Hydrogen Peroxide as it relates to Kidney Dialysis


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The following information was generated from the Hazardous Substances Databank (HSDB), a database of the National Library of Medicine's TOXNET system (http://toxnet.nlm.nih.gov) on August 18, 2000. Query: Information added from CHEMID: hydrogen peroxide Chemid Name: albone [7722-84-1] ( hioxyl, hydroperoxide, inhibine, perhydrol, peroxan, peroxide, superoxol ) Registry Numbers: 7722-84-1 1 NAME: HYDROGEN PEROXIDE HSN: 547 RN: 7722-84-1 HUMAN HEALTH EFFECTS: EVIDENCE FOR CARCINOGENICITY: No data are available in humans. Limited evidence of carcinogenicity in animals. OVERALL EVALUATION: Group 3: The agent is not classifiable as to its carcinogenicity to humans. [IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer,1972-PRESENT. (Multivolume work).,p. S7 64 (1987)]**PEER REVIEWED** HUMAN TOXICITY EXCERPTS: Large doses presumably produce gastritis and esophagitis. Cases of rupture of the colon, proctitis and ulcerative colitis have been reported following hydrogen peroxide enemas. [Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984.,p. II-107]**PEER REVIEWED** THE CONTINUED USE OF HYDROGEN PEROXIDE SOLUTION AS A MOUTHWASH, EVEN IN HALF STRENGTH, MAY CAUSE HYPERTROPHIED FILIFORM PAPILLAE OF THE TONGUE ("HAIRY TONGUE") BUT THESE DISAPPEAR AFTER DRUG IS DISCONTINUED. [Gilman, A. G., L. S. Goodman, and A. Gilman. (eds.). Goodman and Gilman's The Pharmacological Basis of Therapeutics. 6th ed. New York: Macmillan Publishing Co., Inc. 1980. 974]**PEER REVIEWED** Although ingestion is unlikey to occur, if it does the hydrogen peroxide will cause irritation of the upper GI tract. Decomposition results in rapid liberation of oxygen, leading to distension of the esophagus or stomach, and possibly severe damage and internal bleeding. [International Labour Office. Encyclopedia of Occupational Health and Safety. Vols. I&II. Geneva, Switzerland: International Labour Office, 1983. 1089]**PEER REVIEWED** FOR HYDROGEN PEROXIDE, INHALATION OF 7 PPM CAUSES LUNG IRRITATION. [Thienes, C., and T.J. Haley. Clinical Toxicology. 5th ed. Philadelphia: Lea and Febiger, 1972. 191]**PEER REVIEWED** HEMIPLEGIA HAS FOLLOWED ITS USE TO IRRIGATE THE PLEURAL CAVITY; PRESUMABLY ... BY THE PASSAGE OF THE GAS INTO THE VASCULAR SYSTEM, RESULTING IN CEREBRAL EMBOLISM. [American Medical Association. AMA Drug Evaluations Annual 1991. Chicago, IL: American Medical Association, 1991. 1439]**PEER REVIEWED** MAY IRRITATE TONGUE & BUCCAL MUCOSA /WHEN USED TO TREAT STOMATITIS & GINGIVITIS/. [American Medical Association. AMA Drug Evaluations Annual 1991. Chicago, IL: American Medical Association, 1991. 1439]**PEER REVIEWED** WORKERS EXPOSED TO VAPORS FROM 90% H2O2 HAVE NOTED PRIMARILY RESP IRRITATION, BUT SPLASH OF SUCH HIGH CONCN IS GENERALLY FEARED AS POTENTIAL CAUSE OF SEVERE CORNEAL DAMAGE. [Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986. 492]**PEER REVIEWED** The effect of Co(II) ion on the reaction of hydrogen peroxide with DNA was investigated by a DNA sequencing technique using (32)P-5'-end-labeled DNA fragments obtained from human c-Ha-ras-1 protooncogene. 20 uM Co(II) (as cobalt chloride, CoCl2) induced strong DNA cleavage in the presence of 0.4 mM hydrogen peroxide even without alkali treatment. Guanine residues were the most alkali-labile site, and the extent of cleavages at the positions of thymine and cytosine was dependent on the sequence. Adenine residues were relatively resistive. Neither Co(II) nor hydrogen peroxide alone caused DNA cleavage. Diethylenetriaminepentaacetic acid, present in excess over Co(II), inhibited DNA cleavage. Singlet oxygen scavengers (dimethylfuran, 0.05 M sodium azide, 0.05 M 1,4-diazabicyclo(2.2.2)octane, 0.025 M dGMP), sulfur compounds (methional, methionine), and superoxide dismutase inhibited DNA cleavage completely. Hydroxyl radical scavengers, such as dimethyl sulfoxide and sodium formate, were not so effective as singlet oxygen scavengers. Electron spin resonance studies performed in the presence of ADP using 2,2,6,6-tetramethyl-4-piperidone as a singlet oxygen trap suggest that Co(II) reacts with hydrogen peroxide to produce singlet oxygen or its equivalent. Electron spin resonance studies using 5,5-dimethylpyrroline N-oxide showed that the hydroxyl radical adduct of 5,5-dimethylpyrroline N-oxide was also formed. [Yamamoto K et al; Chem Res Toxicol 4 (2): 234-9 (1989)]**PEER REVIEWED** A 33 yr old woman unintentionally ingested a 1 pint bottle of 35% hydrogen peroxide. She vomited, collapsed, and experienced a brief tonic-clonic seizure within minutes. On examination, the patient was intermittently seizing and markedly cyanotic and had copious white foam emanating from her mouth. Vital signs were blood pressure 156/118 mm Hg; pulse, 126; respirations, 32; and temp, 38.2 deg C. Pupils were 6 mm and weakly reactive to light. The heart was rapid and regular, and no SC emphysema was noted. Deep tendon reflexes were 2/4, and plantar responses were flexor. The patient was given 5 mg diazepam, 4 mg naloxone hydrochloride, 100 mg thiamine, and 50 ml of 50% dextrose iv. Within 30 sec after nasotracheal intubation, the patient became apneic and dependent on mechanical ventilation. Gastric lavage was performed. Preoperative esophagogastroduodenoscopy showed mild erythema of the distal esophagus and diffuse hemorrhages and edema of the gastric mucosa. Recurrent postoperative seizures were well controlled with phenytoin therapy. Bilateral cerebral hemisphere swelling was determined; intracranial pressure of 30 cm H2O responded to hyperventilation. Later neurologic examination demonstrated patchy areas of weakness in the upper and lower extremities and truncal ataxia with inability to maintain a sitting position. After 9 days, the patient was transferred to a rehabilitation facility. [Giberson TP et al; Ann Emerg Med 18 (7): 778-9 (1989)]**PEER REVIEWED** Respiratory effects - Acute lung damage/edema. [Cralley, L.J., L.V. Cralley (eds.). Patty's Industrial Hygiene and Toxicology. Volume III: Theory and Rationale of Industrial Hygiene Practice. 2nd ed., 3A:The Work Environment. New York, NY: John Wiley Sons, 1985. 171]**PEER REVIEWED** If swallowed, the sudden evolution of oxygen may cause injury by acute distension of the stomach and also nausea, vomiting, and internal bleeding. [Armour, M.A. Hazardous Laboratory Chemicals Disposal Guide. Boca Raton, FL: CRC Press Inc., 1991. 183]**PEER REVIEWED** Large ingestions may produce a mild gastritis from the decomposition of peroxide, which releases large volumes of oxygen and causes gastric distension. [Ellenhorn, M.J. and D.G. Barceloux. Medical Toxicology - Diagnosis and Treatment of Human Poisoning. New York, NY: Elsevier Science Publishing Co., Inc. 1988. 907]**PEER REVIEWED** Repeated use of hydrogen peroxide topical solution as a mouthwash or gargle may produce a condition known as "hairy tongue" or may cause irritation of the buccal mucous membrane. Concentrated solutions (20-30% or more) of hydrogen peroxide are strongly irritating to skin or mucous membranes and should be handled cautiously. When used rectally in a colonic lavage, the drug has caused gas embolism, rupture of the colon, proctitis, ulcerative colitis, and gangrene of the intestine. [McEvoy, G.K. (ed.). American Hospital Formulary Service - Drug Information 93. Bethesda, MD: American Society of Hospital Pharmacists, Inc., 1993 (Plus Supplements, 1993). 1753]**PEER REVIEWED** In treatment of corneal ulcerations, particularly in herpetic dendritic keratitis, 20% solution has been applied, after local anesthetic, every two hr as a localized cautery to the ulcer, and has been reported to have had good effect in numerous patients. In one instance a 10% solution was dropped on one eye of a patient after application of cocaine, and this eye was normal by the next day. [Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986. 492]**PEER REVIEWED** Dropping 1 to 3% hydrogen peroxide solution on the human eye causes severe pain, but this soon subsides. [Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986. 493]**PEER REVIEWED** DNA strand breaks and chromosomal aberrations were studied in human cells treated with hydrogen peroxide or with ionizing radiation. DNA strand breaks could be produced at dose levels of hydrogen peroxide much lower than those which induced chromosomal aberrations. Doses as low as 0.5 mM of hydrogen peroxide produced about as many DNA strand breaks as 2 Gy of (60)Co gamma-radiation. On the other hand, as much as 20 mM hydrogen peroxide produced only half as many chromosomal aberrations as 1 Gy of (60)Co gamma-radiation. [Rueff J et al; Mutat Res 289 (2): 197-204 (1993)]**PEER REVIEWED** SKIN, EYE AND RESPIRATORY IRRITATIONS: Marked irritation - eye, nose, throat, skin [Cralley, L.J., L.V. Cralley (eds.). Patty's Industrial Hygiene and Toxicology. Volume III: Theory and Rationale of Industrial Hygiene Practice. 2nd ed., 3A:The Work Environment. New York, NY: John Wiley Sons, 1985. 171]**PEER REVIEWED** DRUG WARNINGS: Hydrogen peroxide topical solution is acidic to the taste and to litmus paper and produces a froth in the mouth; because hydrogen-peroxide concentrate is caustic, it should not be tasted undiluted. [McEvoy, G.K. (ed.). American Hospital Formulary Service - Drug Information 93. Bethesda, MD: American Society of Hospital Pharmacists, Inc., 1993 (Plus Supplements, 1993). 1753]**PEER REVIEWED** PROBABLE ROUTES OF HUMAN EXPOSURE: Inhalation of vapor or mist, ingestion, eye and skin contact. [Sittig, M. Handbook of Toxic and Hazardous Chemicals and Carcinogens, 1985. 2nd ed. Park Ridge, NJ: Noyes Data Corporation, 1985. 510]**PEER REVIEWED** EMERGENCY MEDICAL TREATMENT: EMERGENCY MEDICAL TREATMENT: EMT COPYRIGHT DISCLAIMER: Portions of the POISINDEX(R) database are provided here for general reference. THE COMPLETE POISINDEX(R) DATABASE, AVAILABLE FROM MICROMEDEX, SHOULD BE CONSULTED FOR ASSISTANCE IN THE DIAGNOSIS OR TREATMENT OF SPECIFIC CASES. Copyright 1974-1998 Micromedex, Inc. Denver, Colorado. All Rights Reserved. Any duplication, replication or redistribution of all or part of the POISINDEX(R) database is a violation of Micromedex' copyrights and is strictly prohibited.
The following Overview, *** HYDROGEN PEROXIDE ***, is relevant for this HSDB record chemical. LIFE SUPPORT: o This overview assumes that basic life support measures have been instituted. CLINICAL EFFECTS: SUMMARY OF EXPOSURE 0.2.1.1 ACUTE EXPOSURE o Hydrogen peroxide is an oxidizing agent which liberates oxygen on contact with tissue. o HOUSEHOLD hydrogen peroxide (3%) is mildly irritating to mucus membranes. In general, ingestion, ocular, or dermal exposure to small amounts of dilute hydrogen peroxide will cause no serious problems. Vomiting and diarrhea are common after ingestion. Gastric injury has rarly been reported after accidental ingestion. o HIGH CONCENTRATIONS of hydrogen peroxide (greater than 10% industrial strength or 35% "Food Grade" solutions) are strong oxidizers and are corrosive, causing severe burns to mucus membranes, gastrointestinal mucosa, skin and eyes. Complications of ingestion include ruptured viscus, coma, seizures, and gas embolization with subsequent shock and cardiac arrest. 1. Dermal and ocular exposures may result in severe burns with corneal ulceration or perforation. Corneal injury is in rare cases delayed. o Inhalation of low concentration mist or spray causes mild ocular and respiratory irritation. Higher concentrations can cause severe mucus membrane irritation and inflammation, pulmonary edema, and systemic poisoning with shock, coma and seizures. o Rare reports of gas emboli have been described following surgical irrigation with 3% hydrogen peroxide due to the formation of microbubbles. VITAL SIGNS 0.2.3.1 ACUTE EXPOSURE o Hypotension and apnea have been reported with severe poisonings. HEENT 0.2.4.1 ACUTE EXPOSURE o Eye exposure to 3% hydrogen peroxide (household strength) may result in immediate pain and irritation, however, severe eye injury is rare. o Ocular exposure to industrial strength hydrogen peroxide solutions (greater than 10%) may result in ulceration or perforation of the cornea. CARDIOVASCULAR 0.2.5.1 ACUTE EXPOSURE o Systemic embolization has occurred resulting in EKG changes and rarely, cardiac arrest and death. RESPIRATORY 0.2.6.1 ACUTE EXPOSURE o Inhalation of vapors from concentrated (greater than 10%) solutions may result in severe pulmonary irritation. Interstitial lung disease and respiratory arrest have also been reported following massive exposures. NEUROLOGIC 0.2.7.1 ACUTE EXPOSURE o Cerebral edema, cerebral embolism, and seizures have been reported following ingestion of concentrated (35%) solutions. Death has been reported as a result of embolic cerebrovascular injury. GASTROINTESTINAL 0.2.8.1 ACUTE EXPOSURE o Serious GI complications have resulted from the ingestion of concentrated solutions and enemas with dilute peroxide solutions. o DILUTE - Exposure to dilute (3%) solutions may result in spontaneous vomiting, mild irritation to mucosal tissue, burns in the mouth, throat, esophagus, and stomach, colitis, enteritis, tenesmus, and papillae hypertrophy. Gastric ulcer has been reported in a young child exposed to a small amount of hydrogen peroxide 3%. 1. Gastric distention and possible rupture of the colon secondary to liberation of oxygen may occur but is probably rare especially following accidental ingestion of household solutions. o CONCENTRATED - Exposure to concentrated (greater than 10%) solutions may cause extreme irritation and inflammation, intestinal gangrene, hemorrhagic gastritis, burns in the mouth, throat, esophagus, and stomach, rupture of the colon, intestinal gangrene with gas embolization, a fulminant acute ulcerating colitis resulting in death, and near fatal gas embolization. DERMATOLOGIC 0.2.14.1 ACUTE EXPOSURE o Dermal exposure to dilute (3%) solutions generally results in a bleaching of the affected area in association with a tingling sensation and lasts 2 to 3 hours, if washed promptly after contact. o Dermal exposure to concentrated solutions has resulted in burns and gangrene. CARCINOGENICITY 0.2.21.1 IARC CATEGORY o IARC (Hydrogen Peroxide, 30%) (RTECS, 1991) 1. Animal: Limited evidence 2. Group 3 o IARC (Hydrogen Peroxide, 90%) (RTECS, 1991) 1. Animal: Limited evidence 2. Human: No adequate data 3. Group 3 OTHER 0.2.23.1 ACUTE EXPOSURE o Sepsis may develop as complication resulting from use of H2O2 enema. o Following ingestion or instillation into a body cavity gas may develop within the body cavity and may progress to gas embolism. LABORATORY: o Plasma hydrogen peroxide levels are not clinically useful. TREATMENT OVERVIEW: ORAL EXPOSURE o ADMINISTER WATER immediately to dilute the peroxide. Spontaneous vomiting is common. In general, exposure to small amounts of a dilute solution will NOT result in serious complications and requires little treatment. o EMESIS SHOULD NOT BE INITIATED in those patients with a history of vomiting or ingesting highly concentrated solutions of hydrogen peroxide. 1. Following ingestion of industrial strength (greater than 10%) solutions, patients should be monitored for burns to the mouth, throat, esophagus, and stomach. Serious complications are possible. o GASTRIC DISTENTION may require decompression via a nasogastric tube. o Many chemicals cause irritation of the eyes, skin, and respiratory tract. Respiratory tract irritation, if severe, can progress to pulmonary edema, which may be delayed in onset for up to 24 to 72 hours in some cases. o Irritation or burns of the esophagus or gastrointestinal tract are also possible if caustic or irritant chemicals are ingested. F. PULMONARY EDEMA (NONCARDIOGENIC): Maintain ventilation and oxygenation and evaluate with frequent arterial blood gas or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed. EYE EXPOSURE o DECONTAMINATION: Exposed eyes should be irrigated with copious amounts of tepid water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist, the patient should be seen in a health care facility. o Ocular exposure to HOUSEHOLD STRENGTH (3%) solutions usually requires little more than thorough irrigation, since serious complications are rare. However, ocular exposure to INDUSTRIAL STRENGTH (greater than 10%) solutions not only requires thorough irrigation, but given the possibility of corneal ulceration or perforation, evaluation in a health care facility is recommended. DERMAL EXPOSURE o DECONTAMINATION: Wash exposed area extremely thoroughly with soap and water. A physician may need to examine the area if irritation or pain persists. RANGE OF TOXICITY: o Oral ingestion, dermal exposure, or eye exposure to 3% hydrogen peroxide solutions (household strength) generally does not result in severe toxicity. Gastric ulcers developed in a young child who drank 2 to 4 ounces of 3% hydrogen peroxide. o However, exposure to industrial strength solutions (greater than 10 to 30%) may result in burns of the mouth, throat, esophagus, stomach, and exposed skin. Concentrations exceeding 10% should be considered potentially very toxic. o GAS EMBOLI secondary to irrigation with hydrogen peroxide has occurred during surgical procedures. Its been suggested (extrapolating from animal data) that a 10 kg infant may only need 2 mL/kg of gas (20 mL) to sustain a cardiac arrest; 3% hydrogen peroxide 2 mL can release 20 mL of oxygen microbubbles. ANIMAL TOXICITY STUDIES: EVIDENCE FOR CARCINOGENICITY: No data are available in humans. Limited evidence of carcinogenicity in animals. OVERALL EVALUATION: Group 3: The agent is not classifiable as to its carcinogenicity to humans. [IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer,1972-PRESENT. (Multivolume work).,p. S7 64 (1987)]**PEER REVIEWED** NON-HUMAN TOXICITY EXCERPTS: DOGS /EXPOSED/ 6 HR/DAY; 5 DAYS/WK FOR 6 MO AT AN AVG VAPOR CONCN OF 7 PPM OF 90% HYDROGEN PEROXIDE ... DEVELOPED EXTERNAL BODY IRRITATION, SNEEZING, LACRIMATION AND BLEACHING OF THE HAIR. /90% SOLN/ [American Conference of Governmental Industrial Hygienists. Documentation of the Threshold Limit Values and Biological Exposure Indices. 5th ed. Cincinnati, OH:American Conference of Governmental Industrial Hygienists, 1986. 316]**PEER REVIEWED** DOGS /WERE EXPOSED/ 6 HR/DAY, 5 DAYS PER WEEK FOR 6 MO @ AVG VAPOR CONCN OF 7 PPM OF 90% HYDROGEN PEROXIDE. ... AUTOPSY DISCLOSED GREATLY THICKENED SKIN BUT NO HAIR FOLLICLE DESTRUCTION. THE LUNGS WERE FOUND TO BE IRRITATED. NO SIGNIFICANT CHANGES IN BLOOD OR URINARY CONSTITUENTS WERE OBSERVED. /90% SOLN/ [American Conference of Governmental Industrial Hygienists. Documentation of the Threshold Limit Values and Biological Exposure Indices. 5th ed. Cincinnati, OH:American Conference of Governmental Industrial Hygienists, 1986. 316]**PEER REVIEWED** RABBITS EXPOSED DAILY FOR 3 MONTHS @ 22 PPM SHOWED NO EYE INJURY, ALTHOUGH THE HAIR WAS BLEACHED AND IRRITATION WAS NOTED AROUND NOSE. /90% SOLN/ [American Conference of Governmental Industrial Hygienists. Documentation of the Threshold Limit Values and Biological Exposure Indices. 5th ed. Cincinnati, OH:American Conference of Governmental Industrial Hygienists, 1986. 316]**PEER REVIEWED** DROP APPLICATION OF 0.5% SOLN ON RABBIT CORNEA CAUSES DISTURBANCES OF EPITHELIUM, BUT EYE RETURNS TO NORMAL WITHIN 24 HR. HOWEVER, INTRACORNEAL INJECTION OF 0.1%-0.3% SOLN CAUSES RATHER SEVERE REACTION. [Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986. 493]**PEER REVIEWED** A DROP OF 5%-30% H2O2 APPLIED TO RABBIT EYES HAVING NORMAL EPITHELIUM CAUSES SUPERFICIAL CLOUDING, WHICH IS PERSISTENT WHEN GREATER THAN 10% IS APPLIED. EVEN 5% SOLN HAS BEEN OBSERVED TO CAUSE SEVERE CORNEAL EDEMA, FLARE IN AQUEOUS, INTENSE CONGESTION OF IRIS, & VASCULARIZATION OF CORNEA IN RABBITS ... . [Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986. 493]**PEER REVIEWED** SINGLE STRAND SCISSIONS WERE PRODUCED IN T7 DNA UPON INCUBATION WITH H2O2 IN AQ SOLN @ NEUTRAL PH. INHIBITION OF SCISSIONS BY HYDROXYL RADICAL SCAVENGERS INDICATES INTERMEDIACY OF HYDROXYL RADICALS. [LESKO SA ET AL; BIOCHEMISTRY 19 (13): 3023 (1980)]**PEER REVIEWED** Pregnant rats were fed a diet containing up to 10% hydrogen peroxide. Maternal and fetal weights were reduced but no significant malformations were reported. [Shepard, T.H. Catalog of Teratogenic Agents. 5th ed. Baltimore, MD: The Johns Hopkins University Press, 1986. 296]**PEER REVIEWED** In rabbits and cats that died after iv administration of hydrogen peroxide, the lungs were found to be pale and emphysematous, with considerable amounts of gas in the great veins and in the right side of the heart. [IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer,1972-PRESENT. (Multivolume work).,p. V36 297 (1985)]**PEER REVIEWED** After ip injection of 0.5 ml of 5% hydrogen peroxide into adult mice, a radiation like effect was observed; pyknotic nuclei were induced in the intestine and thymus within 2 hr and persisted for up to 24 hr. [IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer,1972-PRESENT. (Multivolume work).,p. V36 297 (1985)]**PEER REVIEWED** Prophages are induced by treatment of lysogenized bacteria with hydrogen peroxide. In Escherichia coli, hydrogen peroxide induced single strand breaks in DNA and was positive in DNA repair assays. [IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer,1972-PRESENT. (Multivolume work).,p. V36 300 (1985)]**PEER REVIEWED** Hydrogen peroxide was mutagenic to Salmonella typhimurium TA92 and TA102 and was positive in a forward mutation test in Salmonella typhimurium SV50. [IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer,1972-PRESENT. (Multivolume work).,p. V36 301 (1985)]**PEER REVIEWED** Experiments on rabbit eyes ... showed corneal injury from dropped application todepend not only on the conc of hydrogen peroxide, but also on the integrity of the corneal epithelium, which had a protecive influence. Application of a drop of 10 to 30% caused superficial corneal haze, and, if there were defects in the epithelium, could cause localized swelling and opacitites in the corneal stroma. Also, 5% solution caused superficial corneal haze and much conjunctival reaction, but these effects were gone in 24 hr. The effect of 10% solution usually took longer to disappear, and occasionally could result in lasting localized opacities. [Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986. 