure. J Occup Med 1989; 31:854-856.
    249) Workrite: Chemical Splash Protection Garments, Technical Data and Application Guide, W.L. Gore Material Chemical Resistance Guide, Workrite, Oxnard, CA, 1997.