493]**PEER REVIEWED** The effect of hydrogen peroxide on perfusion flow, airway conductance and dynamic compliance of isolated perfused and ventilated guinea pig lungs was investigated. Hydrogen peroxide (50 uM in the perfusion buffer) induced a decrease in airway conductance and dynamic compliance and perfusion flow during 5 min. of exposure. Hydrogen peroxide also caused an increase in the levels of thromboxane in the perfusate of the lung. The constrictor effects as well as the formation of thromboxane were inhibited by the cyclooxygenase inhibitor ibuprofen (50 uM). The thromboxane/prostaglandin endoperoxide receptor antagonist L-670,596 (1 uM) abolished the effects of hydrogen peroxide on perfusion flow, airway conductance and dynamic compliance, but did not affect the formation of thromboxane. The thromboxane synthetase inhibitor carboxyheptylimidazole (100 uM) reduced both the hydrogen peroxide induced formation of thromboxane and vaso and bronchoconstriction, suggesting a predominant role for thromboxane A2 versus prostaglandin H2 in these effects. A role for platelet activating factor in mediating the effect of hydrogen peroxide could not be supported, as the platelet activating factor receptor antagonist WEB 2086 (10 uM) did not affect hydrogen peroxide induced vaso and brochoconstriction. Hydrogen peroxide induces thromboxane A2 mediated vaso and bronchoconstriction in the isolated perfused an ventilated guinea pig lung. Platelet activating factor does not appear to play a significant role in the hydrogen peroxide induced vaso and bronchoconstriction. The perfused guinea pig lung is more sensitive to hydrogen peroxide than the perfused rat lung. [Bannenberg G et al; Pharmacol Toxicol 72 (4-5): 1993 314-20 (1993)]**PEER REVIEWED** Hydrogen peroxide resistant sublines of Chinese hamster ovary cells were isolated by in vitro exposure to the oxidant (treatment for 1 hr followed by 3 days of growth in peroxide free medium). Stepwise increase in low level hydrogen peroxide concn produced variants which were progressively more resistant to the growth inhibitory effect elicited by the oxidant. Removal from hydrogen peroxide decreased resistance and the curve describing this process was biphasic in nature. The protein content constantly increased during the adaptation process and decreases upon removal from hydrogen peroxide. Catalase activity did not show large variations in resistant sublines with respect to the parental cell line, and these changes were at least partially related to differences in cell size/amount of total cell proteins of the sublines. In addition, the minor changes observed for catalase activity did not correlate with the degree of resistance to growth inhibition elicited by the oxidant. [Cantoni O et al; Biochem Pharmacol 45 (11): 2251-57 (1993)]**PEER REVIEWED** To understand the role of protein-thiol mixed disulfide formation in relation to the sequence of events during cataract induction, we conducted a long term hydrogen peroxide exposure study for up to 96 hr to monitor the dynamic changes in glutathione and protein-glutathione mixed disulfide levels, the formation of protein-protein disulfide aggregate, protein solubility, and the progression in lens opacity. Rat lenses were cultured in 0.5 mM hydrogen peroxide and harvested at intervals of 24, 48, 72 and 96 hr for the examination of morphological and biochemical changes. Contralateral lenses cultured in hydrogen peroxide free media were used as controls. It was found that the lenses had only patchy opacity at the equatorafter 24 hr, but became hydrated suddenly at 48 hr (31% heavier than the control), with an opacity which involved the entire outer cortical region. By 72 hr incubation, the nucleus was opacified. Lens glutathione progressively decreased with time of hydrogen peroxide exposure, 40% was lost by 24 hr and over 95% by 48 hr. There was a concomitant elevation of protein-glutathione mixed disulfide, 16 fold over the controls by 24 hr and 45 fold by 48 hr followed by a decline to 34 fold after 72 hr. In addition, the level of protein-cysteine mixed disulfide was elevated after 48 hr incubation in hydrogen peroxide. At this time, protein-protein disulfide aggregates began to appear both in water soluble and urea soluble fractions along with a drastic reduction in protein solubility. Western blot analysis of the protein fractions identified beta and gamma, but not alpha-crystallin in the disulfide containing aggregates. The lens clarity and biochemical changes partially recovered if the oxidant was removed within 24 hr, indicating a potential therapeutic role for antioxidants. [Cui XL, Lou MF; Exp Eye Res 57 (2): 157-67 (1993)]**PEER REVIEWED** DNA damage induced by oxidants includes formation of DNA strand breaks as well as oxidative damage to DNA bases. Both forms of DNA damage were measured concurrently in two model human breast epithelial cell lines treated with hydrogen peroxide to compare the dose-dependent induction of each form of DNA damage with growth inhibition. MCF-7 breast cancer cells had relatively higher levels of non-protein thiols, oxidized glutathione (GSSG) reductase, catalase, and superoxide dismutase than did the MCF-10A line of immortalized, but not transformed human breast epithelial cells. The levels of antioxidant defenses were not predictive of endogenous oxidative DNA damage levels nor of toxicity and DNA damage induced by hydrogen peroxide. The endogenous levels of 5-hydroxymethyl-2'-deoxyuridine were higher in MCF-7 than MCF-10A cells. The cells were treated with 10-200 uM hydrogen peroxide for 15 min at 37 C in complete media. Low concn of hydrogen peroxide were growth stimulatory to both cell lines. At higher concn, growth inhibition by hydrogen peroxide was greater in MC-7 than in MCF-10A cells. Accordingly, induction of both single-strand DNA breaks and 5-hydroxymethyl-2'-deoxyuridine in DNA was greater in MCF-7 than MCF-10A cells. In both cell lines, the dose-dependent induction of single-strand breaks paralleled growth inhibition more closely than did formation of 5-hydroxymethyl-2'-deoxyuridine. [Djuric Z et al; Free Radical Biol Med 14 (5): 541-7 (1993)]**PEER REVIEWED** An oxidant burden established by hydrogen peroxide overload may elicit postischemic myocardial damage. Exposure of neonatal rat cardiomyocytes to 50 uM-1.0 mM hydrogen peroxide bolus rapidly shifted their pyridine-nucleotide redox balance toward oxidation. At least 30% of the observed NADPH oxidation was independent of glutathione cycle activity and appeared chemical in nature with hydrogen peroxide itself, and not a radical metabolite, acting as oxidant. Cell exposure to hydrogen peroxide also depleted cardiomyocyte pyridine nucleotides as a consequence of enhanced utilization. The oxidative stress activated one major route of pyridine nucleotide catabolism (i.e., protein ADP-ribosylation) without acute inhibitory effect upon the other (cleavage by NAD glycohydrolase). The limited NAD sparing by metal chelators and inhibitors of ADP-ribosylation reflected pyridine nucleotide utilization for repair of single-strand DNA breaks caused by hydroxyl-like radicals formed intracellularly through iron-dependent hydrogen peroxide reduction. Cardiomyocyte NAD depletion during hydrogen peroxide induced oxidative stress was independent of cell integrity and lipid peroxidation. The NAD lost after a discrete hydrogen peroxide pulse was only partly replenished over a 24 hr postinjury period. Cardiomyocyte pyridine nucleotide metabolism is a nonperoxidative injury target that is chronically affected by hydrogen peroxide overload. [Janero DR et al; Am J Physiol 264 (6 Pt 1): C1401-10 (1993)]**PEER REVIEWED** The effect of the oxidant hydrogen peroxide on the vulnerability of the myocardium to reperfusion induced arrhythmias following global ischemia was investigated. After a 15 min equilibration period with or without experimental intervention, isolated perfused rat hearts were made globally ischemic for 5 min by cross-clamping the aortic line. No dysrhythmias were evoked upon reperfusion at the 5 min global ischemia time period. Hydrogen peroxide was added to the perfusate 5 min into the equilibration period with a total exposure of 10 min. Global ischemia was then induced for 5 min followed by 10 min of reperfusion. All hearts exposed to 200 uM hydrogen peroxide developed ventricular dysrhythmias during the reperfusion period. Coronary flow increased after 5 min of exposure to 200 uM hydrogen peroxide and remained elevated during reperfusion. Toxic oxygen derivedproducts are capable of increasing the susceptibility of the myocardium to reperfusion induced arrhythmias. [Okabe E et al; Eur J Pharmacol 248 (1): 33-9 (1993)]**PEER REVIEWED** The superoxide dismutase mimic, 4-hydroxy TEMPO (TEMPOL), was used to investigate the mechanism by which hydrogen peroxide damages cultured rabbit lens epithelial cells and to identify some of the targets of hydrogen peroxide insult. Most studies aimed at determining the mechanism by which hydrogen peroxide exerts its cytotoxic effect have used iron chelators to prevent the generation of the damaging hydroxyl radical. TEMPOL does not chelate transition metals. Cells at low or high density were cultured in MEM containing 5 mM TEMPOL and exposed to a single sub-lethal dose of 0.05 or 0.5 mM hydrogen peroxide, respectively. Analysis of EPR spectra indicated that TEMPOL was stable in MEM, did not destroy hydrogen peroxide and penetrated the intracellular fluid. TEMPOL prevented or curtailed the hydrogen peroxide induced inhibition of cell growth, blebbing of the cell membrane, the decrease in NAD+, the activation of poly ADP-ribose polymerase, an enzyme involved in DNA repair, and limited the induction of single strand breaks in DNA normally brought about by hydrogen peroxide. TEMPOL did not prevent the hydrogen peroxide induced decrease in reduced glutathione, lactate production, and the activity of glyceraldehyde 3-phosphate dehydrogenase, or the hydrogen peroxide induced increases in oxidized glutathione and hexose monophosphate shunt activity. Addition of TEMPOL 1-15 min after exposure of cells to hydrogen peroxide offered partial protection from the inhibition of cell division. TEMPOL at 5 mM did not inhibit cell growth. Some of the hydrogen peroxide induced damage in cultured rabbit LECs is mediated by intracellular redox-active metals involved in the Haber-Weiss cycle. Cellular changes not protected by TEMPOL, including attack of hydrogen peroxide on the thiol groups of glutathione (mediated through glutathione peroxidase) and G3PDH, are likely brought about by hydrogen peroxide itself and not by reactions of oxygen free-radicals generated from hydrogen peroxide. [Reddan JR et al; Exp Eye Res 56 (5): 543-54 (1993)]**PEER REVIEWED** The effect of extracellular acidosis on different types of cell injury and death was examined using suspensions of rabbit renal proximal tubules. Cell death produced by the mitochondrial inhibitors rotenone, antimycin A, carbonyl cyanide p-trifluoromethoxyphenylhydrazone and oligomycin and by the ion exchangers valinomycin, nigericin and monensin was ameliorated by reducing extracellular pH from 7.4 to 6.4. The protection lasted for more than 5 hr and was not due to the release of mitochondrial inhibition or to the maintenance of tubular ATP levels. In contrast, extracellular acidosis potentiated the cell injury and death produced by the oxidants t-butyl hydroperoxide, hydrogen peroxide and ochratoxin A. Because a decrease in extracellular pH resulted in an increase in lipid peroxidation and in glutathione disulfide formation, and caused a decrease in glutathione peroxidase and glutathione reductase activities, the mechanism of this potentiation is most likely the result of an increase in free-radical production or a decrease in free-radical detoxification. The findings with the oxidants are in marked contrast to those in hepatocytes. [Rodeheaver DP, Schnellmann RG; J Pharmacol Exp Ther 265 (3): 1355-60 (1993)]**PEER REVIEWED** Hydrogen peroxide induced contractions of isolated rabbit intrapulmonary arteries mounted in standard tissue baths were studied. All vessels were pretreated with a thromboxane A2/prostaglandin H2 receptor antagonist, SQ 29,548, to block immediate transient contractions to hydrogen peroxide and to isolate slowly developing sustained contractions. When exposed to hydrogen peroxide (0.1, 0.2, 0.3, 0.6, and 1.0 mM) for 30 min, vessels contracted in a concn-dependent fashion between 0.1 and 0.3 mM hydrogen peroxide; contractions at 0.6 and 1.0 mM hydrogen peroxide were not significantly different from those at 0.3 mM hydrogen peroxide. During recovery (90 min) from hydrogen peroxide exposures, baseline tension was significantly greater, but active tension (10 uM phenylephrine) was significantly less for vessels previously exposed to 0.6 and 1.0 mM hydrogen peroxide. [Sheehan DW et al; Am J Physiol 264 (5 PART 2): H1542-H1547 (1993)]**PEER REVIEWED** Free radical generation from hydrogen peroxide and lipid hydroperoxides in the presence of chromium(III) was investigated by electron spin resonance spin trapping methodology. Incubation of chromium(III) with hydrogen peroxide at physiological pH generated hydroxyl radical, the yield of which reached saturation level in about 6 min. Deferoxamine reduced the hydroxyl radical yield by only about 20%, diethylenetriamine pentaacetic acid reduced it by about 70%, while cysteine, glutathione, and NADH exhibited no significant effect. The yield of hydroxyl radical formation also depended on the pH being 15 times higher at pH 10 than that at pH 7.2. At pH 3.0, hydroxyl radical generation became nondetectable, and addition of hydrogen peroxide to chromium(III) solution did not affect the intensity of the chromium(III) electron spin resonance signal while at pH 10, addition of hydrogen peroxide reduced the chromium(II) intensity by about 40%, showing that reaction of chromium(III) with hydrogen peroxide occurred only at higher pH. Chromium(III) is capable of producing free radicals from hydrogen peroxide and lipid hydroperoxides. [Shi X et al; Arch Biochem Biophys 302 (1): 294-99 (1993)]**PEER REVIEWED** Electron spin resonance spin trapping was utilized to investigate the generation of free radicals from cumene hydroperoxide, tert-butyl hydroperoxide, and hydrogen peroxide at pH 7.2 by cobalt(II) in the presence of cysteinyl and histidyl chelating agents. Incubation of cobalt(II) with cumene hydroperoxide or tert-butyl hydroperoxide did not generate any detectable amounts of free radicals. However, in the presence of glutathione, cysteine, penicillamine, or N-acetylcysteine, cobalt(II) generated cumene hydroperoxide-derived carbon-centered radicals, cumene alkoxyl radicals, and hydroxyl radicals. Oxidized glutathione and cysteine used instead of reduced glutathione or cysteine did not generate any free radical, indicating an important role of the -SH group in radical generation. While the addition of diethylenetriamine pentaacetic acid prevented radical generation, deferoxamine had only a slightly inhibitory effect. Incubation of cobalt(II) with hydrogen peroxide produced only a small amount of hydroxyl radicals. Addition of glutathione to the mixture of cobalt(II) and hydrogen peroxide resulted in generation of both glutathionyl and hydroxyl radicals, which could be inhibited by diethylenetriamine pentaacetic acid and deferoxamine. Under the same experimental conditions, cysteine, penicillamine, and N-acetylcysteine inhibited free radical generation from the reaction of cobalt(II) with hydrogen peroxide. Histidine and histidyl oligopeptides, homocarnosine, and carnosine did not have a significant effect. However, anserine enhanced the hydroxyl radical generation from this reaction. Cobalt(II) is capable of generating free radicals from lipid hydroperoxides and hydrogen peroxide in the presence of certain chelating agents. [Shi X et al; Chem Res Toxicol 6 (3): 277-83 (1993)]**PEER REVIEWED** A comparison was made between the house mouse (Mus musculus) and the white-footed mouse (Peromyscus leucopus): the latter has > 2 fold greater life span and metabolic potential than the former. Longe life span and higher metabolic potential of Peromyscus were associated with low rates of mitochondrial superoxide radical and hydrogen peroxide generation, higher activities of catalase and glutathione peroxidase and low levels of protein oxidative damage as well as low susceptibility to oxidative damage in response to experimental oxidative stress. Results support the role of oxidative stress in aging. [Sohal RS et al; Biochem Biophys Res Commun 196 (1): 7-11 (1993)]**PEER REVIEWED** Fanconi's anemiacells are highly susceptible to both reactive oxygen species and mitomycin C, a DNA cross-linking agent. In this study we have determined the amounts of 8-hydroxydeoxyguanosine, typical of oxidative DNA damage, in Epstein-Barr virus transformed lymphoblasts from Fanconi's anemia patients and normal controls. Fanconi's anemia cells (HSC72 and 99 cells being assigned to Fanconi's anemia complementation group A) formed 2-3 times more 8-hydroxydeoxyguanosine than control cells after incubation with 20 mM hydrogen peroxide at 37 deg C for 30 min. Fanconi's anemia cells also formed more 8-hydroxyguanosine, typical of oxidative RNA damage, than control cells. Fanconi's anemia cells showed decreased activity to decompose hydrogen peroxide. Although the activity in Fanconi's anemia cells was only 20-30% less than control cells, the remaining, undecomposed hydrogen peroxide concn was almost twice as much in Fanconi's anemia cells as in control cells, and the remaining hydrogen peroxide concn correlated well with the amounts of 8-hydroxydeoxyguanosine formation. The hydrogen peroxide decomposing activity was almost completely inhibited by sodium azide or aminotriazole, both catalase inhibitors. With these inhibitors the amounts of 8-hydroxydeoxyguanosine formation were much higher than in those cells without inhibitors, and were almost the same in control cells as in Fanconi's anemia cells. Catalase activity in Fanconi's anemia cell lysates was 70-80% of controls. [Takeuchi T, Morimoto K; Carcinogenesis 14 (6): 1115-20 (1993)]**PEER REVIEWED** Energy transduction, as measured by myocyte respiration, was inhibited by hydrogen peroxide, but the mitochondrial membrane potential was relatively unaffected. In mitochondrial energy transduction by measuring the sensitivity to hydrogen peroxide of NADH-CoQ reductase, ATP synthase, and adenine nucleotide translocase in situ in myocytes. Adult rat heart cells were isolated and incubated in the presence of 0.1-10 mM hydrogen peroxide for 30 min. The NADH-CoQ reductase and ATP synthase activities were inhibited to 77% and 67% of control, respectively, following an exposure to 10 mM hydrogen peroxide for 30 min. The adenine nucleotide translocase activities were inhibited in a concn- and time-dependent manner and by 10 mM hydrogen peroxide to 44% of control. The dose-response relationship indicated that the translocase was the most susceptible to hydrogen peroxide among the three enzymes studied. Combined treatment of myocytes with 3-amino-1,2,4-triazole, 1,3-bis(2-chloroethyl)-1-nitrosourea and diethyl maleate (to inactivate catalase, to inhibit glutathione reductase activity, and to deplete glutathione, respectively) enhanced the sensitivity of translocase to hydrogen peroxide. Hydrogen peroxide can cause dysfunction in mitochondrial energy transduction, principally as the result of inhibition of adenine nucleotide translocase. [Tatsumi T, Kako KJ; Basic Res Cardiol 88 (3): 199-211 (1993)]**PEER REVIEWED** METABOLISM/PHARMACOKINETICS: METABOLISM/METABOLITES: WHEN HYDROGEN PEROXIDE COMES IN CONTACT WITH CATALASE, AN ENZYME FOUND IN BLOOD AND MOST TISSUES, IT IS RAPIDLY DECOMPOSED INTO OXYGEN AND WATER ... IN WOUNDS & ON MUCOUS MEMBRANES. [American Medical Association. AMA Drug Evaluations Annual 1991. Chicago, IL: American Medical Association, 1991. 1438]**PEER REVIEWED** ABSORPTION, DISTRIBUTION & EXCRETION: WHEN ... APPLIED TO TISSUE ... SOLUTIONS OF HYDROGEN PEROXIDE HAVE POOR PENETRABILITY. [Gilman, A. G., L. S. Goodman, and A. Gilman. (eds.). Goodman and Gilman's The Pharmacological Basis of Therapeutics. 6th ed. New York: Macmillan Publishing Co., Inc. 1980. 974]**PEER REVIEWED** MECHANISM OF ACTION: The pharmacologic activity of the drug depends on the release of nascent oxygen which has a powerful oxidizing effect that destroys some microorganisms and chemically alters many organic substances. When hydrogen peroxide topical solution comes in contact with tissues that contain the enzyme catalase, the solution releases oxygen which exerts antibacterial action; the mechanical effect of effervescence loosens tissue debris and pus. The release of nascent oxygen and effervescence is more rapid on wounds, denuded areas, and mucous membranes than on unbroken skin. The presence of reactive organic material such as pus and blood diminishes the efficiency of hydrogen peroxide. The antibacterial activity of hydrogen peroxide is relatively weak and slow and the drug exhibits poor tissue and wound penetration. Hydrogen peroxide's mechanical effect of effervescence and resultant removal of tissue debris is probably a more effective means of reducing the bacterial content of wounds, denuded areas, and mucous membranes than actual antibacterial activity. The drug also appears to have a styptic effect when applied topically to minor wounds. Concentrated solutions of hydrogen peroxide have a bleaching effect on hair and may injure tissue. [McEvoy, G.K. (ed.). American Hospital Formulary Service - Drug Information 93. Bethesda, MD: American Society of Hospital Pharmacists, Inc., 1993 (Plus Supplements, 1993). 1753]**PEER REVIEWED** PHARMACOLOGY: THERAPEUTIC USES: Anti-Infective Agents, Local; Oxidants [National Library of Medicine's Medical Subject Headings online file (MeSH, 1999)]**QC REVIEWED** Hydrogen peroxide topical solution is used to cleanse wounds, suppurating ulcers, and local infections. Hydrogen peroxide topical solution has been used in the treatment of inflammatory conditions of the external auditory canal and as a mouthwash or gargle (eg, in the treatment of pharyngitis or Vincent's stomatitis). Hydrogen peroxide has also been applied in root canals of teeth or other dental pulp cavities. [McEvoy, G.K. (ed.). American Hospital Formulary Service - Drug Information 93. Bethesda, MD: American Society of Hospital Pharmacists, Inc., 1993 (Plus Supplements, 1993). 1753]**PEER REVIEWED** Hydrogen peroxide topical solution has also been used as a vaginal douche and, following rectal instillation of warm mineral oil, as a rectal enema in the treatment of fecal impaction. More potent solutions (eg, 20-30%) have been used as a hair bleach and as a toothbleaching agent. [McEvoy, G.K. (ed.). American Hospital Formulary Service - Drug Information 93. Bethesda, MD: American Society of Hospital Pharmacists, Inc., 1993 (Plus Supplements, 1993). 1753]**PEER REVIEWED** Hydrogen peroxide topical gel is used to cleanse minor wounds or minor gum inflammation resulting from minor dental procedures, orthodontic appliances, denture irritations, accidental injury, and other mouth and gum irritations (eg, canker sores). [McEvoy, G.K. (ed.). American Hospital Formulary Service - Drug Information 93. Bethesda, MD: American Society of Hospital Pharmacists, Inc., 1993 (Plus Supplements, 1993). 1753]**PEER REVIEWED** DRUG WARNINGS: Hydrogen peroxide topical solution is acidic to the taste and to litmus paper and produces a froth in the mouth; because hydrogen-peroxide concentrate is caustic, it should not be tasted undiluted. [McEvoy, G.K. (ed.). American Hospital Formulary Service - Drug Information 93. Bethesda, MD: American Society of Hospital Pharmacists, Inc., 1993 (Plus Supplements, 1993). 1753]**PEER REVIEWED** ENVIRONMENTAL FATE & EXPOSURE: PROBABLE ROUTES OF HUMAN EXPOSURE: Inhalation of vapor or mist, ingestion, eye and skin contact. [Sittig, M. Handbook of Toxic and Hazardous Chemicals and Carcinogens, 1985. 2nd ed. Park Ridge, NJ: Noyes Data Corporation, 1985. 510]**PEER REVIEWED** NATURAL POLLUTION SOURCES: Gaseous hydrogen peroxide is recognized to be a key component and product of the earth's lower atmospheric photochemical reactions, both in a clean and polluted atmosphere. Atmospheric hydrogen peroxide is believed to be generated exclusively by gas-phase photochemical reactions. [IARC MONOGRAPHS 1972-PRESENT V36 p.291]**PEER REVIEWED** ATMOSPHERIC CONCENTRATIONS: Measurements of hydrogen peroxide concentrations in the gas-phase and in cloud water were obtained in the vicinity of the USA Carolinas coast between late Jan and early Mar 1986. Gas phase concentrations, determined by a fluorometric method, were always less than 2.4 ppb and generally less than 1 ppb. Vertical profiles of hydrogen peroxide in the clear air around clouds and storm systems were highly variable. Concentrations of hydrogen peroxide in cloud water ranged from the detection limit of 0.3 uM to 112 uM, with higher values generally occurring in the vicinity of lightning activity. Hydrogen peroxide concentrations in cloud water were well below those calculated to be in Henry's law equilibrium with gas-phase concentrations of hydrogen peroxide in the cloudy air. [Barth MC et al; Tellus 41B (1): 61-9 (1989)]**PEER REVIEWED** ENVIRONMENTAL STANDARDS & REGULATIONS: FIFRA REQUIREMENTS: In 1988, Congress amended FIFRA to strengthen and accelerate EPA's reregistration program. The nine-year reregistration scheme mandated by "FIFRA 88" applies to each registered pesticide product containing an active ingredient initially registered before November 1, 1984. Pesticides for which EPA had not issued Registration Standards prior to the effective date of FIFRA '88 were divided into three lists based upon their potential for exposure and other factors, with List B being of highest concern and D of least.List: D; Case: Peroxy cmpds.; Case No.: 4072; Pesticide type: Fungicide, Herbicide, Rodenticide, and Antimicrobial; Case Status: Awaiting Data/Data in Review: OPP awaits data from the pesticide's producer(s) regarding its human health and/or environmental effects, or OPP has received and is reviewing such data, in order to reach a decision about the pesticide's eligibility for reregistration. Active Ingredient (AI): HYDROGEN PEROXIDE; AI Status: The producer(s) of the pesticide has made commitments to conduct the studies and pay the fees required for reregistration, and is meeting those commitments in a timely manner. [USEPA/OPP; Status of Pesticides in Reregistration and Special Review p.252 (Mar, 1992) EPA 700-R-92-004]**PEER REVIEWED** CERCLA REPORTABLE QUANTITIES: Releases of CERCLA hazardous substances are subject to the release reporting requirement of CERCLA section 103, codified at 40 CFR part 302, in addition to the requirements of 40 CFR part 355. Hydrogen peroxide (Conc > 52%) is an extremely hazardous substance (EHS) subject to reporting requirements when stored in amounts in excess of its threshold planning quantity (TPQ) of 1,000 lbs. [40 CFR 355 (7/1/97)]**QC REVIEWED** FDA REQUIREMENTS: Hydrogen peroxide may be safely used as a component ofarticles intended for use in packaging, transporting, or holding food in accordance with prescribed conditions. [21 CFR 175.105 (4/1/93)]**PEER REVIEWED** Substance added directly to human food affirmed as generally recognized as safe (GRAS) only when used to treat the following food within /specific/ limitations: milk, whey, dried eggs, tripe, beef feet, herring, wine, starch, instant tea, corn syrup, colored (annatto) cheese whey, wine vinegar, and emulsifiers containing fatty acid esters. [21 CFR 184.1366 (4/1/93)]**PEER REVIEWED** CHEMICAL/PHYSICAL PROPERTIES: MOLECULAR FORMULA: H2-O2 [Budavari, S. (ed.). The Merck Index - Encyclopedia of Chemicals, Drugs and Biologicals. Rahway, NJ: Merck and Co., Inc., 1989. 760]**PEER REVIEWED** MOLECULAR WEIGHT: 34.02 [Budavari, S. (ed.). The Merck Index - Encyclopedia of Chemicals, Drugs and Biologicals. Rahway, NJ: Merck and Co., Inc., 1989. 760]**PEER REVIEWED** COLOR/FORM: A clear, colorless liquid [IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer,1972-PRESENT. (Multivolume work).,p. V36 285 (1985)]**PEER REVIEWED** AT LOW TEMPERATURES A CRYSTALLINE SOLID [Sax, N.I. Dangerous Properties of Industrial Materials. 6th ed. New York, NY: Van Nostrand Reinhold, 1984. 1550]**PEER REVIEWED** Colorless liquid ... [Note: The pure compound is a crystalline solid below 12 degrees F. Often used in an aqueous solution]. [NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997. 168]**QC REVIEWED** ODOR: ODORLESS, OR HAVING AN ODOR RESEMBLING THAT OF OZONE [Osol, A. and J.E. Hoover, et al. (eds.). Remington's Pharmaceutical Sciences. 15th ed. Easton, Pennsylvania: Mack Publishing Co., 1975. 1092]**PEER REVIEWED** ... Slightly sharp odor ... [NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997. 168]**QC REVIEWED** TASTE: SLIGHTLY ACID [Osol, A. and J.E. Hoover, et al. (eds.). Remington's Pharmaceutical Sciences. 15th ed. Easton, Pennsylvania: Mack Publishing Co., 1975. 1092]**PEER REVIEWED** BITTER [Budavari, S. (ed.). The Merck Index - Encyclopedia of Chemicals, Drugs and Biologicals. Rahway, NJ: Merck and Co., Inc., 1989. 760]**PEER REVIEWED** BOILING POINT: 152 DEG C [Budavari, S. (ed.). The Merck Index - Encyclopedia of Chemicals, Drugs and Biologicals. Rahway, NJ: Merck and Co., Inc., 1989. 760]**PEER REVIEWED** MELTING POINT: -0.43 DEG C [Budavari, S. (ed.). The Merck Index - Encyclopedia of Chemicals, Drugs and Biologicals. Rahway, NJ: Merck and Co., Inc., 1989. 760]**PEER REVIEWED** DENSITY/SPECIFIC GRAVITY: 1.463 @ 0 DEG C/4 DEG C [Budavari, S. (ed.). The Merck Index - Encyclopedia of Chemicals, Drugs and Biologicals. Rahway, NJ: Merck and Co., Inc., 1989. 760]**PEER REVIEWED** HEAT OF VAPORIZATION: 51.6 kJ/mol at 25 deg C [Lide, D.R. (ed.). CRC Handbook of Chemistry and Physics. 73rd ed. Boca Raton, FL: CRC Press Inc., 1992-1993.,p. 6-102]**PEER REVIEWED** PH: SLIGHTLY ACID TO LITMUS PAPER [Osol, A. and J.E. Hoover, et al. (eds.). Remington's Pharmaceutical Sciences. 15th ed. Easton, Pennsylvania: Mack Publishing Co., 1975. 1092]**PEER REVIEWED** SOLUBILITIES: MISCIBLE WITH WATER; SOL IN ETHER; INSOL IN PETROLEUM ETHER [Budavari, S. (ed.). The Merck Index - Encyclopedia of Chemicals, Drugs and Biologicals. Rahway, NJ: Merck and Co., Inc., 1989. 760]**PEER REVIEWED** SOL IN ALCOHOL [Lide, D.R. (ed.). CRC Handbook of Chemistry and Physics. 73rd ed. Boca Raton, FL: CRC Press Inc., 1992-1993.,p. 4-62]**PEER REVIEWED** water solubility = 1X10+6 mg/l @ 25 deg C [Radding SB et al; "Review of The Environmental Fate of Selected Chemicals". NTIS 68-01-2681 (1977)]**QC REVIEWED** SPECTRAL PROPERTIES: INDEX OF REFRACTION: 1.414 AT 22 DEG C/D [Lide, D.R. (ed.). CRC Handbook of Chemistry and Physics. 73rd ed. Boca Raton, FL: CRC Press Inc., 1992-1993.,p. 4-62]**PEER REVIEWED** SURFACE TENSION: 80.4 DYNES/CM @ 20 DEG C [Lewis, R.J., Sr (Ed.). Hawley's Condensed Chemical Dictionary. 12th ed. New York, NY: Van Nostrand Rheinhold Co., 1993 617]**PEER REVIEWED** VAPOR PRESSURE: 1.97 mm Hg @ 25 deg C /calculated from experimentally derived coefficients/ [Daubert, T.E., R.P. Danner. Physical and Thermodynamic Properties of Pure Chemicals Data Compilation. Washington, D.C.: Taylor and Francis, 1989.]**QC REVIEWED** VISCOSITY: 1.245 CENTIPOISES [Lewis, R.J., Sr (Ed.). Hawley's Condensed Chemical Dictionary. 12th ed. New York, NY: Van Nostrand Rheinhold Co., 1993 617]**PEER REVIEWED** OTHER CHEMICAL/PHYSICAL PROPERTIES: STRONG OXIDIZER [Budavari, S. (ed.). The Merck Index - Encyclopedia of Chemicals, Drugs and Biologicals. Rahway, NJ: Merck and Co., Inc., 1989. 760]**PEER REVIEWED** DENSITY, SOLID: 1.71 G/CC [Lewis, R.J., Sr (Ed.). Hawley's Condensed Chemical Dictionary. 12th ed. New York, NY: Van Nostrand Rheinhold Co., 1993 617]**PEER REVIEWED** DENSITY OF 3% SOLN: ABOUT 1.00; DENSITY OF 30% SOLN: ABOUT 1.11 [The Merck Index. 9th ed. Rahway, New Jersey: Merck & Co., Inc., 1976. 633]**PEER REVIEWED** Heat of fusion: 12.5 kJ/mol [Lide, D.R. (ed.). CRC Handbook of Chemistry and Physics. 73rd ed. Boca Raton, FL: CRC Press Inc., 1992-1993.,p. 5-95]**PEER REVIEWED** Heat of Decomposition: -1220 Btu/lb = -676 cal/g = -28.3X10+5 J/kg [U.S. Coast Guard, Department of Transportation. CHRIS - Hazardous Chemical Data. Volume II. Washington, D.C.: U.S. Government Printing Office, 1984-5.]**PEER REVIEWED** Heat of Solution: -20.2 Btu/lb = -11.2 cal/g = -0.469X10+5 J/kg [U.S. Coast Guard, Department of Transportation. CHRIS - Hazardous Chemical Data. Volume II. Washington, D.C.: U.S. Government Printing Office, 1984-5.]**PEER REVIEWED** CHEMICAL SAFETY & HANDLING: DOT EMERGENCY GUIDELINES: Fire or explosion: These substances will accelerate burning when involved in a fire. Some may decompose explosively when heated or involved in a fire. May explode from heat or contamination. Some will react explosively with hydrocarbons (fuels). May ignite combustibles (wood, paper, oil, clothing, etc.). Containers may explode when heated. Runoff may create fire or explosion hazard. /Hydrogen peroxide, aqueous solution, with not less than 8% but less than 20% Hydrogen peroxide; Hydrogen peroxide, aqueous solution, with not less than 20% but not more than 60% Hydrogen peroxide (stabilized as necessary)/ [U.S. Department of Transportation. 1996 North American Emergency Response Guidebook. A Guidebook for First Responders During the Initial Phase of aHazardous Materials/Dangerous Goods Incident. U.S. Department of Transportation (U.S. DOT) Research and Special Programs Administration, Office of HazardousMaterials Initiatives and Training (DHM-50), Washington, D.C. (1996).,p. G-140]**QC REVIEWED** Health: Inhalation, ingestion or contact (skin, eyes) with vapors or substance may cause severe injury, burns, or death. Fire may produce irritating, corrosive and/or toxic gases. Runoff from fire control or dilution water may cause pollution. /Hydrogen peroxide, aqueous solution, with not less than 8% but less than 20% Hydrogen peroxide; Hydrogen peroxide, aqueous solution, with not less than 20% but not more than 60% Hydrogen peroxide (stabilized as necessary)/ [U.S. Department of Transportation. 1996 North American Emergency Response Guidebook. A Guidebook for First Responders During the Initial Phase of aHazardous Materials/Dangerous Goods Incident. U.S. Department of Transportation (U.S. DOT) Research and Special Programs Administration, Office of HazardousMaterials Initiatives and Training (DHM-50), Washington, D.C. (1996).,p. G-140]**QC REVIEWED** Public safety: CALL Emergency Response Telephone Number on Shipping Paper first. If Shipping Paper not available or no answer, refer to appropriate telephone number listed on the inside back cover. Isolate spill or leak area immediately for at least 10 to 25 meters (30 to 80 feet) in all directions. Keep unauthorized personnel away. Stay upwind. Keep out of low areas. Ventilate closed spaces before entering. /Hydrogen peroxide, aqueous solution, with not less than 8% but less than 20% Hydrogen peroxide; Hydrogen peroxide, aqueous solution, with not less than 20% but not more than 60% Hydrogen peroxide (stabilized as necessary)/ [U.S. Department of Transportation. 1996 North American Emergency Response Guidebook. A Guidebook for First Responders During the Initial Phase of aHazardous Materials/Dangerous Goods Incident. U.S. Department of Transportation (U.S. DOT) Research and Special Programs Administration, Office of HazardousMaterials Initiatives and Training (DHM-50), Washington, D.C. (1996).,p. G-140]**QC REVIEWED** Protective clothing: Wear positive pressure self-contained breathing apparatus (SCBA). Structural firefighters' protective clothing will only provide limited protection. /Hydrogen peroxide, aqueous solution, with not less than 8% but less than 20% Hydrogen peroxide; Hydrogen peroxide, aqueous solution, with not less than 20% but not more than 60% Hydrogen peroxide (stabilized as necessary)/ [U.S. Department of Transportation. 1996 North American Emergency Response Guidebook. A Guidebook for First Responders During the Initial Phase of aHazardous Materials/Dangerous Goods Incident. U.S. Department of Transportation (U.S. DOT) Research and Special Programs Administration, Office of HazardousMaterials Initiatives and Training (DHM-50), Washington, D.C. (1996).,p. G-140]**QC REVIEWED** Evacuation: Large spill: Consider initial downwind evacuation for at least 100 meters (330 feet). Fire: If tank, rail car or tank truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions. /Hydrogen peroxide, aqueous solution, with not less than 8% but less than 20% Hydrogen peroxide; Hydrogen peroxide, aqueous solution, with not less than 20% but not more than 60% Hydrogen peroxide (stabilized as necessary)/ [U.S. Department of Transportation. 1996 North American Emergency Response Guidebook. A Guidebook for First Responders During the Initial Phase of aHazardous Materials/Dangerous Goods Incident. U.S. Department of Transportation (U.S. DOT) Research and Special Programs Administration, Office of HazardousMaterials Initiatives and Training (DHM-50), Washington, D.C. (1996).,p. G-140]**QC REVIEWED** Fire: Small fires: Do not use dry chemicals, CO2, Halon or foams. Use water only. Large fires: Flood fire area with water from a distance. Move containers from fire area if you can do it without risk. Do not move cargo or vehicle if cargo has been exposed to heat. Fight fire from maximum distance or use unmanned hose holders or monitor nozzles. Cool containers with flooding quantities of water until well after fire is out. ALWAYS stay away from the ends of tanks. For massive fire, use unmanned hose holders or monitor nozzles; if this is impossible, withdraw from area and let fire burn. /Hydrogen peroxide, aqueous solution, with not less than 8% but less than 20% Hydrogen peroxide; Hydrogen peroxide, aqueous solution, with not less than 20% but not more than 60% Hydrogen peroxide (stabilized as necessary)/ [U.S. Department of Transportation. 1996 North American Emergency Response Guidebook. A Guidebook for First Responders During the Initial Phase of aHazardous Materials/Dangerous Goods Incident. U.S. Department of Transportation (U.S. DOT) Research and Special Programs Administration, Office of HazardousMaterials Initiatives and Training (DHM-50), Washington, D.C. (1996).,p. G-140]**QC REVIEWED** Spill or leak: Keep combustibles (wood, paper, oil, etc.) away from spilled material. Do not touch damaged containers or spilled material unless wearing appropriate protective clothing. Stop leak if you can do it without risk. Do not get water inside containers. Small dry spills: With clean shovel place material into clean, dry container and cover loosely; move containers from spill area. Small liquid spills: Use a non-combustible material like vermiculite, sand or earth to soak up the product and place into a container for later disposal. Large spills: Dike far ahead of liquid spill for later disposal. Following product recovery, flush area with water. /Hydrogen peroxide, aqueous solution, with not less than 8% but less than 20% Hydrogen peroxide; Hydrogen peroxide, aqueous solution, with not less than 20% but not more than 60% Hydrogen peroxide (stabilized as necessary)/ [U.S. Department of Transportation. 1996 North American Emergency Response Guidebook. A Guidebook for First Responders During the Initial Phase of aHazardous Materials/Dangerous Goods Incident. U.S. Department of Transportation (U.S. DOT) Research and Special Programs Administration, Office of HazardousMaterials Initiatives and Training (DHM-50), Washington, D.C. (1996).,p. G-140]**QC REVIEWED** First aid: Move victim to fresh air. Call emergency medical care. Apply artificial respiration if victim is not breathing. Administer oxygen if breathing is difficult. Remove and isolate contaminated clothing and shoes. In case of contact with substance, immediately flush skin or eyes with running water for at least 20 minutes. Keep victim warm and quiet. Ensure that medical personnel are aware of the material(s) involved, and take precautions to protect themselves. /Hydrogen peroxide, aqueous solution, with not less than 8% but less than 20% Hydrogen peroxide; Hydrogen peroxide, aqueous solution, with not less than 20% but not more than 60% Hydrogen peroxide (stabilized as necessary)/ [U.S. Department of Transportation. 1996 North American Emergency Response Guidebook. A Guidebook for First Responders During the Initial Phase of aHazardous Materials/Dangerous Goods Incident. U.S. Department of Transportation (U.S. DOT) Research and Special Programs Administration, Office of HazardousMaterials Initiatives and Training (DHM-50), Washington, D.C. (1996).,p. G-140]**QC REVIEWED** Fire or explosion: May explode from friction, heat or contamination. These substances will accelerate burning when involved in a fire. May ignite combustibles (wood, paper, oil, clothing, etc.). Some will react explosively with hydrocarbons (fuels). Containers may explode when heated. Runoff may create fire or explosion hazard. /Hydrogen peroxide, aqueous solution, stabilized, with more than 60% Hydrogen peroxide; Hydrogen peroxide, stabilized/ [U.S. Department of Transportation. 1996 North American Emergency Response Guidebook. A Guidebook for First Responders During the Initial Phase of aHazardous Materials/Dangerous Goods Incident. U.S. Department of Transportation (U.S. DOT) Research and Special Programs Administration, Office of HazardousMaterials Initiatives and Training (DHM-50), Washington, D.C. (1996).,p. G-143]**QC REVIEWED** Health: TOXIC; inhalation, ingestion or contact (skin, eyes) with vapors, dusts or substance may cause severe injury, burns, or death. Fire may produce irritating and/or toxic gases. Toxic fumes or dust may accumulate in confined areas (basement, tanks, hopper/tank cars, etc.). Runoff from fire control or dilution water may cause pollution. /Hydrogen peroxide, aqueous solution, stabilized, with more than 60% Hydrogen peroxide; Hydrogen peroxide, stabilized/ [U.S. Department of Transportation. 1996 North American Emergency Response Guidebook. A Guidebook for First Responders During the Initial Phase of aHazardous Materials/Dangerous Goods Incident. U.S. Department of Transportation (U.S. DOT) Research and Special Programs Administration, Office of HazardousMaterials Initiatives and Training (DHM-50), Washington, D.C. (1996).,p. G-143]**QC REVIEWED** Public safety: CALL Emergency Response Telephone Number on Shipping Paper first. If Shipping Paper not available or no answer, refer to appropriate telephone number listed on the inside back cover. Isolate spill or leak area immediately for at least 50 to lOO meters (160 to 330 feet) in all directions. Keep unauthorized personnel away. Stay upwind. Keep out of low areas. Ventilate closed spaces before entering. /Hydrogen peroxide, aqueous solution, stabilized, with more than 60% Hydrogen peroxide; Hydrogen peroxide, stabilized/ [U.S. Department of Transportation. 1996 North American Emergency Response Guidebook. A Guidebook for First Responders During the Initial Phase of aHazardous Materials/Dangerous Goods Incident. U.S. Department of Transportation (U.S. DOT) Research and Special Programs Administration, Office of HazardousMaterials Initiatives and Training (DHM-50), Washington, D.C. (1996).,p. G-143]**QC REVIEWED** Protective clothing: Wear positive pressure self-contained breathing apparatus (SCBA). Wear chemical protective clothing which is specifically recommended by the manufacturer. Structural firefighters' protective clothing is recommended for fire situations ONLY; it is not effective in spill situations. /Hydrogen peroxide, aqueous solution, stabilized, with more than 60% Hydrogen peroxide; Hydrogen peroxide, stabilized/ [U.S. Department of Transportation. 1996 North American Emergency Response Guidebook. A Guidebook for First Responders During the Initial Phase of aHazardous Materials/Dangerous Goods Incident. U.S. Department of Transportation (U.S. DOT) Research and Special Programs Administration, Office of HazardousMaterials Initiatives and Training (DHM-50), Washington, D.C. (1996).,p. G-143]**QC REVIEWED** Evacuation: Spill: See the Table of Initial Isolation and Protective Action Distances for highlighted substances. For non-highlighted substances, increase, in the downwind direction, as necessary, the isolation distance shown under "PUBLIC SAFETY". Fire: If tank, rail car or tank truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions. /Hydrogen peroxide, aqueous solution, stabilized, with more than 60% Hydrogen peroxide; Hydrogen peroxide, stabilized/ [U.S. Department of Transportation. 1996 North American Emergency Response Guidebook. A Guidebook for First Responders During the Initial Phase of aHazardous Materials/Dangerous Goods Incident. U.S. Department of Transportation (U.S. DOT) Research and Special Programs Administration, Office of HazardousMaterials Initiatives and Training (DHM-50), Washington, D.C. (1996).,p. G-143]**QC REVIEWED** Fire: Small fires: Do not use dry chemicals, CO2, Halon or foams. Use water only. Large fires: Flood fire area with water from a distance. Do not move cargo or vehicle if cargo has been exposed to heat. Move containers from fire area if you can do it without risk. Do not get water inside containers: a violent reaction may occur. Cool containers with flooding quantities of water until well after fire is out. Dike fire-control water for later disposal. ALWAYS stay away from the ends of tanks. For massive fire, use unmanned hose holders or monitor nozzles; if this is impossible, withdraw from area and let fire burn. /Hydrogen peroxide, aqueous solution, stabilized, with more than 60% Hydrogen peroxide; Hydrogen peroxide, stabilized/ [U.S. Department of Transportation. 1996 North American Emergency Response Guidebook. A Guidebook for First Responders During the Initial Phase of aHazardous Materials/Dangerous Goods Incident. U.S. Department of Transportation (U.S. DOT) Research and Special Programs Administration, Office of HazardousMaterials Initiatives and Training (DHM-50), Washington, D.C. (1996).,p. G-143]**QC REVIEWED** Spill or leak: Keep combustibles (wood, paper, oil, etc.) away from spilled material. Do not touch damaged containers or spilled material unless wearing appropriate protective clothing. Use water spray to reduce vapors or divert vapor cloud drift. Prevent entry into waterways, sewers, basements or confined areas. Small spills: Flush area with flooding quantities of water. Large spills: DO NOT CLEAN-UP OR DISPOSE OF, EXCEPT UNDER SUPERVISION OF A SPECIALIST. /Hydrogen peroxide, aqueous solution, stabilized, with more than 60% Hydrogen peroxide; Hydrogen peroxide, stabilized/ [U.S. Department of Transportation. 1996 North American Emergency Response Guidebook. A Guidebook for First Responders During the Initial Phase of aHazardous Materials/Dangerous Goods Incident. U.S. Department of Transportation (U.S. DOT) Research and Special Programs Administration, Office of HazardousMaterials Initiatives and Training (DHM-50), Washington, D.C. (1996).,p. G-143]**QC REVIEWED** First aid: Move victim to fresh air. Call emergency medical care. Apply artificial respiration if victim is not breathing. Administer oxygen if breathing is difficult. Remove and isolate contaminated clothing and shoes. In case of contact with substance, immediately flush skin or eyes with running water for at least 20 minutes. Keep victim warm and quiet. Ensure that medical personnel are aware of the material(s) involved, and take precautions to protect themselves. /Hydrogen peroxide, aqueous solution, stabilized, with more than 60% Hydrogen peroxide; Hydrogen peroxide, stabilized/ [U.S. Department of Transportation. 1996 North American Emergency Response Guidebook. A Guidebook for First Responders During the Initial Phase of aHazardous Materials/Dangerous Goods Incident. U.S. Department of Transportation (U.S. DOT) Research and Special Programs Administration, Office of HazardousMaterials Initiatives and Training (DHM-50), Washington, D.C. (1996).,p. G-143]**QC REVIEWED** SKIN, EYE AND RESPIRATORY IRRITATIONS: Marked irritation - eye, nose, throat, skin [Cralley, L.J., L.V. Cralley (eds.). Patty's Industrial Hygiene and Toxicology. Volume III: Theory and Rationale of Industrial Hygiene Practice. 2nd ed., 3A:The Work Environment. New York, NY: John Wiley Sons, 1985. 171]**PEER REVIEWED** FIRE POTENTIAL: DANGEROUS/FIRE HAZARD/ BY CHEMICAL REACTION WITH FLAMMABLE MATERIALS. HYDROGEN PEROXIDE IS A POWERFUL OXIDIZER, PARTICULARLY IN THE CONCENTRATED STATE. IT IS IMPORTANT TO KEEP CONTAINERS ... COVERED BECAUSE 1) UNCOVERED CONTAINERS ... MORE PRONE TO REACT WITH FLAMMABLE VAPORS, GASES, ETC.; 2) ... IF UNCOVERED, THEWATER FROM HYDROGEN PEROXIDE SOLN CAN EVAPORATE, CONCENTRATING THE /REMAINING/ MATERIAL AND THUS INCREASING THE FIRE HAZARD. [Sax, N.I. Dangerous Properties of Industrial Materials. 6th ed. New York, NY: Van Nostrand Reinhold, 1984. 1551]**PEER REVIEWED** ... SOLN OF HYDROGEN PEROXIDE OF CONCN IN EXCESS OF 65 WT% HEAT UP SPONTANEOUSLYWHEN DECOMPOSING TO WATER + 1/2 OXYGEN. THUS 90 WT% SOLN, WHEN CAUSED TO DECOMPOSE RAPIDLY DUE TO THE INTRODUCTION OF A CATALYTIC DECOMPOSITION AGENT, CAN GET QUITE HOT AND PERHAPS START FIRES. [Sax, N.I. Dangerous Properties of Industrial Materials. 6th ed. New York, NY: Van Nostrand Reinhold, 1984. 1551]**PEER REVIEWED** CONCENTRATIONS OF 50% OR LESS WILL NOT USUALLY IGNITE COMBUSTIBLE MATERIALS IMMEDIATELY UPON CONTACT, BUT PREFERENTIAL EVAPORATION OF H2O CAN INCREASE PEROXIDE CONCN SUFFICIENTLY TO CAUSE DELAYED IGNITION. [International Labour Office. Encyclopedia of Occupational Health and Safety. Volumes I and II. New York: McGraw-Hill Book Co., 1971. 696]**PEER REVIEWED** Hydrogen peroxide is not itself flammable but can cause spontaneous combustion of flammable materials and continued support of the combustion because it liberates oxygen as it decomposes. [International Labour Office. Encyclopedia of Occupational Health and Safety. Vols. I&II. Geneva, Switzerland: International Labour Office, 1983. 1089]**PEER REVIEWED** FIRE INVOLVING HYDROGEN PEROXIDE CAN BE OF THE FLARING TYPE BUT ARE NOT EXPLOSIVE UNLESS CONFINED. [International Labour Office. Encyclopedia of Occupational Health and Safety. Volumes I and II. New York: McGraw-Hill Book Co., 1971. 696]**PEER REVIEWED** Drying of concentrated product on clothing or other combustible material may cause fire. [Armour, M.A. Hazardous Laboratory Chemicals Disposal Guide. Boca Raton, FL: CRC Press Inc., 1991. 181]**PEER REVIEWED** Leakage from drums of 35% hydrogen peroxide onto a wooden pallet caused ignition of the latter when it was moved. Combustion, though limited in area, was fierce and took some time to extinguish. Leakage of 50% peroxide onto supporting pallets under polythene sheeting led to spontaneous ignition and a fierce fire. Contact of 50% peroxide with wood does not usually lead to spontaneous ignition, but hot weather, dry wood and the thermal insulation of the cover may have contributed to ignition. [Bretherick, L. Handbook of Reactive Chemical Hazards. 3rd ed. Boston, MA: Butterworths, 1985. 1163]**PEER REVIEWED** FIRE FIGHTING PROCEDURES: Fires caused by the compound are best controlled by large amounts of water. Chemical extinguishers should be used as they hasten decomposition of the peroxide. Fire fighters should wear goggles and self contained breathing apparatus. [International Labour Office. Encyclopedia of Occupational Health and Safety. Vols. I&II. Geneva, Switzerland: International Labour Office, 1983. 1089]**PEER REVIEWED** Water for fires resulting from spillage. [U.S. Coast Guard, Department of Transportation. CHRIS - Hazardous Chemical Data. Volume II. Washington, D.C.: U.S. Government Printing Office, 1984-5.]**PEER REVIEWED** EXPLOSIVE LIMITS & POTENTIAL: VAPOR CONCENTRATIONS GREATER THAN 40% BY WEIGHT CAN BE DECOMPOSED EXPLOSIVELY @ 1 ATM PRESSURE. [International Labour Office. Encyclopedia of Occupational Health and Safety. Volumes I and II. New York: McGraw-Hill Book Co., 1971. 698]**PEER REVIEWED** EXPLOSION HAZARD: SEVERE, WHEN HIGHLY CONCENTRATED OR PURE H2O2 IS EXPOSED TO HEAT, MECHANICAL IMPACT, DETONATION OF A BLASTING CAP, OR CAUSED TO DECOMPOSE CATALYTICALLY BY METALS & THEIR SALTS, DUSTS & ALKALIES. [Martin, E. W. (ed.). Hazards of Medication. 2nd ed. Philadelphia: J.B. Lippincott Co., l978. 730]**PEER REVIEWED** ALTHOUGH MANY MIXTURES OF HYDROGEN PEROXIDE & ORG MATERIALS DO NOT EXPLODE UPON CONTACT, THE RESULTANT COMBINATION IS DETONATABLE EITHER UPON CATCHING FIRE OR BY IMPACT. DETONATION VELOCITY OF AQ SOLN ... FOUND TO BE ABOUT 6500 M/SEC FOR SOLN OF BETWEEN 96 WT% & 100 WT% HYDROGEN PEROXIDE. [Sax, N.I. Dangerous Properties of Industrial Materials. 6th ed. New York, NY: Van Nostrand Reinhold, 1984. 1551]**PEER REVIEWED** ANOTHER SOURCE OF HYDROGEN PEROXIDE EXPLOSIONS IS FROM SEALING THE MATERIAL IN STRONG CONTAINERS. UNDER SUCH CONDITIONS EVEN GRADUAL DECOMPOSITION OF HYDROGEN PEROXIDE TO WATER + 1/2 OXYGEN CAN CAUSE LARGE PRESSURES TO BUILD UP IN THE CONTAINERS WHICH MAY BURST EXPLOSIVELY. [Sax, N.I. Dangerous Properties of Industrial Materials. 6th ed. New York, NY: Van Nostrand Reinhold, 1984. 1551]**PEER REVIEWED** UNDER ORDINARY STORAGE CONDITIONS, PEROXIDE VAPORS ARE NOT LIKELY TO BECOME EXPLOSIVE. A SOURCE OF EXTERNAL HEAT COULD ... INCREASE VAPOR TEMP OF HIGHLY CONCENTRATED PEROXIDE SUFFICIENTLY FOR THE VAPOR TO BECOME EXPLOSIVE. [International Labour Office. Encyclopedia of Occupational Health and Safety. Volumes I and II. New York: McGraw-Hill Book Co., 1971. 696]**PEER REVIEWED** AT ATMOSPHERIC PRESSURE VAPOR CONTAINING 40% OR MORE BY WT OF H202 MAY DECOMPOSE EXPLOSIVELY @ TEMP BELOW THE BOILING POINT OF THE LIQUID. THESE EXPLOSIONS CAN BE INITIATED BY A HOT WIRE, BY CATALYTIC IMPURITIES, BY ALUMINUM SURFACES AT 150 DEG C ETC. [International Labour Office. Encyclopedia of Occupational Health and Safety. Volumes I and II. New York: McGraw-Hill Book Co., 1971. 696]**PEER REVIEWED** Soluble fuels (acetone, ethanol, glycerol) will detonate on admixture with peroxide of over 30% concentration, the violence increasing with concentration. [Bretherick, L. Handbook of Reactive Chemical Hazards. 3rd ed. Boston, MA: Butterworths, 1985. 1150]**PEER REVIEWED** An organic sulfur compound containing an acetal function had been oxidized to the sulfone with 30% hydrogen peroxide in acetic acid. After the liquor had been concentrated by vacuum distillation at 50-60 deg C, the residue exploded during handling. ... Interaction /with acetaldehyde/ gives the extremely explosive poly(ethylidene) peroxide. [Bretherick, L. Handbook of Reactive Chemical Hazards. 3rd ed. Boston, MA: Butterworths, 1985. 1151]**PEER REVIEWED** Acetone and hydrogen peroxide readily form explosive dimeric and trimeric cyclic peroxides, particularly during evaporation of the mixture. Many explosions have occurred during work-up of peroxide reactions run in acetone solvent, including partial hydrolysis of a nitrile and oxidation of 2,2'-thiodiethanol and of an unspecified material. [Bretherick, L. Handbook of Reactive Chemical Hazards. 3rd ed. Boston, MA: Butterworths, 1985. 1152]**PEER REVIEWED** Homogeneous mixtures of concentrated peroxide with alcohols or other peroxide miscible organic liquids are capable of detonation by shock or heat. ... During conversion of alcohols to hydroperoxides, the order of mixing of reagents is important. Addition of concentrated acid to mixtures of an alcohol and concentrated peroxide almost inevitably leads to explosion, particularly if the mixture is inhomogeneous and the alcohol is a solid. [Bretherick, L. Handbook of Reactive Chemical Hazards. 3rd ed. Boston, MA: Butterworths, 1985. 1153]**PEER REVIEWED** Conversion of the acid to diperoxyazelaic acid in hydrogen peroxide/sulfuric acid medium at 45-50 deg C was uncontrollabley exothermic and led to explosion. [Bretherick, L. Handbook of Reactive Chemical Hazards. 3rd ed. Boston, MA: Butterworths, 1985. 1154]**PEER REVIEWED** Evaporation of an ethereal solution of hydrogen peroxide gave a residue of which a drop on a platinum spatula exploded weakly on exposure to flame. When the sample (1-2 g) was stirred with a glass rod (not fire polished), an extremely violent detonation occurred. [Bretherick, L. Handbook of Reactive Chemical Hazards. 3rd ed. Boston, MA: Butterworths, 1985. 1155]**PEER REVIEWED** Interaction gives a hydrated basic peroxide which decomposes explosively at 80-90 deg C. [Bretherick, L. Handbook of Reactive Chemical Hazards. 3rd ed. Boston, MA: Butterworths, 1985. 1156]**PEER REVIEWED** Addition of 30% peroxide and sulfuric acid to 2-methylpyridine and iron(II) sulfate caused a sudden exotherm, followed by a vapor phase explosion and ignition. [Bretherick, L. Handbook of Reactive Chemical Hazards. 3rd ed. Boston, MA: Butterworths, 1985. 1157]**PEER REVIEWED** Interaction with excess ketene rapidly forms explosive diacetyl peroxide. [Bretherick, L. Handbook of Reactive Chemical Hazards. 3rd ed. Boston, MA: Butterworths, 1985. 1157]**PEER REVIEWED** Directions given for the preparation of 2-phenyl-1,1-dimethylethyl hydroperoxideby adding sulfuric acid to a mixture of the alcohol and 90% hydrogen peroxide are wrong and will lead to explosion. [Bretherick, L. Handbook of Reactive Chemical Hazards. 3rd ed. Boston, MA: Butterworths, 1985. 1161]**PEER REVIEWED** Preparative reactions involving oxidation of tetrahydrothiophene to the sulfoxide by slow addition of 37% peroxide solutions exploded violently on 3 occasions. No explanation is apparent, and similar reactions had been run uneventfully over a period of 10 years. [Bretherick, L. Handbook of Reactive Chemical Hazards. 3rd ed. Boston, MA: Butterworths, 1985. 1162]**PEER REVIEWED** HAZARDOUS REACTIVITIES & INCOMPATIBILITIES: Oxidizable materials, iron, copper, brass, bronze, chromium, zinc, lead, silver, manganese [Note: Contact with combustible material may result in SPONTANEOUS combustion]. [NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997. 168]**QC REVIEWED** Most cellulose materials contain enough catalyst to cause spontaneous ignition with 90% peroxide. Soluble fuels (acetone, ethanol, glycerol) will detonate on admixture with peroxide of over 30% concentration, the violence increasing with concentration. Handling systems must exclude fittings of iron, brass, copper, Monel, and screwed joints caulked with red lead. /Explosive with acetic acid, acetic anhydride, acetone, alcohols, carboxylic acids, nitrogen-containing bases, organic compounds./ Addition of charcoal to concentrated peroxide results in violent decompositon. [Armour, M.A. Hazardous Laboratory Chemicals Disposal Guide. Boca Raton, FL: CRC Press Inc., 1991. 181]**PEER REVIEWED** The solid peroxide produced by action of hydrogen peroxide and nitric acid on thiourea (and possibly a hydrogen peroxidate of thiourea dioxide) decomposed violently on drying in air, with evolution of sulfur dioxide and free sulfur. [Bretherick, L. Handbook of Reactive Chemical Hazards. 3rd ed. Boston, MA: Butterworths, 1985. 1160]**PEER REVIEWED** HAZARDOUS DECOMPOSITION: Contamination of hydrogen peroxide by such metals as copper, cobalt, manganese, chromium, nickel, iron, lead, and their salts, by dust, dirt, oils, various enzymes, rust and undistilled water results in increased rate of decomposition. Decomposition results in the liberation of oxygen and heat. If the solution is dilute, the heat is readily absorbed by the water present. In more concentrated solutions the heat increases the temp of the solution and its decomposition rate. This may lead to an explosion. Contamination with materials containing metal catalysts can result in immediate decomposition and explosive rupture of the container if it is not properly vented. [International Labour Office. Encyclopedia of Occupational Health and Safety. Vols. I&II. Geneva, Switzerland: International Labour Office, 1983. 1089]**PEER REVIEWED** IMMEDIATELY DANGEROUS TO LIFE OR HEALTH: 75 ppm [NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997. 168]**QC REVIEWED** PROTECTIVE EQUIPMENT & CLOTHING: Proper protective equipment, safety goggles, gloves of polychloroprene rubber, polyvinyl chloride, polyethylene, etc, should be used. Aprons and foot and leg covering of similar materials should be used when working with concentrated solutions. [International Labour Office. Encyclopedia of Occupational Health and Safety. Vols. I&II. Geneva, Switzerland: International Labour Office, 1983. 1089]**PEER REVIEWED** Wear appropriate personal protective clothing to prevent skin contact. [NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997. 169]**QC REVIEWED** Wear appropriate eye protection to prevent eye contact. [NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997. 169]**QC REVIEWED** Eyewash fountains should be provided in areas where there is any possibility that workers could be exposed to the substance; this is irrespective of the recommendation involving the wearing of eye protection. [NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997. 169]**QC REVIEWED** Facilities for quickly drenching the body should be provided within the immediate work area for emergency use where there is a possibility of exposure. [Note: It is intended that these facilities provide a sufficient quantity or flow of water to quickly remove the substance from any body areas likely to be exposed. The actual determination of what constitutes an adequate quick drench facility depends on the specific circumstances. In certain instances, a deluge shower should be readily available, whereas in others, the availability of water from a sink or hose could be considered adequate.] [NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997. 169]**QC REVIEWED** Recommendations for respirator selection. Max concn for use: 10 ppm. Respirator Class(es): Any supplied-air respirator. May require eye protection. [NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997. 169]**QC REVIEWED** Recommendations for respirator selection. Max concn for use: 25 ppm. Respirator Class(es): Any supplied-air respirator operated in a continuous flow mode. May require eye protection. [NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997. 169]**QC REVIEWED** Recommendations for respirator selection. Max concn for use: 50 ppm. Respirator Class(es): Any self-contained breathing apparatus with a full facepiece. Any supplied-air respirator with a full facepiece. [NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997. 169]**QC REVIEWED** Recommendations for respirator selection. Max concn for use: 75 ppm. Respirator Class(es): Any supplied-air respirator that has a full facepiece and is operated in a pressure-demand or other positive-pressure mode. [NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997. 169]**QC REVIEWED** Recommendations for respirator selection. Condition: Emergency or planned entry into unknown concn or IDLH conditions: Respirator Class(es): Any self-contained breathing apparatus that has a full facepiece and is operated in a pressure-demand or other positive pressure mode. Any supplied-air respirator with a full facepiece and operated in pressure-demand or other positive pressure mode in combination with an auxiliary self-contained breathing apparatus operated in pressure-demand or other positive pressure mode. [NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997. 169]**QC REVIEWED** Recommendations for respirator selection. Condition: Escape from suddenly occurring respiratory hazards: Respirator Class(es): Any air-purifying, full-facepiece respirator (gas mask) with a chin-style, front- or back-mounted canister providing protection against the compound of concern. Any appropriate escape-type, self-contained breathing apparatus. [NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997. 169]**QC REVIEWED** Protective garments, both outer and inner, made of a woven polyester fabric or of modacrylic or polyvinylidene fabrics; impermeable apron made of polyvinyl chloride or polyethylene film; neoprene gloves and boots; goggles. [U.S. Coast Guard, Department of Transportation. CHRIS - Hazardous Chemical Data. Volume II. Washington, D.C.: U.S. Government Printing Office, 1984-5.]**PEER REVIEWED** PREVENTIVE MEASURES: THE BASIC VENTILATION METHODS ARE LOCAL EXHAUST VENTILATION AND DILUTION OR GENERAL VENTILATION. [Sax, N.I. Dangerous Properties of Industrial Materials. 5th ed. New York: Van Nostrand Rheinhold, 1979. 730]**PEER REVIEWED** ... SUBSTITUTION OF LESS IRRITATING SUBSTANCES ... REDESIGN OF OPERATIONS ... PREVENT CONTACT, PROVISION OF A PHYSICAL BARRIER AGAINST CONTACT, PROPER WASHINGFACILITIES, WORK CLOTHING AND STORAGE FACILITIES, PROTECTIVE CLOTHING, AND BARRIER CREAMS. MEDICAL CONTROL ... . [Sax, N.I. Dangerous Properties of Industrial Materials. 4th ed. New York: Van Nostrand Reinhold, 1975. 819]**PEER REVIEWED** Contact lenses should not be worn when working with this chemical. [NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997. 169]**QC REVIEWED** SRP: The scientific literature for the use of contact lenses in industry is conflicting. The benefit or detrimental effects of wearing contact lenses depend not only upon the substance, but also on factors including the form of the substance, characteristics and duration of the exposure, the uses of other eye protection equipment, and the hygiene of the lenses. However, there may be individual substances whose irritating or corrosive properties are such that the wearing of contact lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In any event, the usual eye protection equipment should be worn even when contact lenses are in place. **PEER REVIEWED** The worker should immediately wash the skin when it becomes contaminated. [NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997. 169]**QC REVIEWED** Work clothing that becomes wet or significantly contaminated should be removed and replaced. [NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997. 169]**QC REVIEWED** STABILITY/SHELF LIFE: HYDROGEN PEROXIDE IS A VERY UNSTABLE COMPOUND THAT BREAKS DOWN READILY TO FORM MOLECULAR OXYGEN AND WATER. [Gilman, A. G., L. S. Goodman, and A. Gilman. (eds.). Goodman and Gilman's The Pharmacological Basis of Therapeutics. 6th ed. New York: Macmillan Publishing Co., Inc. 1980. 974]**PEER REVIEWED** Hydrogen peroxide topical solution deteriorates upon standing or upon repeated agitation, undergoes accelerated decomposition when exposed to light or when in contact with many oxidizing or reducing substances, and decomposes suddenly when heated. Hydrogen peroxide topical solution should be stored in tight, light-resistant containers at 15-30 deg C. To ensure greater stability, the inside surfaces of containers should be as free as possible from rough points since these promote decomposition. [McEvoy, G.K. (ed.). American Hospital Formulary Service - Drug Information 93. Bethesda, MD: American Society of Hospital Pharmacists, Inc., 1993 (Plus Supplements, 1993). 1753]**PEER REVIEWED** PURE HYDROGEN PEROXIDE SOLN, COMPLETELY FREE FROM CONTAMINATION, ARE HIGHLY STABLE [Lewis, R.J., Sr (Ed.). Hawley's Condensed Chemical Dictionary. 12th ed. New York, NY: Van Nostrand Rheinhold Co., 1993 617]**PEER REVIEWED** RELATIVELY STABLE SAMPLE OF HYDROGEN PEROXIDE TYPICALLY DECOMP @ THE RATE OF ABOUT 0.5%/YR @ ROOM TEMP [Lewis, R.J., Sr (Ed.). Hawley's Condensed Chemical Dictionary. 12th ed. New York, NY: Van Nostrand Rheinhold Co., 1993 617]**PEER REVIEWED** SOLN OF H2O2 GRADUALLY DETERIORATE & ARE USUALLY STABILIZED BY ADDITION OF ACETANILIDE OR SIMILAR ORGANIC MATERIALS. AGITATION OR CONTACT WITH ROUGH SURFACES, METALS OR MANY OTHER SUBSTANCES ACCELERATES DECOMP. RAPIDLY DECOMP BY ALKALIES, FINELY DIVIDED METALS; PRESENCE OF MINERAL ACID RENDERS IT MORE STABLE. [Budavari, S. (ed.). The Merck Index - Encyclopedia of Chemicals, Drugs and Biologicals. Rahway, NJ: Merck and Co., Inc., 1989. 760]**PEER REVIEWED** Concentrated peroxide may decompose violently in contact with iron, copper chromium and most other metals and their salts, and dust. [Bretherick, L. Handbook of Reactive Chemical Hazards. 3rd ed. Boston, MA: Butterworths, 1985. 1150]**PEER REVIEWED** The violent decomposition observed on adding charcoal to concentrated hydrogen peroxide is mainly owing to catalysis by metallic impurities present and the active surface of the charcoal, rather than to direct oxidation of the carbon. [Bretherick, L. Handbook of Reactive Chemical Hazards. 3rd ed. Boston, MA: Butterworths, 1985. 1154]**PEER REVIEWED** SHIPMENT METHODS AND REGULATIONS: No person may /transport,/ offer or accept a hazardous material for transportation in commerce unless that person is registered in conformance ... and the hazardous material is properly classed, described, packaged, marked, labeled, and in condition for shipment as required or authorized by ... /the hazardous materials regulations (49 CFR 171-177)./ [49 CFR 171.2 (7/1/96)]**QC REVIEWED** The International Air Transport Association (IATA) Dangerous Goods Regulations are published by the IATA Dangerous Goods Board pursuant to IATA Resolutions 618 and 619 and constitute a manual of industry carrier regulations to be followed by all IATA Member airlines when transporting hazardous materials. [IATA. Dangerous Goods Regulations. 38th ed. Montreal, Canada and Geneva, Switzerland: International Air Transport Association, Dangerous Goods Board, January, 1997. 162]**QC REVIEWED** The International Maritime Dangerous Goods Code lays down basic principles for transporting hazardous chemicals. Detailed recommendations for individual substances and a number of recommendations for good practice are included in the classes dealing with such substances. A general index of technical names has also been compiled. This index should always be consulted when attempting to locate the appropriate procedures to be used when shipping any substance or article. [IMDG; International Maritime Dangerous Goods Code; International Maritime Organization p.5042,5044,5087 (1988)]**QC REVIEWED** STORAGE CONDITIONS: STORE IN ORIGINAL CLOSED CONTAINER. BE SURE THAT CONTAINER VENT IS WORKING... DO NOT ADD ANY OTHER PRODUCT TO CONTAINERS. WHEN EMPTY, RINSE THOROUGHLY WITH CLEAN WATER. /30% SOLN/ [The Merck Index. 9th ed. Rahway, New Jersey: Merck & Co., Inc., 1976. 633]**PEER REVIEWED** Storage tanks should be constructed of high-purity aluminium alloy. Undesirable contamininants must not become imbedded in the aluminium surface, and extreme care should be taken to ensure proper welding techniques. Hydrogen peroxide should be stored only in original containers or in containers of compatible materials which have been properly designed and thoroughly passivated. [International Labour Office. Encyclopedia of Occupational Health and Safety. Vols. I&II. Geneva, Switzerland: International Labour Office, 1983. 1089]**PEER REVIEWED** STORAGE: IN SMALL PACKAGES, SOLN OF H2O2 ARE ALWAYS KEPT IN TIGHT, LIGHT-RESISTANT BOTTLES & PREFERABLY NOT ABOVE 35 DEG C. ... HIGH CONCN OF H2O2 ARE BEST PRESERVED IN PLASTIC (POLYETHYLENE) CONTAINERS, EQUIPPED WITH A PRESSURE RELEASE VALVE IN THE STOPPER, TO MINIMIZE EXPLOSION DUE TO DECOMPOSITION. [Osol, A. and J.E. Hoover, et al. (eds.). Remington's Pharmaceutical Sciences. 15th ed. Easton, Pennsylvania: Mack Publishing Co., 1975. 376]**PEER REVIEWED** Storage Temperature: Ambient; Venting: Safety relief or pressure-vacuum. [U.S. Coast Guard, Department of Transportation. CHRIS - Hazardous Chemical Data. Volume II. Washington, D.C.: U.S. Government Printing Office, 1984-5.]**PEER REVIEWED** Once removed from the original container, the hydrogen peroxide must not be returned to it. Storage containers should be properly vented and kept away from direct heat and sun and combustible materials. [International Labour Office. Encyclopedia of Occupational Health and Safety. Vols. I&II. Geneva, Switzerland: International Labour Office, 1983. 1089]**PEER REVIEWED** DISPOSAL METHODS: Wear butyl rubber gloves, eye protection, and laboratory coat. A body shield should be available. In the fume hood, prepare, a dilute solution (5%) of peroxide by cautiously adding to a large volume of water. Gradually, with stirring, add to a 50% excess of aqueous sodium metabisulfite in a round bottom flask equipped with a thermometer. An increase in temperature indicates that the reaction is taking place. Acidify the reaction if it does not proceed spontaneously. Neutralize the reaction mixture and wash down the drain with at least 50 times its volume of water. [Armour, M.A. Hazardous Laboratory Chemicals Disposal Guide. Boca Raton, FL: CRC Press Inc., 1991. 183]**PEER REVIEWED** Dilute and drain with abundant water. Recommended method: Discharge to sewer. Recommendable method: Discharge to sewer. Not recommendable methods: Evaporation & oxidation. Peer-review: Extreme caution - potentially explosive. Strong oxidizing agent. Handle in new glass or polished clean aluminum. Avoid inhalation. Highly unstable material. (Peer-review conclusions of an IRPTC expert consultation (May 1985)) [United Nations. Treatment and Disposal Methods for Waste Chemicals (IRPTC File). Data Profile Series No. 5. Geneva, Switzerland: United Nations Environmental Programme, Dec. 1985. 191]**PEER REVIEWED** Dilute and drain into the sewer with abundant water. [ITII. Toxic and Hazardous Industrial Chemicals Safety Manual. Tokyo, Japan: The International Technical Information Institute, 1988. 278]**PEER REVIEWED** OCCUPATIONAL EXPOSURE STANDARDS: OSHA STANDARDS: Permissible Exposure Limit: Table Z-1 8-hr Time Weighted Avg: 1 ppm (1.4 mg/cu m). [29 CFR 1910.1000 (7/1/98)]**QC REVIEWED** THRESHOLD LIMIT VALUES: 8 hr Time Weighted Avg (TWA) 1 ppm [American Conference of Governmental Industrial Hygienists. Threshold Limit Values (TLVs) for Chemical Substances and Physical Agents Biological Exposure Indices for 1998. Cincinnati, OH: ACGIH, 1998. 42]**QC REVIEWED** Excursion Limit Recommendation: Excursions in worker exposure levels may exceed three times the TLV-TWA for no more than a total of 30 min during a work day, and under no circumstances should they exceed five times the TLV-TWA, provided that the TLV-TWA is not exceeded. [American Conference of Governmental Industrial Hygienists. Threshold Limit Values (TLVs) for Chemical Substances and Physical Agents Biological Exposure Indices for 1998. Cincinnati, OH: ACGIH, 1998. 6]**QC REVIEWED** NIOSH RECOMMENDATIONS: Recommended Exposure Limit: 10 Hr Time-Weighted Avg: 1 ppm (1.4 mg/cu m). [NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997. 168]**QC REVIEWED** IMMEDIATELY DANGEROUS TO LIFE OR HEALTH: 75 ppm [NIOSH. NIOSH Pocket Guide to Chemical Hazards. DHHS (NIOSH) Publication No. 97-140. Washington, D.C. U.S. Government Printing Office, 1997. 168]**QC REVIEWED** OTHER OCCUPATIONAL PERMISSIBLE LEVELS: Emergency Response Planning Guidelines (ERPG): ERPG(1) 10 ppm (no more than mild, transient effects) for up to 1 hr exposure; ERPG(2) 50 ppm (without serious, adverse effects) for up to 1 hr exposure; ERPG(3) 100 ppm (not life threatening) up to 1 hr exposure. [American Industrial Hygiene Association. The AIHA 1999 Emergency Response Planning Guidelines and Workplace Environmental Exposure Level Guides Handbook.American Industrial Hygiene Association. Fairfax, VA 1999. 26]**QC REVIEWED** MANUFACTURING/USE INFORMATION: MAJOR USES: IN PLASTICS INDUST; WHITE DISCHARGE PRINTING ON INDIGO-DYED WOOL; BLEACHING FEATHERS, HAIR, SILK, STRAWS, IVORY, FLOUR, BONE, GELATIN, & TEXTILE FABRICS; OXIDIZER IN MFR DYES; RENOVATING OLD PAINTING, ENGRAVINGS; DISINFECTING WATER & HIDES; ARTIFICIALLY AGING WINES, LIQUORS, ETC; REFINING OILS & FATS; AS ANTICHLOR; WITH PARAPHENYLENEDIAMINE AS DYE FOR FURS, DEAD HAIR, ETC; IN PHOTOGRAPHY AS HYPO ELIMINANT; WITH NAOH FOR CLEANING METAL SURFACES, FOR GILDING, SILVERING, ETC; IN PHARMACEUTICAL PREPN, MOUTHWASHES, DENTIFRICES, SANITARY LOTIONS /3% SOLN/ [The Merck Index. 9th ed. Rahway, New Jersey: Merck & Co., Inc., 1976. 633]**PEER REVIEWED** INT FOR EPOXIDIZED OIL & ESTER PLASTICIZERS, GLYCERIN, PERACIDS, ORG PEROXIDES; BLEACH FOR GROUNDWOOD & CHEMICAL PULP, FOOD PRODUCTS, MISC APPLICATIONS; IN WASTEWATER TREATMENT; IN BLEACHING CREAM & OTHER COSMETICS. [SRI]**PEER REVIEWED** WHEN DILUTED WITH ONE OR MORE PARTS OF WATER ... IS SOMETIMES EMPLOYED AS A MOUTHWASH, BUT ITS USE TO TREAT STOMATITIS AND GINGIVITIS MAY IRRITATE TONGUE AND BUCCAL MUCOSA. THE 3% SOLUTION OR A SOLUTION DILUTED TO 1.5% IS OFTEN INSTILLED IN EXTERNAL EAR TO AID IN REMOVAL OF CERUMEN. [American Medical Association. AMA Drug Evaluations Annual 1991. Chicago, IL: American Medical Association, 1991. 1439]**PEER REVIEWED** Used to make inorganic peroxide derivatives and organic peroxides [CHEMICAL PRODUCTS SYNOPSIS: Hydrogen Peroxide (1984)]**PEER REVIEWED** Used for hydroxylation and epoxidation [CHEMICAL PRODUCTS SYNOPSIS: Hydrogen Peroxide (1984)]**PEER REVIEWED** Used in food and pharmaceuticals as a bleach and disinfectant [CHEMICAL PRODUCTS SYNOPSIS: Hydrogen Peroxide (1984)]**PEER REVIEWED** Used to leach uranium, hydrometallurgical processing, metal finishing and pollution control [CHEMICAL PRODUCTS SYNOPSIS: Hydrogen Peroxide (1984)]**PEER REVIEWED** 90% soln is used in rocket propulsion; as dough conditioner, maturing and bleaching agent in food; medication: anti-infective; medication (vet): topical antiseptic & cleansing agent (as a dilute soln) [Budavari, S. (ed.). The Merck Index - Encyclopedia of Chemicals, Drugs and Biologicals. Rahway, NJ: Merck and Co., Inc., 1989. 760]**PEER REVIEWED** Hydrogen peroxide is used in the manufacture of acetone, antichlor, antiseptics, benzoyl peroxide, buttons, disinfectants, pharmaceuticals, felt hats, plastic foam, rocket fuel, sponge rubber and pesticides. It is also used in bleaching bone, feathers, flour, fruit, fur, gelatin, glue, hair, ivory, silk, soap, straw, textiles, was, and wood pulp, and as an oxygen source in respiratory protective equipment. [Sittig, M. Handbook of Toxic and Hazardous Chemicals and Carcinogens, 1985. 2nd ed. Park Ridge, NJ: Noyes Data Corporation, 1985. 510]**PEER REVIEWED** Deodorizing of textiles, wood pulp, hair, fur; source of organic and inorganic peroxides; pulp and paper industry; plasticizers; rocket fuel; foam rubber; manufacture of glycerol; antichlor; dyeing; electroplating; antiseptic; laboratory reagent; epozidation, hydroxylation, oxidation, and reduction; viscosity control for starch and cellulose derivatives; refining and cleaning metals; bleaching and oxidizing agent in foods; neutralizing agent in wine distillation; seed disinfectant; substitute for chlorine in water and sewage treatment. [Lewis, R.J., Sr (Ed.). Hawley's Condensed Chemical Dictionary. 12th ed. New York, NY: Van Nostrand Rheinhold Co., 1993 617]**PEER REVIEWED** Wastewater treatment. [Eul W et al; Chem Oxid, Proc Int Symp, 1st; 68-77 (1992)]**PEER REVIEWED** Sterilization and disinfection in industry, water purification. [Fraser JA L; Effluent Water Treat J 26 (5-6): 186-99 (1986)]**PEER REVIEWED** Degradation of organic pollutants by advanced oxidation. [Yue PL; Process Saf Environ Prot 70 (B3): 145-8 (1992)]**PEER REVIEWED** Removal of organic cmpd from wastewater by chemical oxidation with ozone or hydrogen peroxide. [Assink JW; Proces Technol 2 (10): 42-6 (1992)]**PEER REVIEWED** MEDICATION **QC REVIEWED** MANUFACTURERS: DeGussa Corporation, Hq, 65 Challenger Rd, Ridgefield Park, NJ 07660, (201) 641-6100; Production site: Theodore, AL 36590 [SRI. 1992 Directory of Chemical Producers-United States of America. Menlo Park, CA: SRI International, 1992. 706]**PEER REVIEWED** Du Pont Co, Hq, 1007 Market St, Wilmington, DE 19898, (302) 774-1000, (800) 441-7515 (Product Information); Du Pont Chemicals, (800) 441-9442 (Customer Service Center); Production site: Memphis, TN 38127 [SRI. 1992 Directory of Chemical Producers-United States of America. Menlo Park, CA: SRI International, 1992. 706]**PEER REVIEWED** Eka Nobel Inc, Hq, 1519 Johnson Ferry Rd, Suite 200, Marietta, GA 30062, (404) 578-0858, (800) 241-3900; Production site: Columbus, MS 39702 [SRI. 1992 Directory of Chemical Producers-United States of America. Menlo Park, CA: SRI International, 1992. 706]**PEER REVIEWED** FMC Corporation, Hq, 200 E Randolph Dr, Chicago, IL 60601, (312) 861-6000; Chemical Products Group, 1735 Market St, Philadelphia, PA 19103; Peroxygen Chemicals Div; Production sites: Bayport, TX 77062; Spring Hill, WV 25303 [SRI. 1992 Directory of Chemical Producers-United States of America. Menlo Park, CA: SRI International, 1992. 706]**PEER REVIEWED** Fort Howard Corp, Hq, 1919 S Broadway, PO Box 19130, Green Bay, WI 54307-9130, (414) 435-8821; Production site: Muskogee, OK 74401 [SRI. 1992 Directory of Chemical Producers-United States of America. Menlo Park, CA: SRI International, 1992. 706]**PEER REVIEWED** Interox America, Hq, 3333 Richmond Ave, Houston, TX 77227, (713) 522-4155; Production sites: Deer Park, TX 77536, Longview, WA 98632 [SRI. 1992 Directory of Chemical Producers-United States of America. Menlo Park, CA: SRI International, 1992. 706]**PEER REVIEWED** METHODS OF MANUFACTURING: CYCLIC REDUCTION AND OXIDATION OF ALKYL ANTHRAQUINONES [SRI]**PEER REVIEWED** PREPD BY TREATING BARIUM PEROXIDE WITH ACID. [Budavari, S. (ed.). The Merck Index - Encyclopedia of Chemicals, Drugs and Biologicals. Rahway, NJ: Merck and Co., Inc., 1989. 760]**PEER REVIEWED** PRODN OF ANHYDROUS HYDROGEN PEROXIDE BY CONTINUOUS FRACTIONAL CRYSTALLIZATION. [Budavari, S. (ed.). The Merck Index - Encyclopedia of Chemicals, Drugs and Biologicals. Rahway, NJ: Merck and Co., Inc., 1989. 760]**PEER REVIEWED** AUTOXIDATION OF AN ALKYL ANTHRAHYDROQUINONE, SUCH AS THE 2-ETHYL DERIVATIVE, IN A CYCLIC CONTINUOUS PROCESS IN WHICH THE QUINONE FORMED IN THE OXIDATION STEP IS REDUCED TO THE STARTING MATERIAL BY HYDROGEN IN THE PRESENCE OF A SUPPORTED PALLADIUM CATALYST; BY ELECTROLYTIC PROCESSES IN WHICH AQUEOUS SULFURIC ACID OR ACIDIC AMMONIUM BISULFATE IS CONVERTED ELECTROLYTICALLY TO THE PEROXYDISULFATE, WHICH IS THEN HYDROLYZED TO FORM HYDROGEN PEROXIDE; BY AUTOXIDATION OF ISOPROPYL ALC. [Lewis, R.J., Sr (Ed.). Hawley's Condensed Chemical Dictionary. 12th ed. New York, NY: Van Nostrand Rheinhold Co., 1993 617]**PEER REVIEWED** Electrolysis of potassium bisulfate solution to form the corresponding persulfate radical, which was then heated and hydrolysed in an evaporator to remove water and hydrogen peroxide vapors [CHEMICAL PRODUCTS SYNOPSIS: Hydrogen Peroxide, 1984]**PEER REVIEWED** Oxidation of isopropyl alcohol to acetone and hydrogen peroxide [CHEMICAL PRODUCTS SYNOPSIS: Hydrogen Peroxide, 1984]**PEER REVIEWED** GENERAL MANUFACTURING INFORMATION: INCOMPATIBILITIES: ALKALIES, AMMONIA AND THEIR CARBONATES, ALBUMIN, BALSAM PERU, PHENOL, CHARCOAL, CHLORIDES, ALKALI CITRATES; FERROUS, MERCUROUS OR GOLD SALTS; HYPOPHOSPHITES, IODIDES, LIME WATER, PERMANGANATES, SULFITES, TINCTURES, AND ORGANIC MATTER IN GENERAL. /3% SOLN/ [The Merck Index. 9th ed. Rahway, New Jersey: Merck & Co., Inc., 1976. 633]**PEER REVIEWED** IT IS USED AS DISINFECTING GARGLE IN PHARYNGITIS & AS DEODORIZING MOUTH WASH IN STOMATITIS. ... IT IS ALSO EMPLOYED AS MEANS OF CLEANSING WOUNDS & SUPPURATING ULCERS. ... MAIN VALUE IS PROBABLY DUE TO ITS BUBBLING ACTION WHICH REMOVES ORGANIC DETRITUS THAN TO ANY ANTIBACTERIAL EFFECT. [American Hospital Formulary Service. Volumes I and II. Washington, DC: American Society of Hospital Pharmacists, to 1984.,p. 52:28]**PEER REVIEWED** (VET): FORMERLY, AS AN ORAL EMETIC WITH SECONDARY ANTHELMINTIC BENEFITS IN CATS, DOGS, & PIGS, & OF LOW EFFICACY AS WHIPCIDE BY ENEMA. EXPERIMENTALLY, AS AN IV SOURCE OF OXYGEN; TO HELP LOCALIZE ISOTOPES IN CERTAIN TUMORS & POTENTIATE EFFECTS OF RADIATION ON TUMORS; & TO INCR CIRCULATING PLATELETS. [Rossoff, I.S. Handbook of Veterinary Drugs. New York: Springer Publishing Company, 1974. 267]**PEER REVIEWED** MEAT INSPECTION DIVISION OF US DEPARTMENT OF AGRICULTURE REGULATION: BLEACHING AGENT IN TRIPE; MUST BE REMOVED FROM THE PRODUCT BY RINSING WITH CLEAR WATER. [Furia, T.E. (ed.). CRC Handbook of Food Additives. 2nd ed. Cleveland: The Chemical Rubber Co., 1972. 867]**PEER REVIEWED** MATERIALS SUITABLE FOR LIMITED CONTACT, EG 7 DAYS @ ATMOSPHERIC TEMP, INCLUDE: 99% PURE ALUMINUM: CERTAIN LOW-COPPER, STD ALUMINUM PIPING ALLOYS & ALUMINUM-SILICON-MAGNESIUM CASTING ALLOYS; 18% CHROMIUM-8% NICKEL STAINLESS STEELS; CERTAIN FLUOROCARBON LUBRICANTS; POLYVINYL CHLORIDE & SILICONE SYNTHETIC RUBBERS. [International Labour Office. Encyclopedia of Occupational Health and Safety. Volumes I and II. New York: McGraw-Hill Book Co., 1971. 697]**PEER REVIEWED** IRON, STEEL, BRASS, ETC MUST NOT BE USED ... IN CONTACT WITH H2O2. MATERIALS RECOMMENDED FOR UNLIMITED CONTACT ...: SPECIAL MAGNESIUM-ALUMINUM ALLOYS WITH LO COPPER & MANGANESE CONTENTS; BOROSILICATE GLASS; WHITE CHEM PORCELAIN; POLYTETRAFLUORETHYLENE; POLYCHLOROTRIFLUOROETHYLENE; & POLYETHYLENE ... . [International Labour Office. Encyclopedia of Occupational Health and Safety. Volumes I and II. New York: McGraw-Hill Book Co., 1971. 697]**PEER REVIEWED** ... IT IS A SUBSTANCE WHICH MIGRATES TO FOOD FROM PACKAGING MATERIALS. [Sax, N.I. Dangerous Properties of Industrial Materials. 6th ed. New York, NY: Van Nostrand Reinhold, 1984. 1551]**PEER REVIEWED** A low percentage of an inhibitor such as acetanilide or sodium stannate, is usually added to counteract the catalytic effect of traces of impurities such as iron, copper, and other heavy metals. [Lewis, R.J., Sr (Ed.). Hawley's Condensed Chemical Dictionary. 12th ed. New York, NY: Van Nostrand Rheinhold Co., 1993 617]**PEER REVIEWED** Potency of hydrogen peroxide is often described in terms of volume of active oxygen it yields. Each 1% w/w hydrogen peroxide is equivalent to 3.3% by volume; 100 volume hydrogen peroxide is approximately equivalent to 30% w/w, 30 volume to 9% w/w, and 10 volume to 3% w/w, respectively. [McEvoy, G.K. (ed.). American Hospital Formulary Service - Drug Information 93. Bethesda, MD: American Society of Hospital Pharmacists, Inc., 1993 (Plus Supplements, 1993). 1753]**PEER REVIEWED** FORMULATIONS/PREPARATIONS: GRADES: USP (3%); TECHNICAL (3, 6, 27.5, 30, 35, 50 & 90%); FCC /Food Chemical Codex/ [Lewis, R.J., Sr (Ed.). Hawley's Condensed Chemical Dictionary. 12th ed. New York, NY: Van Nostrand Rheinhold Co., 1993 617]**PEER REVIEWED** HYDROGEN PEROXIDE SOLUTION 3%. ... CONTAINS 2.5-3.5% BY WT OF H2O2= 8-12 VOL OXYGEN. ... HYDROGEN PEROXIDE SOLN 30%. CONTAINS 30% BY WT OF H2O2= 100 VOL OF OXYGEN. /3% & 30% SOLN/ [The Merck Index. 9th ed. Rahway, New Jersey: Merck & Co., Inc., 1976. 633]**PEER REVIEWED** HYDROGEN PEROXIDE SOLUTIONS CONTAIN 3% OF H2O2 IN WATER WITH 0.5% OF ACETANILID OR ACETOPHENETIDIN AS A STABILIZING AGENT. [American Hospital Formulary Service. Volumes I and II. Washington, DC: American Society of Hospital Pharmacists, to 1984.,p. 52:28]**PEER REVIEWED** NOW REPLACING THE 3% SOLN FOR INDUSTRIAL USES; DILUTED TO THE REQUIRED STRENGTH IMMEDIATELY BEFORE USE. IT ALSO IS USED FOR MAKING THE 3% SOLN. /30% SOLN/ [The Merck Index. 9th ed. Rahway, New Jersey: Merck & Co., Inc., 1976. 633]**PEER REVIEWED** DOSE: TOPICAL, FOR CLEANSING WOUNDS, 1.5-3% SOLN; AS A MOUTHWASH, 3% SOLN; INTRAVAGINAL, 2% SOLN. [Osol, A. and J.E. Hoover, et al. (eds.). Remington's Pharmaceutical Sciences. 15th ed. Easton, Pennsylvania: Mack Publishing Co., 1975. 1092]**PEER REVIEWED** Hydrogen peroxide is available only as aqueous solutions containing 3-98% hydrogen peroxide. [IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer,1972-PRESENT. (Multivolume work).,p. V36 286 (1985)]**PEER REVIEWED** Marketed as a soln in water in concentrations of 3-90% by wt. [Budavari, S. (ed.). The Merck Index - Encyclopedia of Chemicals, Drugs and Biologicals. Rahway, NJ: Merck and Co., Inc., 1989. 760]**PEER REVIEWED** Common commercial strengths are 27.5%, 35%, 50%, 70%, 90%, and 98%. "High strength" means greater than 52%. ... The hazard increases with the strength. [U.S. Coast Guard, Department of Transportation. CHRIS - Hazardous Chemical Data. Volume II. Washington, D.C.: U.S. Government Printing Office, 1984-5.]**PEER REVIEWED** Topical concentrate: 30.5% (w/w) (available by nonproprietary name); Gel: 1.5% Peroxyl Oral Spot Treatment, Colgate-Hoyt; Solution: 1.5% Peroxyl Mouthrinse (with alcohol 6%), Colgate-Hoyt; 3% (available by nonproprietary name) [McEvoy, G.K. (ed.). American Hospital Formulary Service - Drug Information 93. Bethesda, MD: American Society of Hospital Pharmacists, Inc., 1993 (Plus Supplements, 1993). 1753]**PEER REVIEWED** CONSUMPTION PATTERNS: 30% IN TEXTILES; 28% IN PLASTICIZERS & OTHER CHEMS; 9% FOR GLYCERIN; 8% FOR PULP & PAPER; 4% IN WASTEWATER TREATMENT; 21% IN MISC APPLICATIONS (1974). [SRI]**PEER REVIEWED** Pulp and paper, 25%; Chemical synthesis, 25%; Environmental, 20%; Textile, 10%; Mining and Uranium, 5%; Miscellaneous, 15% (1984). [CHEMICAL PRODUCTS SYNOPSIS: Hydrogen Peroxide (1984)]**PEER REVIEWED** CHEMICAL PROFILE: Hydrogen Peroxide. Chemical synthesis, 24%; pulp and paper, 23%; environmental uses (includes municipal and industrial water treatment and geothermal steam treatment), 18%; textiles, 14%; mining, 3%; electronics, 3%; miscellaneous (including food and cosmetic uses and the distribution market, 15%. [Kavaler AR; Chemical Marketing Reporter 230 (17): 58 (1986)]**PEER REVIEWED** CHEMICAL PROFILE: Hydrogen peroxide. Demand: 1985: 300 million lb; 1986: 320 million lb; 1990 /projected/: 410 million lb. (Canada and US) [Kavaler AR; Chemical Marketing Reporter 230 (17): 58 (1986)]**PEER REVIEWED** CHEMICAL PROFILE: Hydrogen peroxide. Pulp and paper, 38%; chemical synthesis, 18%; environmental uses (including municipal and industrial water treatment), 17%; textiles, 11%; exports, 5%; miscellaneous (including mining, electronic, food and cosmetic uses and distributor market), 11%. [Kavaler AR; Chemical Marketing Reporter 236 (14): 50 (1989)]**PEER REVIEWED** CHEMICAL PROFILE: Hydrogen peroxide. Demand: 1988: 425 million lb; 1989: 475 million lb; 1993 /projected/: 720 million lb (Includes net exports of 20 million lb). 1993 /projected/: 720 million lb (Includes net exports of 20 million lb). [Kavaler AR; Chemical Marketing Reporter 236 (14): 50 (1989)]**PEER REVIEWED** U. S. PRODUCTION: (1972) 6.83X10+10 GRAMS [SRI]**PEER REVIEWED** (1984) 1.26X10+11 g [BUREAU OF THE CENSUS. CURRENT INDUSTRIAL REPORTS: INORGANIC CHEMICALS 1984 p.9]**PEER REVIEWED** U. S. IMPORTS: (1972) 3.84X10+9 GRAMS [SRI]**PEER REVIEWED** (1984) 1.74X109+10 g [BUREAU OF THE CENSUS. U.S. IMPORTS FOR CONSUMPTION AND GENERAL IMPORTS 1984 p.1-353]**PEER REVIEWED** U. S. EXPORTS: (1984) 2.32X10+10 g [BUREAU OF THE CENSUS. U.S. EXPORTS, SCHEDULE E, 1984 p.2-94]**PEER REVIEWED** LABORATORY METHODS: ANALYTIC LABORATORY METHODS: DETERMINE H2O2 CONTENT BY KMNO4 TITRATION, DILUTE TO ABOUT 6% H2O2, NEUTRALIZE TO METHYL RED, (B), & DILUTE TO CALCULATED VOL TO GIVE 3.0%. [Association of Official Analytical Chemists. Official Methods of Analysis. 10th ed. and supplements. Washington, DC: Association of Official Analytical Chemists, 1965. New editions through13th ed. plus supplements, 1982.,p. 13/339 20.106]**PEER REVIEWED** An iodometric method for the flow injection amperometric determination of hydrogen peroxide in water is described. The range of 1x10-3 to 1x10-6 M for hydrogen peroxide. When this method was used to determine 3X10-6 M hydrogen peroxide in the presence of chloride, bromide, sulfate and carbonate ions, no interference from these ions was observed. In addition, organic peroxides present in a variety of natural water did not interfere with this method. [Abdalla MA, Al-Swaidan HM; Anal Lett 22 (7): 1729-42 (1989)]**PEER REVIEWED** Determination of hydrogen peroxide in milk by using qualitative color test. Prepare reagent by dissolving 1 g vanadium oxide in 100 ml sulfuric acid (6 + 94). Add 10-20 drops reagent in ca 10 ml sample and mix. Pink or red indicates hydrogen peroxide. [Association of Official Analytical Chemists. Official Methods of Analysis. 15th ed. and Supplements. Washington, DC: Association of Analytical Chemists, 1990,p. V2 1149]**PEER REVIEWED** SPECIAL REFERENCES: SPECIAL REPORTS: Cantoni O et al; Role of Metal Ions in Oxidant Cell Injury. Biol Trace Elem Res 21): 277-81 (1989). This paper represents a short review of recent data on the molecular mechanism(s) of hydrogen peroxide cytotoxicity. Ward PA; Mechanisms of Endothelial Cell Killing by H2O2 or Products of Activated Neutrophils. Am J Med 91 (3C): 89S-94S (1991). SYNONYMS AND IDENTIFIERS: SYNONYMS: ALBONE [Budavari, S. (ed.). The Merck Index - Encyclopedia of Chemicals, Drugs and Biologicals. Rahway, NJ: Merck and Co., Inc., 1989. 760]**PEER REVIEWED** ALBONE DS **PEER REVIEWED** Hioxyl [Budavari, S. (ed.). The Merck Index - Encyclopedia of Chemicals, Drugs and Biologicals. Rahway, NJ: Merck and Co., Inc., 1989. 760]**PEER REVIEWED** HYDROGEN DIOXIDE [Budavari, S. (ed.). The Merck Index - Encyclopedia of Chemicals, Drugs and Biologicals. Rahway, NJ: Merck and Co., Inc., 1989. 760]**PEER REVIEWED** HYDROGEN DIOXIDE SOLUTION **PEER REVIEWED** HYDROGEN PEROXIDE SOLUTION [Sax, N.I. Dangerous Properties of Industrial Materials. 6th ed. New York, NY: Van Nostrand Reinhold, 1984. 1550]**PEER REVIEWED** HYDROPEROXIDE [Budavari, S. (ed.). The Merck Index - Encyclopedia of Chemicals, Drugs and Biologicals. Rahway, NJ: Merck and Co., Inc., 1989. 760]**PEER REVIEWED** INHIBINE [Sax, N.I. Dangerous Properties of Industrial Materials. 6th ed. New York, NY: Van Nostrand Reinhold, 1984. 1550]**PEER REVIEWED** PERHYDROL [Sax, N.I. Dangerous Properties of Industrial Materials. 6th ed. New York, NY: Van Nostrand Reinhold, 1984. 1550]**PEER REVIEWED** PEROSSIDO DI IDROGENO (ITALIAN) [U.S. Department of Health and Human Services, Public Health Service, Center for Disease Control, National Institute for Occupational Safety & Health. Registry of ToxicEffects of Chemical Substances 1979 edition. Volumes 1 and 2. Washington, DC: U.S. Government Printing Office, 1980.,p. V1 763]**PEER REVIEWED** PEROXAAN **PEER REVIEWED** PEROXAN [Sax, N.I. Dangerous Properties of Industrial Materials. 6th ed. New York, NY: Van Nostrand Reinhold, 1984. 1550]**PEER REVIEWED** Peroxide [U.S. Coast Guard, Department of Transportation. CHRIS - Hazardous Chemical Data. Volume II. Washington, D.C.: U.S. Government Printing Office, 1984-5.]**PEER REVIEWED** PEROXYDE D'HYDROGENE (FRENCH) [U.S. Department of Health and Human Services, Public Health Service, Center for Disease Control, National Institute for Occupational Safety & Health. Registry of ToxicEffects of Chemical Substances 1979 edition. Volumes 1 and 2. Washington, DC: U.S. Government Printing Office, 1980.,p. V1 763]**PEER REVIEWED** SUPEROXOL **PEER REVIEWED** WASSERSTOFFPEROXID (GERMAN) [U.S. Department of Health and Human Services, Public Health Service, Center for Disease Control, National Institute for Occupational Safety & Health. Registry of ToxicEffects of Chemical Substances 1979 edition. Volumes 1 and 2. Washington, DC: U.S. Government Printing Office, 1980.,p. V1 763]**PEER REVIEWED** WATERSTOFPEROXYDE (DUTCH) [U.S. Department of Health and Human Services, Public Health Service, Center for Disease Control, National Institute for Occupational Safety & Health. Registry of ToxicEffects of Chemical Substances 1979 edition. Volumes 1 and 2. Washington, DC: U.S. Government Printing Office, 1980.,p. V1 763]**PEER REVIEWED** FORMULATIONS/PREPARATIONS: GRADES: USP (3%); TECHNICAL (3, 6, 27.5, 30, 35, 50 & 90%); FCC /Food Chemical Codex/ [Lewis, R.J., Sr (Ed.). Hawley's Condensed Chemical Dictionary. 12th ed. New York, NY: Van Nostrand Rheinhold Co., 1993 617]**PEER REVIEWED** HYDROGEN PEROXIDE SOLUTION 3%. ... CONTAINS 2.5-3.5% BY WT OF H2O2= 8-12 VOL OXYGEN. ... HYDROGEN PEROXIDE SOLN 30%. CONTAINS 30% BY WT OF H2O2= 100 VOL OF OXYGEN. /3% & 30% SOLN/ [The Merck Index. 9th ed. Rahway, New Jersey: Merck & Co., Inc., 1976. 633]**PEER REVIEWED** HYDROGEN PEROXIDE SOLUTIONS CONTAIN 3% OF H2O2 IN WATER WITH 0.5% OF ACETANILID OR ACETOPHENETIDIN AS A STABILIZING AGENT. [American Hospital Formulary Service. Volumes I and II. Washington, DC: American Society of Hospital Pharmacists, to 1984.,p. 52:28]**PEER REVIEWED** NOW REPLACING THE 3% SOLN FOR INDUSTRIAL USES; DILUTED TO THE REQUIRED STRENGTH IMMEDIATELY BEFORE USE. IT ALSO IS USED FOR MAKING THE 3% SOLN. /30% SOLN/ [The Merck Index. 9th ed. Rahway, New Jersey: Merck & Co., Inc., 1976. 633]**PEER REVIEWED** DOSE: TOPICAL, FOR CLEANSING WOUNDS, 1.5-3% SOLN; AS A MOUTHWASH, 3% SOLN; INTRAVAGINAL, 2% SOLN. [Osol, A. and J.E. Hoover, et al. (eds.). Remington's Pharmaceutical Sciences. 15th ed. Easton, Pennsylvania: Mack Publishing Co., 1975. 1092]**PEER REVIEWED** Hydrogen peroxide is available only as aqueous solutions containing 3-98% hydrogen peroxide. [IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer,1972-PRESENT. (Multivolume work).,p. V36 286 (1985)]**PEER REVIEWED** Marketed as a soln in water in concentrations of 3-90% by wt. [Budavari, S. (ed.). The Merck Index - Encyclopedia of Chemicals, Drugs and Biologicals. Rahway, NJ: Merck and Co., Inc., 1989. 760]**PEER REVIEWED** Common commercial strengths are 27.5%, 35%, 50%, 70%, 90%, and 98%. "High strength" means greater than 52%. ... The hazard increases with the strength. [U.S. Coast Guard, Department of Transportation. CHRIS - Hazardous Chemical Data. Volume II. Washington, D.C.: U.S. Government Printing Office, 1984-5.]**PEER REVIEWED** Topical concentrate: 30.5% (w/w) (available by nonproprietary name); Gel: 1.5% Peroxyl Oral Spot Treatment, Colgate-Hoyt; Solution: 1.5% Peroxyl Mouthrinse (with alcohol 6%), Colgate-Hoyt; 3% (available by nonproprietary name) [McEvoy, G.K. (ed.). American Hospital Formulary Service - Drug Information 93. Bethesda, MD: American Society of Hospital Pharmacists, Inc., 1993 (Plus Supplements, 1993). 1753]**PEER REVIEWED** SHIPPING NAME/ NUMBER DOT/UN/NA/IMO: UN 2014; Hydrogen peroxide solution (8% to 40% peroxide) UN 2015; Hydrogen peroxide solution (over 52% peroxide) UN 2984; Hydrogen peroxide, aqueous solutions, stabilized, with more than 8% but less than 20% hydrogen peroxide (stabilized as necessary) UN 2014; Hydrogen peroxide, aqueous solutions with more than 40% but 60% or less hydrogen peroxide (stabilized as necessary) IMO 5.1; Hydrogen peroxide, aqueous solutions with not less than 8% but less than 20% hydrogen peroxide (stabilized as necessary); Hydrogen peroxide, aqueous solutions with not less than 20% but 60% or less hydrogen peroxide (stabilized as necessary); Hydrogen peroxide, stabilized, or hydrogen peroxide, aqueous solutions, stabilized, with more than 60% hydrogen peroxide UN 2015; Hydrogen peroxide, stabilized, or hydrogen peroxide, aqueous solutions, stabilized, with more than 60% hydrogen peroxide UN 1511; Hydrogen peroxide, solid RTECS NUMBER: NIOSH/MX0900000 ADMINISTRATIVE INFORMATION: HAZARDOUS SUBSTANCES DATABANK NUMBER: 547 LAST REVISION DATE: 20000612 LAST REVIEW DATE: Reviewed by SRP on 3/2/1994 UPDATE HISTORY: Field Update on 06/12/2000, 1 field added/edited/deleted. Field Update on 06/12/2000, 1 field added/edited/deleted. Complete Update on 02/09/2000, 1 field added/edited/deleted. Complete Update on 02/08/2000, 1 field added/edited/deleted. Complete Update on 12/27/1999, 1 field added/edited/deleted. Complete Update on 11/18/1999, 1 field added/edited/deleted. Complete Update on 06/07/1999, 8 fields added/edited/deleted. Complete Update on 05/04/1999, 1 field added/edited/deleted. Complete Update on 01/27/1999, 1 field added/edited/deleted. Complete Update on 11/12/1998, 13 fields added/edited/deleted. Field Update on 10/29/1998, 1 field added/edited/deleted. Field Update on 10/17/1997, 1 field added/edited/deleted. Field Update on 05/01/1997, 2 fields added/edited/deleted. Complete Update on 05/17/1996, 1 field added/edited/deleted. Complete Update on 05/10/1996, 1 field added/edited/deleted. Complete Update on 04/23/1996, 7 fields added/edited/deleted. Complete Update on 01/19/1996, 1 field added/edited/deleted. Complete Update on 01/20/1995, 1 field added/edited/deleted. Complete Update on 12/21/1994, 1 field added/edited/deleted. Complete Update on 08/09/1994, 1 field added/edited/deleted. Complete Update on 05/18/1994, 60 fields added/edited/deleted. Field Update on 03/21/1994, 1 field added/edited/deleted. Complete Update on 08/07/1993, 1 field added/edited/deleted. Complete Update on 08/04/1993, 1 field added/edited/deleted. Complete Update on 02/05/1993, 1 field added/edited/deleted. Field update on 12/13/1992, 1 field added/edited/deleted. Complete Update on 04/27/1992, 1 field added/edited/deleted. Complete Update on 01/23/1992, 1 field added/edited/deleted. Field update on 11/09/1990, 1 field added/edited/deleted. Complete Update on 10/22/1990, 11 fields added/edited/deleted. Field Update on 05/14/1990, 1 field added/edited/deleted. Field Update on 05/04/1990, 1 field added/edited/deleted. Field Update on 01/15/1990, 1 field added/edited/deleted. Complete Update on 01/11/1990, 8 fields added/edited/deleted. Express Update on 10/13/1989, 2 fields added/edited/deleted. Field Update on 05/05/1989, 1 field added/edited/deleted. Field Update on 03/01/1989, 1 field added/edited/deleted. Complete Update on 12/09/1988, 2 fields added/edited/deleted. Complete Update on 11/09/1988, 4 fields added/edited/deleted. Complete Update on 03/08/1988, 2 fields added/edited/deleted. Complete Update on 10/14/1986 RECORD LENGTH: 136435 Better Health Through Better Dialysis

Human Studies on Acedic Acid Kidney Dialysis


Acedic Acid - reuse
The following information was generated from the Hazardous Substances Databank (HSDB), a database of the National Library of Medicine's TOXNET system (http://toxnet.nlm.nih.gov) on August 18, 2000. Query: Information added from CHEMID: acetic acid Chemid Name: vosol [64-19-7] Registry Numbers: 64-19-7 1 NAME: ACETIC ACID HSN: 40 RN: 64-19-7 HUMAN HEALTH EFFECTS: HUMAN TOXICITY EXCERPTS: WORKERS EXPOSED FOR A NUMBER OF YEARS TO CONCN OF UP TO 200 PPM HAVE BEEN FOUND TO SUFFER FROM PALPEBRAL EDEMA WITH HYPERTROPHY OF LYMPH NODES, CONJUNCTIVAL HYPEREMIA. ... FOLLOWING REPEATED EXPOSURES, WORKERS MAY COMPLAIN OF DIGESTIVE DISORDERS WITH PYROSIS AND CONSTIPATION. SKIN ON PALMS OF HANDS ... BECOME DRY, CRACKED AND HYPERKERATOTIC. [International Labour Office. Encyclopedia of Occupational Health and Safety. Vols. I&II. Geneva, Switzerland: International Labour Office, 1983. 37]**PEER REVIEWED** ... STUDIED 5 WORKERS EXPOSED 7-12 YEARS TO HIGH CONCENTRATIONS (80-200 PPM @ PEAK CONCN). THE PRINCIPAL FINDINGS WERE BLACKENING & HYPERKERATOSIS OF THE SKIN ... . [Patty, F. (ed.). Industrial Hygiene and Toxicology: Volume II: Toxicology. 2nd ed. New York: Interscience Publishers, 1963. 1779]**PEER REVIEWED** SKIN SENSITIZATION TO ACETIC ACID IS RARE, BUT HAS OCCURRED. [Patty, F. (ed.). Industrial Hygiene and Toxicology: Volume II: Toxicology. 2nd ed. New York: Interscience Publishers, 1963. 1778]**PEER REVIEWED** /IN/ ... WORKERS EXPOSED FOR 7-12 YR @ CONCN OF 60 PPM, PLUS 1 HR DAILY @ 100-200 PPM ... /SOME INVESTIGATORS/ FOUND CONJUNCTIVITIS, BRONCHITIS, PHARYNGITIS, & EROSION OF EXPOSED TEETH ... . [American Conference of Governmental Industrial Hygienists, Inc. Documentation of the Threshold Limit Values and Biological Exposure Indices. 6th ed. Volumes I,II, III. Cincinnati, OH: ACGIH, 1991. 6]**PEER REVIEWED** BOTH /ACETIC/ ACID & ITS ANHYDRIDE ... ARE POTENT LACRIMATORS. [Hamilton, A., and H. L. Hardy. Industrial Toxicology. 3rd ed. Acton, Mass.: Publishing Sciences Group, Inc., 1974. 349]**PEER REVIEWED** Six patients with frequent episodes of symptomatic hypotension during acetate dialysis were treated with bicarbonate dialysis. In all patients, blood pressure, heart rate, and arterial acid-base values were monitored every 30 min during each of the 5 treatments with acetate dialysis and bicarbonate dialysis. Hemodynamic parameters were measured in all patients during bicarbonate dialysis and in three of them also during acetate dialysis. Long-term monitoring with electroencephalography was performed during both bicarbonate and acetate dialysis. During acetate dialysis, the patients showed a frequent onset of sudden hypotension and arrhythmia with concomitant symptoms of the so-called disequilibrium syndrome. None of these symptoms were seen during bicarbonate dialysis. /Acetate/ [Hampl H et al; Artif Organs 6 (4): 410-6 (1982)]**PEER REVIEWED** ... As little as 1.0 ml of glacial acetic acid has resulted in perforation of the esophagus. [Mackison, F. W., R. S. Stricoff, and L. J. Partridge, Jr. (eds.). NIOSH/OSHA - Occupational Health Guidelines for Chemical Hazards. DHHS(NIOSH) PublicationNo. 81-123 (3 VOLS). Washington, DC: U.S. Government Printing Office, Jan. 1981. 2]**PEER REVIEWED** ... Unacclimatized humans experience extreme eye and nasal irritation at concentrations in excess of 25 ppm; conjunctivitis from concentrations below 10 ppm has been reported. ... Glacial (100%) acetic acid ... has caused permanent corneal opacification. [Mackison, F. W., R. S. Stricoff, and L. J. Partridge, Jr. (eds.). NIOSH/OSHA - Occupational Health Guidelines for Chemical Hazards. DHHS(NIOSH) PublicationNo. 81-123 (3 VOLS). Washington, DC: U.S. Government Printing Office, Jan. 1981.,p. 1-2]**PEER REVIEWED** ... A splash of vinegar (4 to 10% acetic acid soln) in the human eye causes immediate pain and conjunctival hyperemia, sometimes with injury of the corneal epithelium. [Mackison, F. W., R. S. Stricoff, and L. J. Partridge, Jr. (eds.). NIOSH/OSHA - Occupational Health Guidelines for Chemical Hazards. DHHS(NIOSH) PublicationNo. 81-123 (3 VOLS). Washington, DC: U.S. Government Printing Office, Jan. 1981. 2]**PEER REVIEWED** Bronchopneumonia and pulmonary edema may develop following acute overexposure. Chronic exposure may result in pharyngitis and catarrhal bronchitis. Ingestion, though not likely to occur in industry, may result in penetration of the esophagus, bloody vomiting, diarrhea, shock, hemolysis, and hemoglobinuria ... followed by anuria. [Sittig M; Handbook of Toxic and Hazardous Chemicals p.20-21 (1981)]**PEER REVIEWED** In two patients accidental application of acetic acid followed very quickly by irrigation with water resulted in immediate corneal opacification. The corneas cleared sufficiently in a few days to reveal severe iritis and small pupils fixed by posterior synechias. Regeneration of the epithelium took many months, but corneal anesthesia and opacity were permanent. [Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986. 39]**PEER REVIEWED** SYMPTOMATOLOGY (AFTER INGESTION OR SKIN CONTACT): 1) CORROSION OF MUCOUS MEMBRANES OF MOUTH, THROAT, AND ESOPHAGUS, WITH IMMEDIATE PAIN AND DYSPHAGIA. THE NECROTIC AREAS ARE AT FIRST GRAYISH WHITE BUT SOON ACQUIRE A BLACKISH DISCOLORATION AND SOMETIMES A SHRUNKEN OR WRINKLED TEXTURE; THE PROCESS IS DESCRIBED AS A "COAGULATION NECROSIS." 2) EPIGASTRIC PAIN, WHICH MAY BE ASSOCIATED WITH NAUSEA AND THE VOMITING OF MUCOID AND "COFFEE-GROUND" MATERIAL. AT TIMES, GASTRIC HEMORRHAGE MAY BE INTENSE, AND THE VOMITUS THEN CONTAINS FRESH BLOOD. PROFOUND THIRST. 3) ULCERATION OF ALL MEMBRANES AND TISSUES WITH WHICH THE ACID COMES IN CONTACT ... . 4) CIRCULATORY COLLAPSE WITH CLAMMY SKIN, WEAK AND RAPID PULSE, SHALLOW RESPIRATIONS, AND SCANTY URINE. CIRCULATORY SHOCK IS OFTEN THE IMMEDIATE CAUSE OF DEATH. 5) ASPHYXIAL DEATH DUE TO GLOTTIC EDEMA. 6) LATE ESOPHAGEAL, GASTRIC AND PYLORIC STRICTURES AND STENOSES, WHICH MAY REQUIRE MAJOR SURGICAL REPAIR, SHOULD BE ANTICIPATED. SIGNS OF OBSTRUCTION COMMONLY APPEAR WITHIN A FEW WEEKS BUT MAY BE DELAYED FOR MONTHS AND EVEN YEARS. PERMANENT SCARS MAY ALSO APPEAR IN THE CORNEA, SKIN AND OROPHARYNX. 7) UNCORRECTED CIRCULATORY COLLAPSE OF SEVERAL HOURS' DURATION MAY LEAD TO RENAL FAILURE AND ISCHEMIC LESIONS IN THE LIVER AND HEART. [Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984.,p. II-102]**PEER REVIEWED** Long-term exposure can lead to darkening of the skin, erosion of tooth enamel and chronic inflammation of the respiratory tract. [Anon; Canadian Centre for Occupational Health and Safety L8N 1H6 14p (1984)]**PEER REVIEWED** The use of Silastic Medical Adhesive Type A in the fabrication of facial prostheses may cause health hazards to the patient and the operator because of acetic acid emissions. Caution must be exercised to remove acetic acid vapors from the air and unliberated acetic acid from material applied directly to the skin. [McElroy TH et al; J Prosthet Dent 53 (1): 86-7 (1985)]**PEER REVIEWED** LOW MOLECULAR WEIGHT ORGANIC ACIDS SUCH AS ACETIC ARE STRONG IRRITANTS BUT SOMEWHAT LESS CORROSIVE THAN THE MINERAL ACIDS. [Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984.,p. III-10]**PEER REVIEWED** PURE ACETIC ACID IS TOXIC BY INGESTION, & INHALATION ... . [Sax, N.I. and R.J. Lewis, Sr. (eds.). Hawley's Condensed Chemical Dictionary. 11th ed. New York: Van Nostrand Reinhold Co., 1987. 7]**PEER REVIEWED** A human poison... . Moderately toxic by various routes. A severe eye and skin irritant. Human systemic effects by ingestion: changes in the esophagus, ulceration or bleeding from the small and large intestines. Human systemic irritant effects and mucous membrane irritant. [Lewis, R.J. Sax's Dangerous Properties of Industrial Materials. 9th ed. Volumes 1-3. New York, NY: Van Nostrand Reinhold, 1996. 12]**PEER REVIEWED** Produces burns of the skin. ... Ingestion may cause severe corrosion of mouth & tract, with vomiting, hematemesis, diarrhea, circulatory collapse, uremia, death. Chronic exposure may cause erosion of dental enamel, bronchitis, eye irritation ... . [Budavari, S. (ed.). The Merck Index - Encyclopedia of Chemicals, Drugs and Biologicals. Rahway, NJ: Merck and Co., Inc., 1989. 9]**PEER REVIEWED** A case study is reported where an individual ingested 200 ml of an 80% solution of acetic acid. ... Repeated shock due to myocardial infarction and massive intestinal bleeding led to an organic brain psychosyndrome. [Hakenbeck H et al; Z Urol Nephrol 77 (5): 311-4 (1984)]**PEER REVIEWED** A 37 year old man who worked as a maintenance fitter developed both reversible airways obstruction and steroid responsive interstitial pneumonitis after accidental exposure to glacial acetic acid. He was exposed to a blow back of the acid in a petrochemical works, and suffered first degree burns on the face and arms. He developed progressive exertional dyspnea, limiting him to quiet walking on flat areas. Physical examination revealed burns to the face and arms and inspiratory basal crackles. Chest radiograph indicated patchy bilateral reticulonodular infiltration dominantly of the bases. Even after 3 months, there was no improvement in his condition. Bronchoscopy showed widespread bronchial inflammatory changes. A doubling of macrophages and a ten fold increase in lymphocytes were noted which amounted to 34% of the total inflammatory cells. A diffuse, moderate, mainly mononuclear, interstitial pneumonitis was noted on transbronchial biopsy. He was treated with high dose nebulized bronchodilators and corticosteroids. A prompt and sustained improvement was noted in spirometry and clearing of his chest radiograph. Progress was maintained for at least 18 months. [Rajan KG, Davies BH; Br J Ind Med 46 (1): 67-68 (1989)]**PEER REVIEWED** Two patients admitted after ingestion of 80% acetic acid are described. Only the first patient developed hemolysis, slight intravascular coagulation and oliguric kidney insufficiency. They were treated with a nasogastric tube and total parenteral feeding. During the first week after admission urinary excretion of beta 2-microglobulin, alanine-aminopeptidase and N-acetyl-glucosaminidase was significantly increased. The patients remained hemodynamically stable and did not develop fever. The above-mentioned elevated excretions returned to normal levels. Both patients showed similar patterns of tubular proteinuria. The observations in the second patient suggest a direct toxic effect of acetic acid on the proximal tubule of the kidney. [Schardijn GH et al; Ned Tijdschr Geneeskd 133 (11): 556-59 (1989)]**PEER REVIEWED** The ototoxicity of an otic drop preparation containing 2% acetic acid and 3% propylene glycol ... was investigated according to measurements of endocochlear potential and inner ear fluid pH. The application of this preparation to the round window membrane for 30 minutes caused a depression in endocochlear potential from 80.5 +/- 2.5 mV (mean +/- SD; n= 6) to 11.7 +/- 7.7 mV, and lowered inner ear fluid pH from 7.55 +/- 0.09 to 5.06 +/- 0.19 (n= 6) in perilymph and from 7.52 +/- 0.07 to 5.88 +/- 0.63 (n= 6) in endolymph. Two percent acetic acid produced similar changes after 30 minutes: endocochlear potential was reduced from 83.0 +/- 2.2 mV to 34.0 +/- 2.9 mV and endolymphatic pH from 7.49 +/- 0.04 to 6.83 +/- 0.21 (n= 4). However, the application of artificial perilymph of pH 4 titrated with hydrochloric acid induced no significant changes in either endocochlear potential or endolymphatic pH. [Ideda K, Morizono T; Am J Otolaryngol 10 (6): 382-85 (1989)]**PEER REVIEWED** A 22 year old woman developed anaphylactic reations to pure ethyl alcohol (ethanol) and an immediate type allergy to acetic acid. Prick tests with ethyl alcohol, wine, and beer were negative, whereas vinegar and acetic acid (9.6 and 0.96%) gave +++ reactions. Control tests with acetic acid in 10 patients yielded negative or (+) reactions to the 9.6% concentration and negative reactions to the 0.96% concentration. Oral provocation tests led to severe anaphylaxis with urticaria, facial flushing, itching of the mucous membranes, hoarseness, dyspnea, tachycardia, and painful uterine cramps after the ingestion of one ml of ethyl alcohol or 50 ml of beer. The severe anaphylactic reation after ingestion of as little as one ml of ethyl alcohol associated with a +++ prick test reaction to acetic acid in a definitely non-irritating concentration strongly suggests that the patient's anaphylactic reactions are based on an immediate type allergy to acetic acid, the main metabolite of ethyl alcohol. [Przybilla B, Ring J; Lancet 1 (Feb 26): 483 (1983)]**PEER REVIEWED** A case study is reported where an individual ingested 200 ml of an 80% solution of acetic acid. The patient survived the intoxication by use of hemodialysis and intensive care therapy. Repeated shock due to myocardial infarction and massive intestinal bleeding led to an organic brain psychosyndrome. [Hakenbeck H et al; Z Urol Nephrol 77 (5): 311-4 (1984)]**PEER REVIEWED** SKIN, EYE AND RESPIRATORY IRRITATIONS: ... Eye irritation has been noted at a concentration below 10 ppm. [Mackison, F. W., R. S. Stricoff, and L. J. Partridge, Jr. (eds.). NIOSH/OSHA - Occupational Health Guidelines for Chemical Hazards. DHHS(NIOSH) PublicationNo. 81-123 (3 VOLS). Washington, DC: U.S. Government Printing Office, Jan. 1981. 2]**PEER REVIEWED** The vapor of acetic acid is irritating to the eyes and nose, causing lacrimation and hyperemia. [Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986. 40]**PEER REVIEWED** Irritating concn: 25 mg/cu m. [Ruth JH; Am Ind Hyg J 47: A142-51 (1986)]**PEER REVIEWED** Strong irritant to skin & tissue. [Sax, N.I. and R.J. Lewis, Sr. (eds.). Hawley's Condensed Chemical Dictionary. 11th ed. New York: Van Nostrand Reinhold Co., 1987. 7]**PEER REVIEWED** Respiratory irritant [Ellenhorn, M.J. and D.G. Barceloux. Medical Toxicology - Diagnosis and Treatment of Human Poisoning. New York, NY: Elsevier Science Publishing Co., Inc. 1988. 889]**PEER REVIEWED** DRUG WARNINGS: The antiseptic ... 0.25% acetic acid was directly applied to cultured human fibroblasts to quantitatively assess its cytotoxicity. It was cytotoxic and adversely affected wound healing in an animal model. Comparison of bactericidal and cytotoxic effects of serial dilutions indicated that cellular toxicity exceeded its bacterial potency. ... This experiment provides evidence that 0.25% acetic acid is unsuitable for use in wound care. [Lineaweaver W, et al; Arch Surg 120 (3): 267-70 (1985)]**PEER REVIEWED** MEDICAL SURVEILLANCE: EMPLOYMENT & PERIODIC MEDICAL EXAM SHOULD BE CARRIED OUT TO ENSURE THAT WORKERS WITH RESP AILMENTS, SKIN DISORDERS OR KERATOCONJUNCTIVITIS ARE /PROTECTED FROM EXPOSURE/ TO ACETIC ACID. [International Labour Office. Encyclopedia of Occupational Health and Safety. Vols. I&II. Geneva, Switzerland: International Labour Office, 1983. 38]**PEER REVIEWED** Employees should be screened for history of ... /chronic respiratory, skin and, eye diseases/ ... which might place the employee at an increased risk from acetic acid exposure. [Mackison, F. W., R. S. Stricoff, and L. J. Partridge, Jr. (eds.). NIOSH/OSHA - Occupational Health Guidelines for Chemical Hazards. DHHS(NIOSH) PublicationNo. 81-123 (3 VOLS). Washington, DC: U.S. Government Printing Office, Jan. 1981. 1]**PEER REVIEWED** POPULATIONS AT SPECIAL RISK: Employees with /chronic respiratory, skin, or eye disease are/ at increased risk from acetic acid exposure. [Mackison, F. W., R. S. Stricoff, and L. J. Partridge, Jr. (eds.). NIOSH/OSHA - Occupational Health Guidelines for Chemical Hazards. DHHS(NIOSH) PublicationNo. 81-123 (3 VOLS). Washington, DC: U.S. Government Printing Office, Jan. 1981. 1]**PEER REVIEWED** PROBABLE ROUTES OF HUMAN EXPOSURE: Acetic acid detn in rainwater. [Gillett RW, Ayers GP; Anal Chim Acta 177: 273-7 (1985)]**PEER REVIEWED** NIOSH (NOES Survey 1981-1983) has statistically estimated that 595,346 workers (236,213 of these are female) are potentially exposed to acetic acid in the US(1). Acetic acid occurs ubiquitously and is a normal metabolite in animals; therefore, the general population is continually exposed to the compound. Primary routes of exposure to the general population are through consumption of foods and inhalation of air. Occupational exposure occurs through inhalation and dermal contact(SRC). [(1) NIOSH; National Occupational Exposure Survey (NOES) (1983)]**PEER REVIEWED** Emission of acetic acid during extrusion of polyethylene resins was measured as < 0.17 lbs/million lbs for blown film and blow molding and ranged from < 0.17 to 2.0 lbs/million lbs for extrusion coating (higher value for extrusion at higher melt temperature)(1). [(1) Barlow A et al; J Air & Waste Manage Assoc 46: 569-80 (1996)]**PEER REVIEWED** BODY BURDEN: Acetic acid was qualitatively detected in 2 of 12 human milk samples collected from volunteers in four US cities(1). Acetic acid at 19.9 mg/day was measured from non-specified human emissions(2). [(1) Pellizzari ED et al; Bull Environ Contam Toxicol 28: 322-8 (1982) (2) Otson R, Fellin P; in Gas Pollut: Charactization and Cycling. Nriagu JO (ed), NY,NY: John Wiley & Sons, Inc (1989)]**PEER REVIEWED** AVERAGE DAILY INTAKE: AIR INTAKE: Assume ambient atmospheric concns of 0.1-1.6 ug/cu m(1); 2-32 ug/day; WATER INTAKE: insufficient data; FOOD INTAKE: insufficient data(SRC). [(1) Kawamura K et al; Environ Sci Technol 19: 1082-6 (1985)]**PEER REVIEWED** EMERGENCY MEDICAL TREATMENT: EMERGENCY MEDICAL TREATMENT: EMT COPYRIGHT DISCLAIMER: Portions of the POISINDEX(R) database are provided here for general reference. THE COMPLETE POISINDEX(R) DATABASE, AVAILABLE FROM MICROMEDEX, SHOULD BE CONSULTED FOR ASSISTANCE IN THE DIAGNOSIS OR TREATMENT OF SPECIFIC CASES. Copyright 1974-1998 Micromedex, Inc. Denver, Colorado. All Rights Reserved. Any duplication, replication or redistribution of all or part of the POISINDEX(R) database is a violation of Micromedex' copyrights and is strictly prohibited.
The following Overview, *** ACIDS ***, is relevant for this HSDB record chemical. LIFE SUPPORT: o This overview assumes that basic life support measures have been instituted. CLINICAL EFFECTS: SUMMARY OF EXPOSURE 0.2.1.1 ACUTE EXPOSURE o INGESTION - Oral ingestion may produce mild to moderately severe oral and esophageal burns with more severe burns occurring in the stomach. Perforations are rare but may occur. The pyloric end of the stomach is most severely affected and is the site of delayed stricture occurring generally at 3 weeks after the ingestion. 1. Initial signs and symptoms may not reliably predict the extent of injury to the gastrointestinal tract. o DERMAL - Severe dermal burns may occur with dermal exposure. Complications seen with dermal burns include cellulitis, sepsis, contractures, osteomyelitis, and systemic toxicity from absorbed acid. Chromic acid burns can result in systemic toxicity. o INHALATION - Inhalation of acid vapors, mists or aerosols may result in dyspnea, pleuritic chest pain, pulmonary edema, hypoxemia, bronchospasm, pneumonitis, tracheobronchitis and persistent pulmonary function abnormalities. Pulmonary dysfunction similar to asthma has been reported. o EYE - Irritation may develop after exposure to mists, aerosols or vapors. Splash contact may cause corneal erosions. HEENT 0.2.4.1 ACUTE EXPOSURE o Eye exposure may result in pain, swelling, corneal erosions and blindness. CARDIOVASCULAR 0.2.5.1 ACUTE EXPOSURE o Cardiovascular collapse may develop soon after severe poisonings. Cardiac ischemia may occur after several hours of uncorrected circulatory collapse. RESPIRATORY 0.2.6.1 ACUTE EXPOSURE o Exposure to acids may produce dyspnea, pleuritic chest pain, pulmonary edema, hypoxemia, bronchospasm, pneumonitis, and persistent pulmonary function abnormalities. Airway hyperreactivity has also been reported. 1. The onset of respiratory symptoms may be delayed for several hours. NEUROLOGIC 0.2.7.1 ACUTE EXPOSURE o Abnormal neuropsychologic function has been reported following hydrochloric acid exposure from a leaking tanker truck. GASTROINTESTINAL 0.2.8.1 ACUTE EXPOSURE o Ingestion of acids may result in burns, gastrointestinal bleeding, gastritis, perforations, dilation, edema, necrosis, vomiting, stenosis, fistula, and duodenal/jejunal injury. HEPATIC 0.2.9.1 ACUTE EXPOSURE o Systemic toxicity may result in acute hepatic injury. Hepatic injury has been reported following chronic exposure to chromic acid. GENITOURINARY 0.2.10.1 ACUTE EXPOSURE o Renal failure is a rare complication of severe poisonings. Hemoglobinuria may develop secondary to hemolysis. Nephritis may develop after hydrochloric acid ingestion. ACID-BASE 0.2.11.1 ACUTE EXPOSURE o Metabolic acidosis may be noted following significant acid ingestion and may be due to systemic absorption of acid. Acidosis may also be secondary to severe chemical burns and shock. FLUID-ELECTROLYTE 0.2.12.1 ACUTE EXPOSURE o Massive fluid and electrolyte shifts may occur with extensive dermal or gastrointestinal burns. Hyperkalemia may occur with hemolysis. Hyperphosphatemia, hypocalcemia and hyperchloremia have been reported. HEMATOLOGIC 0.2.13.1 ACUTE EXPOSURE o Hemolysis may occur following significant acid ingestion. Disseminated intravascular coagulation has been reported. DERMATOLOGIC 0.2.14.1 ACUTE EXPOSURE o Chemical burns to the skin are often associated with concurrent thermal burns and trauma. Complications seen with thermal burns including cellulitis, sepsis, contractures, osteomyelitis, may occur as well as systemic toxicity from absorbed acid. Deep or extensive burns may require grafting. 0.2.14.2 CHRONIC EXPOSURE o Prolonged or repeated exposure to chromic acid mist can result in dermatitis. Ulcerations may also occur. IMMUNOLOGIC 0.2.19.1 ACUTE EXPOSURE o Hypersensitivity has been reported. LABORATORY: o Obtain baseline CBC and lytes, if needed. TREATMENT OVERVIEW: SUMMARY EXPOSURE o EMESIS CONTRAINDICATED - Do not induce vomiting, do not give bicarbonate to neutralize. Activated charcoal is of no value. Passing a nasogastric or orogastric tube into the stomach is controversial at this time. o IRRIGATION - Irrigate all contaminated areas with copious amounts of water. ORAL EXPOSURE o MUCOSAL DECONTAMINATION: If no respiratory compromise is present, dilute immediately with milk or water; use no more than 8 ounces in adults and 4 ounces in children. o GASTRIC DECONTAMINATION: Ipecac is contraindicated. Consider insertion of a small, flexible nasogastric or orogastric tube to suction gastric contents after recent large ingestions; the risk of further mucosal injury must be weighed against potential benefits. C. ENDOSCOPY: Because acid ingestion may cause severe gastric burns with relatively few initial signs and symptoms, endoscopic evaluation is recommended within 24 hours in any patient with a definite history of ingesting a strong acid, even if asymptomatic. If burns are found, follow 10 to 20 days later with a barium swallow. XB D. PHARMACOLOGIC TREATMENT: Corticosteroids are controversial. Consider use in second degree burns within 48 hours of ingestion in patients without gastrointestinal bleeding or evidence of perforation. Antibiotics are indicated for suspected perforation or infection and in patients receiving corticosteroids. XB E. SURGICAL OPTIONS: Initially, if severe esophageal burns are found a string may be placed in the stomach to facilitate later dilation. Insertion of a specialized nasogastric tube after confirmation of a circumferential burn may prevent strictures. Dilation is indicated after 2 to 4 weeks if strictures are confirmed; if unsuccessful, either colonic intraposition or gastric tube placement may be performed. Consider early laparotomy in patients with severe esophageal and/or gastric burns. INHALATION EXPOSURE o DECONTAMINATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer 100 percent humidified supplemental oxygen with assisted ventilation as required. o INHALATION INJURY: Administer oxygen, obtain chest x-ray and blood gases and, if pulmonary edema is present, consider PEEP. Steroids may provide benefit but antibiotics are useful only if there is evidence of infection. 1. Evaluate for esophageal and other burns in severe cases. 2. Monitor patient for respiratory distress; if a cough or difficulty in breathing develops, evaluate for respiratory tract irritation, bronchitis, and pneumonia. EYE EXPOSURE o DECONTAMINATION: Exposed eyes should be irrigated with copious amounts of tepid water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist, the patient should be seen in a health care facility. o IRRIGATION: In a medical facility, irrigate with sterile saline for at least an hour or until the superior and inferior cul-de-sacs have been examined for particulate matter and returned to neutrality (pH paper touched to lower cul-de-sac). o EYE DAMAGE ASSESSMENT: It may take 48 to 72 hours after the burn to correctly assess the degree of ocular damage. The basis of such an evaluation is the degree of corneal opacification and perilimbal whitening. o EYE DAMAGE TREATMENT: If ocular damage is minor, topical mydriatics and antibiotics may be sufficient. If more extensive, one or more of the following may be tried, only with ophthalmologic consultation: acetazolamide, timolol, steroids, EDTA, cysteine, NAC, penicillamine, tetracycline, soft contact lenses, insertion of a methylmethacrylate ring, or saran wrap suturing. DERMAL EXPOSURE o DECONTAMINATION: Wash exposed area extremely thoroughly with soap and water. A physician may need to examine the area if irritation or pain persists. RANGE OF TOXICITY: o Undiluted acids are caustic especially to the oropharynx and pyloric end of the stomach. Dilute solutions are less hazardous. ANIMAL TOXICITY STUDIES: NON-HUMAN TOXICITY EXCERPTS: ... DEATH OF 2 OUT OF SIX HORSES DOSED ... WITH 15 L OF A 2.5% SOLUTION OF ACETIC ACID; TWO OTHER HORSES WERE SERIOUSLY AFFECTED AND ALL SHOWED SYMPTOMS OF ENTERITIS. ... DULLNESS, LOSS OF APPETITE, RED AND JAUNDICED APPEARANCE OF THE VISIBLE MUCOUS MEMBRANES AND RAPID PULSE AND RESPIRATION. POST MORTEM FINDINGS INCLUDED HEMORRHAGES IN THE SMALL INTESTINE AND ITS MESENTERY, HYPEREMIA OF THE MESENTERIC LYMPH NODES, DIPHTHERITIC INFLAMMATION OF THE SMALL COLON WITH SUBSEROUS HEMORRHAGES AND EDEMA OF THE RECTUM. [Clarke, M. L., D. G. Harvey and D. J. Humphreys. Veterinary Toxicology. 2nd ed. London: Bailliere Tindall, 1981. 171]**PEER REVIEWED** ... CONCN OF ACETIC ACID OF 0.5% OR MORE WERE FATAL TO RABBITS IF GIVEN ORALLY OR PER RECTUM. [Clarke, M. L., D. G. Harvey and D. J. Humphreys. Veterinary Toxicology. 2nd ed. London: Bailliere Tindall, 1981. 171]**PEER REVIEWED** STUDIES ON EFFECT OF ACETIC ACID ON GUINEA PIG SKIN INDICATE THAT CONCN FROM 80% TO GLACIAL PRODUCE SEVERE BURNS; FROM 50-80%, MODERATE TO SEVERE BURNS; & BELOW 50%, RELATIVELY MILD INJURY. [Patty, F. (ed.). Industrial Hygiene and Toxicology: Volume II: Toxicology. 2nd ed. New York: Interscience Publishers, 1963. 1778]**PEER REVIEWED** Suckling rats were exposed to one of three soln, 2.6X10-3 M lead acetate, 5X10-3 M acetic acid or water, from parturition until the pups were 18 days old. Male offspring from dams on acetic acid demonstrated above normal preweaning body weights and were significantly less active than normals in the open field by day 44. [Barrett J, Livesey PJ; Neurobehav Toxicol Teratol 4 (1): 105-8 (1982)]**PEER REVIEWED** Acetic acid is harmful to aquatic life. High concentrations will produce pH levels toxic to oxidizing bacteria, inhibiting oxygen demand. [Environment Canada; Tech Info for Problem Spills: Acetic acid (Draft) p.1 (1981)]**PEER REVIEWED** Liquid glacial acetic acid causes devastating injury when applied to the eyes of rabbits. [Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986. 39]**PEER REVIEWED** /ACETIC ACID/ ... PENETRATES INTACT CORNEAL EPITHELIUM RAPIDLY & REACHES IRIS IN CONCN HIGH ENOUGH TO CAUSE IRITIS. [Klaassen, C.D., M.O. Amdur, Doull J. (eds.). Casarett and Doull's Toxicology. The Basic Science of Poisons. 5th ed. New York, NY: McGraw-Hill, 1995. 589]**PEER REVIEWED** Ethanol and its metabolites acetaldehyde and acetic acid were injected into the eggs during incubation, and the course of the egg development was observed during 21 days covering 3 stages (early, middle, and terminal). Lethal eggs occurred mainly in the early stage. The toxicity was the highest for acetaldehyde, followed by ethanol and acetic acid in decreasing order. Chickens with some deformities were hatched from treated eggs. A strong resemblance was shown between the deformities in the chickens during the early stage of development and the fetal alc syndrome in man at the 3rd month of gestation. [Kawamoto K; Nichidai Igaku Zasshi 40 (3): 249-59 (1981)]**PEER REVIEWED** ... Inhalation of 16,000 ppm killed one of six exposed rats. ... Minor changes in respiration in guinea pigs inhaling 5 ppm acetic acid, with more pronounced effects at 100 ppm. [American Conference of Governmental Industrial Hygienists, Inc. Documentation of the Threshold Limit Values and Biological Exposure Indices. 6th ed. Volumes I,II, III. Cincinnati, OH: ACGIH, 1991. 6]**PEER REVIEWED** A major class of disinfection by-products found in drinking water are the haloacetic acids. Haloacetic acids can be formed by a variety of processes, e.g. chloroacetic acids can be formed during chlorination and bromoacetic acids can be by-products of ozonation. Both dichloro- and trichloroacetic acids have been reported to be teratogenic. There is little information regarding the developmental toxicity of bromoacetates and no structure-activity analysis of haloacetates. Therefore, 3-6 somite CD-1 mouse embryos were exposed to acetic acid (AA), or mono (M), di (D), and tri (T) substituted chloro (C) or bromo (B)-acetic acids (A) (e.g. DCA= dichloroacetic acid) in whole embryo culture and the morphological effects were evaluated. Conceptuses exposed to these agents for 24 hours exhibited malformations. Neural tube defects ranged from prosencephalic hypoplasia to non-closure throughout the cranial region. Other craniofacial defects included optic, otic and pharyngeal arch dysmorphogenesis. Benchmark concentrations (BC) for a 5% increase in NTDs for the studied chemicals in order of increasing potency are dichloroacetic acid (2452 uM)less than acetic acid (1888 uM) less than tribromoacetic acid (1403 uM) less than trichloroacetic acid (1336 uM) less than dibromoacetic acid (162 uM) less than monochloroacetic acid (91.5 uM) less than monobromoacetic acid (2.68 uM). Quantitative structure-activity relationships were derived from these data and other (iodo(I) and fluoro (F)) haloacetic acid data not presented (monoiodoacetic acid, monofluoroacetic acid, difluoroacetic acid, trifluoroacetic acid). The best regression was derived by excluding acetic acid (n=10) and relating log (1/BC) to Elumo and pKa with r = 0.96, adj.r2 = 0.90. These studies indicate that all of the haloacetates can directly alter development and there is a wide range of concentration that produce dysmorphogenesis. [Rogers EH et al; Teratology 51 (3): 195 (1995)]**PEER REVIEWED** NON-HUMAN TOXICITY VALUES: LC50 Guinea pig inhalation 5,000 ppm/1 hr [Verschueren, K. Handbook of Environmental Data of Organic Chemicals. 2nd ed. New York, NY: Van Nostrand Reinhold Co., 1983. 146]**PEER REVIEWED** LC50 Mouse inhalation 5,000 ppm/1 hr [Verschueren, K. Handbook of Environmental Data of Organic Chemicals. 2nd ed. New York, NY: Van Nostrand Reinhold Co., 1983. 146]**PEER REVIEWED** LDL0 Rabbit rectal 600 mg/kg [ITII. Toxic and Hazarous Industrial Chemicals Safety Manual. Tokyo, Japan: The International Technical Information Institute, 1982. 2]**PEER REVIEWED** Pseudomonas putida (bacteria) 2850 mg/l toxic effect: cell multiplication inhibition [Verschueren, K. Handbook of Environmental Data of Organic Chemicals. 2nd ed. New York, NY: Van Nostrand Reinhold Co., 1983. 145]**PEER REVIEWED** LD50 Rat oral 3.53 g/kg [Budavari, S. (ed.). The Merck Index - Encyclopedia of Chemicals, Drugs and Biologicals. Rahway, NJ: Merck and Co., Inc., 1989. 9]**PEER REVIEWED** ECOTOXICITY VALUES: LC50 Fathead minnows > 315 mg/l/1 hr; 122 mg/l/24 hr; 92 mg/l/48 hr; 88 mg/l/72 hr; 88 mg/l/96 hr (static bioassay in reconstituted water at 18-22 deg C) [Verschueren, K. Handbook of Environmental Data of Organic Chemicals. 2nd ed. New York, NY: Van Nostrand Reinhold Co., 1983. 145]**PEER REVIEWED** LC50 Fathead minnows 175 mg/l/1 hr; 106 mg/l/24 hr; 106 mg/l/48 hr; 79 mg/l/72 hr; 79 mg/l/96 hr (static bioassay in reconstituted water at 18-22 deg C, pH < 5.9) [Verschueren, K. Handbook of Environmental Data of Organic Chemicals. 2nd ed. New York, NY: Van Nostrand Reinhold Co., 1983. 145]**PEER REVIEWED** TLm Culex (larvae) 1,500 mg/l/24-48 hr /Conditions of bioassay not specified/ [Verschueren, K. Handbook of Environmental Data of Organic Chemicals. 2nd ed. New York, NY: Van Nostrand Reinhold Co., 1983. 146]**PEER REVIEWED** LD0 Creek chub 100 mg/l/24 hr; Detroit river /Conditions of bioassay not specified/ [Verschueren, K. Handbook of Environmental Data of Organic Chemicals. 2nd ed. New York, NY: Van Nostrand Reinhold Co., 1983. 145]**PEER REVIEWED** LD100 Creek chub 200 mg/l/24 hr; Detroit river /Conditions of bioassay not specified/ [Verschueren, K. Handbook of Environmental Data of Organic Chemicals. 2nd ed. New York, NY: Van Nostrand Reinhold Co., 1983. 145]**PEER REVIEWED** TLm Daphnia magna (Arthropoda) 47 mg/l/24 hr /Conditions of bioassay not specified/ [Verschueren, K. Handbook of Environmental Data of Organic Chemicals. 2nd ed. New York, NY: Van Nostrand Reinhold Co., 1983. 145]**PEER REVIEWED** TLm Bluegill 75 mg/l/96 hr /Conditions of bioassay not specified/ [Verschueren, K. Handbook of Environmental Data of Organic Chemicals. 2nd ed. New York, NY: Van Nostrand Reinhold Co., 1983. 145]**PEER REVIEWED** TLm Lepomis macrochirus 100-1000 mg/l/24 hr /Conditions of bioassay not specified/ [Verschueren, K. Handbook of Environmental Data of Organic Chemicals. 2nd ed. New York, NY: Van Nostrand Reinhold Co., 1983. 145]**PEER REVIEWED** TLm Mosquito fish 251 mg/l/24-96 hr /Conditions of bioassay not specified/ [Verschueren, K. Handbook of Environmental Data of Organic Chemicals. 2nd ed. New York, NY: Van Nostrand Reinhold Co., 1983. 145]**PEER REVIEWED** Goldfish: lethal dose at 423 mg/l 20 hr, period of survival at pH 6.8 is 48 hr to 4 days at 100 ppm; period of survival at pH 7.3 is 4 days at 10 ppm [Verschueren, K. Handbook of Environmental Data of Organic Chemicals. 2nd ed. New York, NY: Van Nostrand Reinhold Co., 1983. 145]**PEER REVIEWED** TLm Sunfish 75 mg/l/96 hr 18-20 deg C, soft water [Environment Canada; Tech Info for Problem Spills: Acetic Acid (Draft) p.76 (1981)]**PEER REVIEWED** LC50 Shrimp 100-300 mg/l/48 hr aerated water [Environment Canada; Tech Info for Problem Spills: Acetic Acid (Draft) p.76 (1981)]**PEER REVIEWED** TLm Brine shrimp 22 mg/l/48 hr /Conditions of bioassay not specified/ [Environment Canada; Tech Info for Problem Spills: Acetic Acid (Draft) p.76 (1981)]**PEER REVIEWED**
Content copyright 2005 Arlene Mullin


Formaldehyde Studies on Kidneys

 

DE logo
The following information was generated from the Hazardous Substances Databank (HSDB), a database of the National Library of Medicine's TOXNET system (http://toxnet.nlm.nih.gov) on August 18, 2000.

Query: Information added from CHEMID: formaldehyde ( fannoform, formalith, formol, fyde, lysoform, morbicid, oxomethane, oxymethylene, superlysoform ) Registry Numbers: 50-00-0 1 NAME: FORMALDEHYDE HSN: 164 RN: 50-00-0 HUMAN HEALTH EFFECTS: EVIDENCE FOR CARCINOGENICITY: CLASSIFICATION: B1; probable human carcinogen. BASIS FOR CLASSIFICATION: Based on limited evidence in humans, and sufficient evidence in animals. Human data include nine studies that show statistically significant associations between site-specific respiratory neoplasms and exposure to formaldehyde or formaldehyde-containing products. An increased incidence of nasal squamous cell carcinomas was observed in long-term inhalation studies in rats and in mice. The classification is supported by in vitro genotoxicity data and formaldehyde's structural relationships to other carcinogenic aldehydes such as acetaldehyde. HUMAN CARCINOGENICITY DATA: Limited. ANIMAL CARCINOGENICITY DATA: Sufficient. [U.S. Environmental Protection Agency's Integrated Risk Information System (IRIS) on Formaldehyde (50-00-0) Available from: http://www.epa.gov/ngispgm3/iris on the Substance File List as of March 15, 2000]**QC REVIEWED** A2. A2= Suspected human carcinogen. [American Conference of Governmental Industrial Hygienists. Threshold Limit Values (TLVs) for Chemical Substances and Physical Agents and BiologicalExposure Indices (BEIs) for 1995-1996. Cincinnati, OH: ACGIH, 1995. 22]**QC REVIEWED** Evaluation: There is limited evidence in humans for the carcinogenicity of formaldehyde. There is sufficient evidence in experimental animals for the carcinogenicity of formaldehyde. Overall evaluation: Formaldehyde is probably carcinogenic to humans (Group 2A). [IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer,1972-PRESENT. (Multivolume work).,p. 62 336 (1995)]**QC REVIEWED** HUMAN TOXICITY EXCERPTS: IF SOLN IS INGESTED, MUCOUS MEMBRANES OF MOUTH, THROAT, & INTESTINAL TRACT ARE IRRITATED, & SEVERE PAIN, VOMITING, & DIARRHEA RESULT. AFTER ABSORPTION, FORMALDEHYDE DEPRESSES CNS & SYMPTOMS NOT UNLIKE THOSE OF ALC INTOXICATION ARE NOTED. THEY CONSIST OF VERTIGO, DEPRESSION, & COMA. RARELY CONVULSIONS ARE OBSERVED. [Goodman, L.S., and A. Gilman. (eds.) The Pharmacological Basis of Therapeutics. 5th ed. New York: Macmillan Publishing Co., Inc., 1975. 993]**PEER REVIEWED** ALTERATION OF TISSUE PROTEINS BY FORMALDEHYDE CAUSES LOCAL TOXICITY & PROMOTES ALLERGIC REACTIONS. REPEATED CONTACT WITH SOLN ... MAY CAUSE ECZEMATOID DERMATITIS. DERMATITIS FROM CLOTHING TREATED WITH FORMALDEHYDE ... HAS OCCURRED. [Gilman, A. G., L. S. Goodman, and A. Gilman. (eds.). Goodman and Gilman's The Pharmacological Basis of Therapeutics. 6th ed. New York: Macmillan Publishing Co., Inc. 1980. 971]**PEER REVIEWED** AQ SOLN ... SPLASHED OR DROPPED ON HUMAN EYES HAVE CAUSED INJURIES RANGING FROM SEVERE PERMANENT CORNEAL OPACIFICATION & LOSS OF VISION TO MINOR TRANSIENT INJURY OR DISCOMFORT, DEPENDING UPON WHETHER SOLN WERE OF HIGH OR LOW CONCN. [Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986. 443]**PEER REVIEWED** INHALATION OF HIGH CONCN ... CAUSED SEVERE IRRITATION OF RESP TRACT, LEADING IN 2 INSTANCES TO DEATH. ... PULMONARY EDEMA, WITH RESIDUAL CARDIAC IMPAIRMENT IN 1 CASE, WAS REPORTEDLY CAUSED BY SINGLE ACUTE INHALATIONS ... . [American Conference of Governmental Industrial Hygienists. Documentation of the Threshold Limit Values and Biological Exposure Indices. 5th ed. Cincinnati, OH:American Conference of Governmental Industrial Hygienists, 1986. 276]**PEER REVIEWED** IN SENSITIZED SUBJECTS SPECIFIC LATE ASTHMATIC REACTIONS MAY BE PROVOKED BY BRIEF EXPOSURES AT APPROX 3 PPM. [HENDRICK DJ ET AL; J OCCUP MED 24 (11): 893 (1982)]**PEER REVIEWED** Ingestion of formaldehyde can cause a reduction in body temperature. [Environment Canada; Tech Info for Problem Spills: Formaldehyde p.83 (1985)]**PEER REVIEWED** Symptoms related to ingestion of formaldehyde include: jaundice, acidosis, and hematuria. Symptoms related to inhalation include: rhinitis, anosmia, laryngospasm, tracheitis, and gastroenteritis. [ITII. Toxic and Hazardous Industrial Chemicals Safety Manual. Tokyo, Japan: The International Technical Information Institute, 1988. 250]**PEER REVIEWED** In a survey of 57 embalmers who were exposed to atmospheric concn below 2 ppm, there was a high incidence of symptoms of irritant effects on the eyes (81%) nose and throat (75%). Other respiratory effects included cough (33%), chest tightness (23%), wheezing (12%), and shortness of breath (11%). On the basis of the results, 10% were acute bronchitics, and 30% were chronic bronchitics. No control group was used and cigarette smoking was not taken into account. [Plunkett ER, Barbela T; Am Ind Hyg Assoc J 38: 61 (1977)]**PEER REVIEWED** Eyes: concn 1-10 ppm may produce appreciable eye irritation on initial exposure; lacrimation occurs at about 4 ppm. [Health and Safety Executive Monograph: Formaldehyde p.8 (1981)]**PEER REVIEWED** CULTURED BRONCHIAL & FIBROBLASTIC CELLS FROM HUMANS WERE USED TO STUDY DNA DAMAGE & TOXICITY. FORMATION OF CROSSLINKS BETWEEN DNA & PROTEINS, CAUSED SINGLE-STRAND BREAKS IN DNA, & INHIBITED RESEALING OF SINGLE-STRAND BREAKS PRODUCED BY IONIZING RADIATION. [GRAFSTROM RC ET AL; SCIENCE 220 (4593): 216-8 (1983)]**PEER REVIEWED** Formaldehyde induced a 1.5-3 fold increase in sister chromatid exchanges in ... human lymphocytes in culture. [Obe G, Beek B; Drug and Alcohol Dependence 4: 91-4 (1979)]**PEER REVIEWED** Formaldehyde was mutagenic for diploid human lymphoblasts in culture ... /inducing an incr number of mutations at/ 130 uM or 4 ppm by weight. [Goldmacher VS et al; Toxicol Epidemiol Mech (Pap Meet) 173-91 (1983)]**PEER REVIEWED** OUTBREAK OF HEMOLYTIC ANEMIA, ATTRIBUTED TO ACCIDENTAL EXPOSURE ... OCCURRED AMONG PATIENTS ON HEMODIALYSIS. 41 YR OLD WOMAN DIED 28 HR AFTER INGESTING 120 ML OF ... SOLN (37% WT/VOL FORMALDEHYDE, 12.5% VOL/VOL METHANOL, CONTAINING NO FORMIC ACID). [IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer,1972-PRESENT. (Multivolume work).,p. V29 369 (1982)]**PEER REVIEWED** EFFECTS IN WOMEN ATTRIBUTED TO EXPOSURE ... INCL MENSTRUAL DISORDERS & SECONDARY STERILITY. [IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer,1972-PRESENT. (Multivolume work).,p. V29 370 (1982)]**PEER REVIEWED** SYMPTOMATOLOGY: A. Inhalation: 1. Irritation of mucous membranes, especially of eyes, nose and upper respiratory tract. 2. With higher concn, cough, dysphagia, bronchitis, pneumonia, edema or spasm of the larynx. Pulmonary edema is uncommon. B. Ingestion. 1. Immediate intense pain in mouth, pharynx and stomach. 2. Nausea, vomiting, hematemesis, abdominal pain and occasionally diarrhea (which may be bloody). 3. Pale, clammy skin and other signs of shock. 4. Difficult micturition, hematuria, anuria. 5. Vertigo, convulsions, stupor, and coma. 6. Death due to respiratory failure. C. Skin contact: 1. Irritation and hardening of skin. Strong solutions produce coagulation necrosis. 2. Dermatitis and hypersensitivity from prolonged or repeated exposure. [Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984.,p. III-197]**PEER REVIEWED** INVESTIGATIONS OF CILIOSTATIC EFFECT OF ALDEHYDES ARE OF SPECIAL INTEREST SINCE MANY HAVE IRRITATING EFFECT ON TRACHEAL MUCOSA. COMPARISON OF CILIOSTATIC EFFECT SHOWED FORMALDEHYDE TO BE MOST TOXIC FOLLOWED BY ACETALDEHYDE & ACROLEIN. CROTONALDEHYDE & METHACROLEIN SHOWED WEAKEST EFFECT. TECHNIQUE USED FOR OBSERVING TRACHEAL CILIARY ACTIVITY WAS THE IN VITRO TECHNIQUE. [DALHAMN T, ROSENGREN A; ARCH OTOLARYNGOL 93 (5): 496-500 (1971)]**PEER REVIEWED** One hundred nine workers and 254 control subjects were studied to evaluate the effects of formaldehyde on the mucous membranes and lungs. A modified, respiratory symptom questionnaire and spirometry were administered to all study participants before and after their work shift, and formaldehyde levels were determined for each test subject. Over the course of the monitored work shift, test subjects demonstrated a dose-dependent excess of irritant symptoms and a statistically significant decline in certain lung function parameters. Baseline spirometry values were not significantly different between test and control groups, and formaldehyde-exposed workers did not report an excess of respiratory symptoms. Formaldehyde is a dose-dependent irritant of the eyes and mucous membranes at low-level exposures. It can exert a small, across-shift effect on airways but after a mean exposure of ten years does not appear to cause permanent respiratory impairment. [Horvath EP et al; J Am Med Assoc 259 (5): 701-7 (1988)]**PEER REVIEWED** The effect of formaldehyde exposure on medical students conducting dissections in the gross anatomy laboratory course /was evaluated using/ self-administered questionnaires designed to assess the frequency of occurrence of various symptoms indicating the acute effects of formaldehyde exposure. The questionnaires were given to a cohort of first-year medical students on completion of the gross anatomy laboratory course. Air sampling of formaldehyde levels in the anatomy laboratories was carried out on one day during the time in which these students were conducting dissections. ... Although the results of the air sampling showed formaldehyde levels to be well below current occupational standards, significant numbers of students reported experiencing symtoms associated with formaldehyde exposure. Estimates of the relative risk of experiencing formaldehyde-related symptoms in the anatomy laboratories compared to the control laboratories ranged from 2.0 to 19.0, depending on the particular symptom. In addition, it was found that female students were three times more likely to report formaldehyde-related symptoms than male students. [Fleischer JM; NY J Med 87 (7): 385-8 (1987)]**PEER REVIEWED** A population based case control study was undertaken in 13 counties of western Washington to determine if occupational formaldehyde exposure was related to cancer of the oropharynx and hypopharynx (OHPC, N= 205), nasopharynx (NPC, N= 27) or sinus and nasal cavity (SNC, N= 53). Controls were selected by random digit dialing (N= 552). A telephone interview inquired about lifetime occupational history as well as a number of potential confounding factors, including smoking and drinking. Approximately half (N= 143) of the case interviews were with next of kin. ... Logistic regression was used to estimate exposure odds ratios STET while taking into account multiple risk factors for each site. No significant associations were found between occupational formaldehyde exposure and any of the cancer sites under study. However, relative risk estimates associated with the highest exposure score categories were evaluated for oropharynx and hypopharynx (OR= 1.3, 95% Confidence Interval= 0.6-3.1) and nasopharynx (OR= 2.1, 95% Cl= 0.4-10.0). When an induction period was accounted for only oropharynx and hypopharynx and nasopharynx increased to 1.7 and 3.1, respectively. Several limitations in the study tend to conservatively bias the results. ... [Vaughn TL et al; Int J Cancer 38 (5): 677-84 (1986)]**PEER REVIEWED** Because of the paucity of scientific data concerning the inhalation toxicity of formaldehyde in humans, determinations of the symptoms and alterations in pulmonary function resulting from inhalation for 1 hr of 3 ppm formaldehyde were studied. The protocol consisted of randomized exposure of each subject to clean air or 3.0 ppm formaldehyde on 2 separate days. Twenty-two healthy normal subjects engaged in intermittent heavy exercise (VE= 65 /min) and 16 asthmatic subjects performed intermittent moderate exercise (VE= 37 /min). Symptoms and pulmonary functions were assessed during the time course of exposure; nonspecific airway reactivity was assessed after exposure. Both groups exhibited similar, significant (p < 0.01) increases in perceived odor, nose/throat irritation, and eye irritation throughout the exposure. The non-asthmatic group had the following slight but statistically significant (p < 0.02) lower pulmonary functions after 55 min of exposure to formaldehyde as compared to clean air: 3.8% in FEV1, 2.6% in FVC, and 2.8% in FEV3. The asthmatic group showed no statistically significant decrements in pulmonary function. [Green DJ et al; Am Rev Respir Dis 135 (6): 1261-6 (1987)]**PEER REVIEWED** A retrospective mortality analysis was conducted in a cohort of 9,365 individuals employed as of 1940 in two chrome leather tanneries in the United States and followed to the end of 1982. Vital status as of the closing date was determined for over 95% of the cohort. Potential hazardous workplace exposures varied with department and included ... formaldehyde. ... Mortality from all causes combined was lower than expected for each tannery. ... Deaths from cancer of each site, including the lung, were also lower than expected compared to those of either the population of the United States or of local state rates. A significant excess of deaths was observed, however, due to accidental causes in one tannery and cirrhosis of the liver, suicide, and alcoholism in the other. These excesses did not appear to be casually associated with occupational exposures. [Stern FB et al; Scand J Work Environ Health 13 (2): 108-17 (1987)]**PEER REVIEWED** Infectivity of human T-cell lymphotropic virus, Type III (HTLV-III) was ... efficiently inactivated by formalin ... . [Quinnan GV et al; Transfusion 26 (5): 481-3 (1986)]**PEER REVIEWED** Eight symptomatic individuals chronically exposed to indoor formaldehyde at low concentrations (0.07-0.55 ppm) were compared to 8 nonexposed subjects with respect to: (1) presence of IgG and IgE antibodies to formaldehyde conjugated to human serum albumin (F-HSA); (2) the percentage of venous blood T- and B-cells by E- and EAC-rosetting; and (3) the ability of T- and B-cells to undergo mitogen (phytohemagglutin and pokeweed) stimulated blastogenesis as measured by the incorporation of tritiated thymidine. Anti-F-HSA IgG, but not IgE, antibodies were detected in the sera of the 8 exposed subjects; none were found in 7 of the controls. T-lymphocytes were decreased in the exposed (48%) compared to the control (65.9%) subjects (p < 0.01). B-cells were 12.6% (exposed group) and 14.75% (controls) (p < 0.05). The incorporation of labeled thymidine by T-cells (phytohemagglutin) was decreased: 17,882 cpm (exposed group) and 28,576 cpm (p < 0.01). T- and B-cell blastogenesis (pokeweed) was 9,698 cpm (exposed group) and 11,279 (controls) (p < 0.1). [Thrasher JD et al; Arch Environ Health 42 (6): 347-50 (1987)]**PEER REVIEWED** Some alcoholic solutions /of formaldehyde/ are used industrially & the physical properties & hazards may be greatly influenced by the solvent. [Sax, N.I. Dangerous Properties of Industrial Materials. 6th ed. New York, NY: Van Nostrand Reinhold, 1984. 1451]**PEER REVIEWED** Both death and survival from 4-oz formalin ingestions have been reported in adults. The probable mean lethal adult dose is 1 to 2 oz. Death may occur within 3 hours; survival past 48 hours usually means recovery. [Ellenhorn, M.J. and D.G. Barceloux. Medical Toxicology - Diagnosis and Treatment of Human Poisoning. New York, NY: Elsevier Science Publishing Co., Inc. 1988. 1002]**PEER REVIEWED** An environmental survey of two wood products (plywood, particle-board) companies revealed mean concentrations in the plywood forming areas of 0.8 ppm and, in two particle-board forming areas, of 1.1 to 1.4 ppm /formaldehyde/. Ophthalmologic evaluations were conducted and eye irritation self-reports were collected from 84 subject workers, including unexposed controls, from various areas in the plants. Results from both were unremarkable, as were tests mapping their visual fields. However, there were subjective reports of at least occasional eye irritation in 67% of the exposed subjects, with more such reports coming from workers in areas of the plant with the higher concentrations. An explosion at the factory closed a major product line and resulted in laying off many of the volunteer subjects prior to performance testing; the remaining 49 workers were tested before and after their workshift (and 13 of them were tested on 2 days) in order to assess acute effects of formaldehyde on visual acuity, depth perception, peripheral vision, accommodation, eye movement and fixation, divided attention, and color vision. Subjective reports of eye irritation on the day of testing did not correlate, or correlated negatively, with formaldehyde concentrations on the test day, which averaged 0.4 ppm. Average visual test scores were better at the end of the day than at the beginning, and there was a trend for those with higher formaldehyde levels to demonstrate greater improvement. Some of the changes reached traditional levels of statistical significance. The results from this investigation, while relevant to the neurotoxicity of formaldehyde, suffer from the small sample size and the possibility that the comparison subjects had also experienced formaldehyde exposure. With these caveats, this study suggests that mean formaldehyde exposures at 0.4 ppm produce no deleterious acute effects on visual performance, but chronic exposures between 0.8 and 1.4 ppm may produce an increased incidence of self reported symptoms of eye irritation in persons who do not have clinical ophthalmologic defects. [O'Donoghue, J.L. (ed.). Neurotoxicity of Industrial and Commercial Chemicals. Volume I. Boca Raton, FL: CRC Press, Inc., 1985. 59]**PEER REVIEWED** Symptoms: Local: Conjunctivitis, corneal burns; brownish discoloration of skin; dermatitis, urticaria (hives), pustulovesicular eruption. Inhalation: rhinitis and anosmia (loss of sense of smell); pharyngitis, laryngospasm; tracheitis and bronchitis; pulmonary edema, cough, constriction in chest; dypsnea (difficult breathing), headache, weakness, palpitation (rapid heart beat), gastro enteritis (inflammation of the stomach and intestines). Ingestion: Burning in mouth and esophagus; nausea and vomiting; abdominal pain, diarrhea, vertigo (dizziness), unconsciousness, jaundice, albuminuria, hematuria, anuria, acidosis, convulsions. [ITII. Toxic and Hazardous Industrial Chemicals Safety Manual. Tokyo, Japan: The International Technical Information Institute, 1988. 249]**PEER REVIEWED** Aldehydes increase airflow at concentrations below those that decrease respiratory frequency. /Aldehydes/ [Gilman, A.G., T.W. Rall, A.S. Nies and P. Taylor (eds.). Goodman and Gilman's The Pharmacological Basis of Therapeutics. 8th ed. New York, NY. Pergamon Press, 1990. 1618]**PEER REVIEWED** Levels of formaldehyde exposure were measured in the dissecting facilities of the biology department of Montclair State College, Montclair, New Jersey during the 1982 through 1983 academic year. An air sampling pump was fitted with two impingers and used to collect air samples at a rate of 1 l/min for 1 hr at each site. A chromotropic acid/sulfuric acid solution was used to form a purple monocationic chromogen with formaldehyde, and absorbance was measured spectrophotometrically at 580 nanometers. Sampling sites and concentrations in ppm at each included a teaching lab (range from 7.0 to 16.5 ppm), rear stock room (range from 1.97 to 2.62 ppm), and a public hallway (less than 1.0 ppm). Both the 7 and the 16.5 ppm levels were above the standard established by OSHA and the standard of 2 ppm established by the American Conference of Governmental Industrial Hygienists. The 2.62 ppm reading was above the standard of 1 ppm for 30 minute exposures as recommended by NIOSH. [Korky JK et al; Bull Environ Contam Toxicol 38 (5): 907-10 (1987)]**PEER REVIEWED** Data on concentration of formaldehyde and 15 organic solvents in Finnish furniture factories from 1975 to 1984 were presented. Workers often complained of severe eye, nose, and upper respiratory tract irritation. Formaldehyde was collected in a 1% sodium bisulfite solution and analyzed by the chromatropic method. The solvents were adsorbed in a charcoal tube, desorbed with carbon-disulfide or dimethylformamide, and analyzed by gas chromatography. All highly exposed workers were monitored. The widest range of formaldehyde concentration was recorded in the operation of the curtain painting furniture receiving operation, which was between 0.2 and 5.4 ppm. The mean concentrations of most organic solvents studied ranged from 4 to 66 ppm. Formaldehyde levels were high and the 1 ppm exposure limit, defined as the 15 minute time weighted average by the Finnish Board of Labor Protection, was exceeded about 40% of the time. [Priha E et al; Ann Occup Hyg 30 (3): 289-94 (1986)]**PEER REVIEWED** A study of 759 histologically verified cancers of the nasal cavity (287 cases), paranasal sinuses (179 cases), and nasopharynx (293 cases) and 2465 cancer controls diagnosed in Denmark between 1970 and 1982 was conducted to investigate the importance of occupational exposure to formaldehyde. Information on job history for cases and controls was derived from a national data linkage system and exposure to formaldehyde and wood dust was assessed by industrial hygienists unaware of the case control status of the patients. The exposure rates for formaldehyde among male and female controls were 4.2% and 0.1% respectively. After proper adjustment for contemporary wood dust exposure, relative risk of 2.3 (95% CI= 0.9-5.8) for squamous cell carcinoma and 2.2 (95% CI= 7-7.2) for adenocarcinoma of the nasal cavity and paranasal sinuses were detected among men who have been exposed to formaldehyde in their job compared with those never exposed. [Olsen JH, Asnaes S; Br J Ind Med 43 (11): 769-74 (1986)]**PEER REVIEWED** The National Cancer Institute study on the relationship between exposure to formaldehyde and mortality from nasophryngeal cancer was evaluated. The study had indicated little evidence of a link between formaldehyde at concentrations normally encountered in the workplace and risk of nasopharyngeal cancer. Although the overall standardized mortality ration was significantly elevated in subjects exposed to formaldehyde, the overall risk did not increase with increasing intensity of exposure. A reanalysis, however, suggested that simultaneous exposure to poarticulates and formaldehyde could be a risk factor. A further review of the National Cancer Institute findings showed that the significant excess mortality was based on deaths occurring in a single factory (factory-A) and occurred primarily in short term employess. When the data were analyzed in terms of cumulative exposures that were known to include both formaldehyde and particulates, only the highest exposure group had a significantly increased excess nasopharyngeal cancer mortality. This excess was clearly located in factory-A. A followup study of factory-A that added 5 more years of followup was initiated. It showed no additional deaths from nasopharyngeal cancer even among workers with the highest formaldehyde and particulate exposures. The four deaths from nasopharyngeal cancer in this factory occurred in workers employed in the same department and hired between 1949 and 1955. Although these workers were exposed to formaldehyde and particulates, they were not among the most highly exposed. [Collins JJ et al; J NCI 80 (5): 376-7 (1988)]**PEER REVIEWED** This study evaluates the histological changes, especially the presence of possible precancerous lesions, in the nasal mucosa of workers exposed to formaldehyde. Nasal biopsies of 37 workers occupationally exposed to formaldehyde for more than five years and 37 age matched referents showed a higher degree of metaplastic alterations in the former group. In addition, three cases of epithelial dysplasia were observed among the exposed. These results indicate that formaldehyde may be potentially carcinogenic in man. Combination of this finding with the inconclusive epidemiological studies suggests that formaldehyde is a weak carcinogen and that occupational exposure to formaldehyde alone is insufficient to induce nasal cancer. [Boysen M et al; Br J Ind Med 47 (2): 116-21 (1990)]**PEER REVIEWED** Clinical and animal studies suggest that formaldehyde adsorbed on respirable particles may elicit a greater pulmonary physiologic and inflammatory effect than gaseous formaldehyde alone. This study was to determine if respirable carbon particles have a synergistic effect on the acute symptomatic and pulmonary physiologic response to formaldehyde inhalation. Normal, nonsmoking, methacholine-nonreactive subjects were exposed to 2 hr each of clean air, 3 ppm formaldehyde, 0.5 mg/cu m respirable activated carbon aerosol, and the combination of 3 ppm formaldehyde plus activated carbon aerosol. The subjects engaged in intermittent heavy exercise (VE= 57 1/min) for 15 min each half hour. Formaldehyde exposure was associated with significant increases in reported eye irritation, nasal irritation, throat irritation, headache, chest discomfort, and odor. Synergistic increases in cough, but not in other irritant respiratory tract symptoms, were observed with inhalation of formaldehyde and carbon. Small (less than 5%) synergistic decreases in FVC and FEV3 were also seen. No formaldehyde effect was observed on FEV1; however, we did observe small (less than 10%) significant decreases in FEF25-75%, which may be indicative of increased airway tone. Overall, results demonstrated synergism, but the effect is small and its clinical significance is uncertain. [Green DJ et al; J Toxicol Environ Health 28 (3): 261-75 (1989)]**PEER REVIEWED** To study the cytotoxic effect of formaldehyde on the human nasal mucosa 75 men with occupational exposure to formaldehyde or to formaldehyde and wood dust, were examined, looking particularly at early signs of irritative effects and histopathological at early signs of irritative effects and histopathological changes in the nasal mucosa. A nasal biopsy specimen was graded from 0-8 according to the morphological changes. A high frequency of nasal symptoms, mostly a running nose and crusting, was related to exposure to formaldehyde. Only three men had a normal mucosa; the remainder has loss of cilia and goblet cell hyperplasia (11%) and squamous metapolasia (78%); in six cases (8%) there was a mild dysplasia. The histological grading showed a significantly higher score when compared with unexposed controls (2.9 v 1.8). There was no dose response relation, no malignancies, and no difference in the histological score between those exposed to formaldehyde or to formaldehyde and wood dust. [Edling C et al; Br J Ind Med 45 (11): 761-5 (1988)]**PEER REVIEWED** A study of respiratory symptoms and pathophysiological effects associated with occupational exposure to formaldehyde and wood dust was conducted. The cohort consisted of 70 Swedish workers exposed to formaldehyde during the production of formaldehyde and formaldehyde based products (formaldehyde group) and 100 furniture workers exposed to formaldehyde and wood dust (formaldehyde/wood dust group). The comparisons consisted of 36 local government clerks. The formaldehyde group was exposed to 0.05 to 0.5 mg/cu m formaldehyde and the furniture workers to 0.2 to 0.3 mg/cu m formaldehyde and 1 to 2 mg/cu m wood dust. Annual formaldehyde exposures of the comparisons averaged 0.09 mg/cu m. Sixty four percent of the formaldehyde group, 53% of the formaldehyde/wood dust group, and 25% of the comparisons reported nasal discomfort. Symptoms from the lower airways were reported by 44% of the formaldehyde group, 39% of the formaldehyde/wood dust group, and 14 % of the comparisons. Symptoms of nasal obstruction and watery discharges were more frequent in the exposed subjects than in the comparisons. More pronounced nasal swelling was found in the cohort than in the comparisons. 20% of the formaldehyde and 15% of the formaldehyde/wood dust group had impaired mucociliary clearance versus only 3% of the comparisons. Both exposed groups had a reduced sense of smell. Forced vital capacity was significantly decreased in the exposed groups. [Holmstorm M, Wilhelmsson B; Scandinavian J Work Environ Health 14 (5): 306-11 (1988)]**PEER REVIEWED** A study was conducted to determine if pathologists with exposure to formaldehyde demonstrate an excess risk of cancer, particularly cancers of the nasopharyngeal and pharyngeal areas. A population of 6411 physicians with occupational formaldehyde exposure participated in the study. The occurrence of these types of cancers was 4.7 times higher in these persons than in a comparable sized group of psychiatrists, but even so it is difficult to determine the importance of this increased risk as being directly tied to formaldehyde exposure. Pathologists and other members of the study group were exposed to other chemicals and infectious agents as well as formaldehyde. There was an apparent excess of mortality from pancreatic cancer and brain cancers as well as leukemia. [Matanoski GM; Risks of Pathologists Exposed to Formaldehyde School of Hygiene and Public Health, Department of Epidemiology, Johns Hopkins University, Baltimore, Maryland, Grant No. RO1-OH-01511 (1989)]**PEER REVIEWED** The relation of chronic respiratory symptoms and pulmonary function to formaldehyde in homes was studied in a sample of 298 children (6-15 years of age) and 613 adults. Formaldehyde measurements were made with passive samplers during two 1 wk periods. Significantly greater prevalence rates of asthma and chronic bronchitis were found in children from houses with formaldehyde levels 60-120 ppb than in those less exposed, especially in children also exposed to environmental tobacco smoke. In children, levels of peak expiratory flow rates decreased linearly with formaldehyde exposur, with the estimated decrease due to 60 ppb of formaldehyde equivalent to 22% of peak expiratory flow rates level in nonexposed children. The effects in asthmatic children exposed to formaldehyde below 50 ppb were greater than in healthy ones. The effects in adults were less evident: decrements in peak expiratory flow rates due to formaldehyde over 40 ppb were seen only in the morning, and mainly in smokers. [Krzyzanowski M et al; Environ Res 52 (2): 117-25 (1990)]**PEER REVIEWED** The long term effects of formaldehyde on the respiratory tract have been investigated in a group of 164 workers exposed daily to the chemical during the production of urea formaldehyde resin, together with 129 workers not exposed to free formaldehyde. Exposure was classified as high (corresponding to an eight hour time weighted exposure of more than 2.0 ppm), medium (0.6 to 2.0 ppm), or low (0.1 to 0.5 ppm). 25% of workers had high exposure at some time and 17% moderate exposure. Both exposed and unexposed groups had an annual assessment that included lung function. The proportion with self reported respiratory symptoms was similar in the two groups, 12% and 16% reporting breathlessness on hurrying and 26% and 20% wheezing. The initial forced expiratory volume in one second was within 0.5 l (approximately on standard deviation) of the predicted value (by age and height) in 65% of the exposed and 59% of unexposed workers and more than 0.5 l below the predicted value in 9% of exposed and 11% unexposed workers. The mean decline in forced expiratory volume in one second was 42 ml a year (standard deviation 45) in the exposed and 41 ml a year in the unexposed group (standard deviation 40 ml a year). The rate of decline showed the expected association with smoking in the unexposed group, but in the exposed group the mean rate of decline in the never smokers was similar to that in current smokers. There were, however, relatively few never smokers and considerable variation in the rates of decline. In the exposed group no association was found between the rate of decline and indices of exposure to formaldehyde. Thus there is no evidence from this study of an excess of respiratory symptoms or decline in lung function in the workers exposed to formaldehyde. The similar rate of decline of forced expiratory volume in one second however in never smokers and smokers of the exposed group is consistent with finding of other studies for workers exposed to formaldehyde. [Nunn AJ et al; Br J Ind Med 47 (11): 747-52 (1990)]**PEER REVIEWED** A prospective evaluation of pulmonary function and respiratory symptoms was conducted among 103 medical students exposed to formaldehyde over a 7 month period to determine the incidence of bronchoconstriction and respiratory symptoms in response to exposure. Time-weighted average formaldehyde exposures were generally less than 1 ppm and peak exposures were less than 5 ppm. Acute symptoms of eye and upper respiratory irritation were significantly associated with exposure. There was no pattern of bronchoconstriction in response to exposure after either 2 weeks or 7 months. Twelve subjects had a history of asthma; they were likely to have symptoms of respiratory irritation or changes in pulmonary function than those without such a history. These findings are consistent with previous case reports that indicate exposure to formaldehyde vapor at levels that are commonly encountered in occupational and residential seetings do not commonly cause significant bronchonconstriction, even among subjects with preexisting asthma. [Uba G et al; Am J Ind Med 15 (1): 91-101 (1989)]**PEER REVIEWED** A case of anaphylactoid reaction to a patch test with formaldehyde was described. The 40 year old woman developed bronchospasm and laryngospasm following the inhalation of formaldehyde vapor. A year later she accidentally entered a hospital room relatively soon after it had been disinfected, and was hospitalized with dyspnea, cyanosis, bronchospasm, and laryngospasm. Days later she did react to a patch test with a 1% solution of formaldehyde in water. Pulmonary function tests 20 min after the patch test revealed a 50% reduction in FEV1 and a 63% reduction in MEF 25. [Orlandini A et al; Contact Dermatitis 19 (5): 383-4 (1988)]**PEER REVIEWED** Four groups of patients with long-term inhalation exposure to formaldehyde were compared with controls who had short-term periodic exposure to formaldehyde. The following were determined for all groups: total white cell, lymphocyte, and T cell counts; T helper/suppressor ratios; total Ta1+, IL2+, and B cell counts; antibodies to formaldehyde-human serum albumin conjugate and autoantibodies. When compared with the controls, the patients had significantly higer antibody titers to formaldehyde-human serum albumin. In addition, significant increases in Ta1+, IL2+, and B cells and autoantibodies were observed. Immune activation, autoantibodies, and anti formaldehyde-human serum albumin antibodies are associated with long-term formaldehyde inhalation. [Thrasher JD et al; Arch Environ Health 45 (4): 217-23 (1990)]**PEER REVIEWED** The incidence of spontaneous abortions among hospital staff who used ethylene oxide, glutaral (glutaraldehyde) and formaldehyde for the chemical sterilization of instruments was studied using data from a questionnaire and a hospital discharge register. ... When the staff were concerned in sterilizing during their pregnancy the frequency was 16.7% compared with 5.6% for the nonexposed pregnancies. The incr frequency ... correlated with exposure to ethylene oxide but not with exposure to glutaral or formaldehyde. [Hemminki K et al; Brit Med J 285: 1461-63 (1982)]**PEER REVIEWED** Employees exposed to formaldehyde in the woodworking industry and nonexposed control subjects were examined by spirometry and the nitrogen washout technique. A dose-response relationship was found between exposure to formaldehyde and decrease in lung function. Industrial exposure to formaldehyde causes transient lung function impairment over a work shift, with a cumulative effect over the years. The impairment, however, can be reversed with 4 wk of no exposure. [Alexandersson R, Hedenstierna G; Arch Environ Health 44 (1): 5-11 (1989)]**PEER REVIEWED** The mortality of 1,332 male workers employed at least 30 days in 1959-1980 in a resins-manufacturing plant was examined. Ambient measurements taken in the plant between 1974 and 1979 documented a potential for exposure to levels of formaldehyde as high or greater than 3.0 mg/cu m. Vital status was ascertained for 98.6% of the cohort members, and their mortality was compared with expected deaths drawn from the national and local population rates. A statistically significant increase in lung cancer was observed, based on 18 deaths, which was not fully accounted for by possible confounding factors linked to personal habits or sociocultural characteristics. This elevated risk, however, could not be attributed specifically to exposure to formaldehyde. Mortality from digestive cancer (14 deaths observed) and hematologic neoplasms (5 deaths observed) was not substantially higher than expected. [Bertazzi PA et al; Scand J Work Environ Health 12 (5): 461-8 (1986)]**PEER REVIEWED** SKIN, EYE AND RESPIRATORY IRRITATIONS: Contact with the skin causes irritation, tanning effect, and allergic sensitization. Contact with eyes causes irritation, itching, & lacrimation. ... [Environment Canada; Tech Info for Problem Spills: Formaldehyde p.2 (1985)]**PEER REVIEWED** MEDICAL SURVEILLANCE: Consider the skin, eyes, & resp tract in any placement or periodic examination, esp if the patient has a history of allergies. [Sittig, M. Handbook of Toxic and Hazardous Chemicals and Carcinogens, 1985. 2nd ed. Park Ridge, NJ: Noyes Data Corporation, 1985. 464]**PEER REVIEWED** PRECAUTIONS FOR "CARCINOGENS": Whenever medical surveillance is indicated, in particular when exposure to a carcinogen has occurred, ad hoc decisions should be taken concerning ... /cytogenetic and/or other/ tests that might become useful or mandatory. /Chemical Carcinogens/ [Montesano, R., H. Bartsch, E.Boyland, G. Della Porta, L. Fishbein, R. A. Griesemer, A.B. Swan, L. Tomatis, and W. Davis (eds.). Handling Chemical Carcinogens in the Laboratory:Problems of Safety. IARC Scientific Publications No. 33. Lyon, France: International Agency for Research on Cancer, 1979. 23]**PEER REVIEWED** POPULATIONS AT SPECIAL RISK: Mean formaldehyde levels are highest in hospital autopsy rooms compared with other commercial settings. /Hospital autopsy workers are possibly exposed/. [Ellenhorn, M.J. and D.G. Barceloux. Medical Toxicology - Diagnosis and Treatment of Human Poisoning. New York, NY: Elsevier Science Publishing Co., Inc. 1988. 1002]**PEER REVIEWED** Release of /formaldehyde/ vapors in mobile homes has been associated with headache and pulmonary and dermal irritation. /Occupants of mobile homes are possibly exposed/. [Ellenhorn, M.J. and D.G. Barceloux. Medical Toxicology - Diagnosis and Treatment of Human Poisoning. New York, NY: Elsevier Science Publishing Co., Inc. 1988. 1002]**PEER REVIEWED** PROBABLE ROUTES OF HUMAN EXPOSURE: Humans are exposed to formaldehyde from a variety of sources. The major source of atmospheric discharge is from combustion processes specifically from auto emissions and also from the photooxidation of hydrocarbons in auto emissions(1,2). Additional exposure to formaldehyde emissions comes from its use as an embalming fluid in anatomy labs, morgues, etc and its use as a fumigant and sterilant(1). Resin treated fabric, rugs, paper, etc and materials such as particle board and plywood which use resin adhesives and foam insulation release formaldehyde which may build up in homes and occupational atmospheres(1,2). Contact with industrial waste water, especially from lumber related operations where formaldehyde is used in adhesives, has resulted in the Pacific Northwest, Northeast, parts of Texas, and lumber areas of the south(1)(SRC). The estimated daily intake of formaldehyde among exposed Finnish workers is 3000 ug, whereas heavily exposed workers (particle-board and glue production, foundry work) is 10,000 ug(3). [(1) Kitchens JF et al; Investigation of Selected Potential Environmental Contaminants: Formaldehyde p. 22-98 USEPA 560/2-76-009 (1976) (2) National Research Council; Formaldehyde and Other Aldehydes p. 2-1 to 5-96 USEPA 600/6-82-002 (1982) (3) Hemminki K, Vainio H; Human Exposure to Potentially Carcinogenic Compounds. IARC Sci Publ 59: 37-45 (1984)]**PEER REVIEWED** Health hazards unique to particle board include the generation of urea-formaldehyde resin bound in wood aerosol and release of formaldehyde gas that can be inhaled by the worker. A particle board aerosol was generated by a sanding process and collected under laboratory conditions that determined the particle size distribution and formaldehyde content. Significant variations (p < 0.005) were observed for the particle board mass and gaseous formaldehyde collected between sample runs. No significant differences were observed for the aerosol size distribution determined and formaldehyde content in particle board aerosol per unit mass for sampling trials. [Stumpf JM et al; Am Indus Hyg Assoc J 47 (12): 725-30 (1986)]**PEER REVIEWED** ... /VAPORS/ GIVEN OFF DURING HOT MOLDING OF SYNTH RESINS (/IS A/ COMMON SOURCE OF EXPOSURE) ... A SURVEY OF 6 FUNERAL HOMES ... REVEALED MEAN CONCN, IN DIFFERENT ESTABLISHMENTS, BETWEEN 0.25 & 1.39 PPM. ... /EXPOSURES ARE ENCOUNTERED/ IN PHENOL-FORMALDEHYDE RESIN MOULDING PLANT ... /FROM WHICH/ CHRONIC AIRWAY OBSTRUCTION LOWERED FORCED EXPIRATORY VOL/FORCED VOL CAPACITY RATIO & EYE, NOSE & THROAT IRRITATION & LOWER RESP TRACT SYMPTOMS /HAVE BEEN OBSERVED/. [American Conference of Governmental Industrial Hygienists. Documentation of the Threshold Limit Values and Biological Exposure Indices. 5th ed. Cincinnati, OH:American Conference of Governmental Industrial Hygienists, 1986. 276]**PEER REVIEWED** ... /EXPOSURES TO/ FORMALDEHYDE VAPOR EMISSIONS IN PERMANENT-PRESS FABRICS INDUSTRY (8 PLANTS) /HAVE BEEN REPORTED IN WHICH/ CONCN RANGING ... FROM 0.3 TO 2.7 PPM (IN SEWING AREA) WITH AVG OF 0.68 PPM /WERE DETECTED/. COMPLAINTS CONSISTED OF ANNOYING ODOR (ODOR THRESHOLD, BELOW 1.0 PPM), CONSTANT PRICKLING IRRITATION OF MUCOUS MEMBRANES & DISTURBED SLEEP. [American Conference of Governmental Industrial Hygienists. Documentation of the Threshold Limit Values and Biological Exposure Indices. 5th ed. Cincinnati, OH:American Conference of Governmental Industrial Hygienists, 1986. 276]**PEER REVIEWED** FORTY-SEVEN SUBJECTS EXPOSED TO FORMALDEHYDE (MEAN AIR CONCN 0.45 MG/CU M) & 20 UNEXPOSED SUBJECTS, ALL EMPLOYED IN CARPENTRY SHOP WERE STUDIED. SYMPTOMS INVOLVING EYES & THROAT AS WELL AS CHEST OPPRESSION WERE SIGNIFICANTLY MORE COMMON IN EXPOSED THAN IN UNEXPOSED. [ALEXANDERSSON R ET AL; ARCH ENVIRON HEALTH 37 (5): 279-84 (1982)]**PEER REVIEWED** NIOSH (NOES 1981-1983) has statistically estimated that 206,935 workers are exposed to formaldehyde in the USA(5). In a 12-week study of exposure in a gross anatomy lab of a medical school, 44% of breathing room samples and 11% of ambient air samples were > 1.0 ppm the ceiling recommended by ACGIH; Half the breathing zone samples were between 0.6-1.0 ppm and the range was 0.3-2.63 ppm(1). A 1976 report estimates that 8000 US workers were potentially exposed to formaldehyde during its production(3). A more recent estimate of the number of exposed workers in industries producing and using formaldehyde and its derivatives range from 1.4-1.75 million(2). Concentrations of formaldehyde in occupational areas dating from the 1960's and early 1970's are: textile plant 0-2.7 ppm, 0.68 ppm avg; garment factory 0.9-2.7 ppm; clothing store 0.9-3.3 ppm; laminating plant 0.04-10 ppm; funeral homes 0.09-5.26 ppm, 0.25-1.39 ppm avg; resin manufacture and paper production 16-30 ppm; paper conditioning 0.9-1.6 ppm; wood processing 31.2 ppm max(2). Concns in occupational settings dating from the late 70's are: textile plants 0.1-0.5 ppm, 0.2 ppm avg; shoe factory 0.9-2.7 ppm, 1.9 ppm avg; particle board plant 0.1-4.9 ppm, 1.15 ppm avg; plywood plant 0.1-1.2 ppm, 0.35 ppm avg; wooden furniture manufacturing plant 0.1-5.4 ppm, 1.35 ppm avg; adhesive plants 0.8-3.5 ppm, 1.75 ppm avg; foundries 0.05-2.0 ppm, 0.6 ppm avg; construction sites 0.5-7.0 ppm, 2.8 ppm avg; hospitals and clinics 0.05-3.5 ppm, 0.7 ppm avg(2). More recent survey results for occupational environments include: fertilizer production 0.2-1.9 ppm; dyestuffs < 0.1-5.8 ppm; textile manufacture < 0.1-1.4 ppm; resins (foundry) < 0.1-5.5 ppm; bronze foundry 0.12-0.8 ppm; iron foundry < 0.02-18.3 ppm; treated paper 0.14-0.99 ppm; hospital autopsy room 2.2-7.9 ppm; plywood industry 1.0-2.5 ppm; urea-formaldehyde foam applicators < 0.08-2.4 ppm(4). [(1) Skisak, CM; Amer Ind Hyg Assoc J 44: 948-50 (1983) (2) IARC; Monograph. Some Industrial Chemicals and Dyestuffs 29: 345-89 (1982) (3) National Research Council; Formaldehyde and other Aldehydes p.2-1 to 5-96 USEPA 600/6-82-002 (1982) (4) Bernstein RS et al; Am Ind Hyg Assoc J; 45: 778-85 (1984) (5) NIOSH; National Occupational Exposure Survey (1985)]**PEER REVIEWED** AVERAGE DAILY INTAKE: AIR INTAKE (assume 2-20 ppb) 50-500 ug; in energy efficient houses (assume 212 ppb day, 114 ppb night) 4500 ug;. The estimated daily exposure of the Finnish population to formaldehyde from community air is 100 ug and from the home environment, 1000 ug(1); WATER INTAKE (assume 0 ppb) 0 ug; FOOD - insufficient data.; TOBACCO - 50 ug(1). [(1) Hemminki K, Vainio H; Human Exposure to Potentially Carcinogenic Compounds. IARC Sci Publ 59: 37-45 (1984)]**PEER REVIEWED** MINIMUM FATAL DOSE LEVEL: Approximate Minimum Lethal Dose (MLD) (150-lb man): 30 ml [Arena, J. M. Poisoning: Toxicology, Symptoms, Treatments. Fourth Edition. Springfield, Illinois: Charles C. Thomas, Publisher, 1979. 97]**PEER REVIEWED** EMERGENCY MEDICAL TREATMENT: EMERGENCY MEDICAL TREATMENT: EMT COPYRIGHT DISCLAIMER: Portions of the POISINDEX(R) database are provided here for general reference. THE COMPLETE POISINDEX(R) DATABASE, AVAILABLE FROM MICROMEDEX, SHOULD BE CONSULTED FOR ASSISTANCE IN THE DIAGNOSIS OR TREATMENT OF SPECIFIC CASES. Copyright 1974-1998 Micromedex, Inc. Denver, Colorado. All Rights Reserved. Any duplication, replication or redistribution of all or part of the POISINDEX(R) database is a violation of Micromedex' copyrights and is strictly prohibited.

Peractic Acid Studies

DE logo

* * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * *
* HAZARDOUS SUBSTANCES DATA BANK (HSDB) *
* *
* Produced by : U.S. National Library of Medicine *
* Provided by : Canadian Centre for Occupational Health and Safety *
* * * * * * * * * * * * * * * * * * * * Issue : 2000-2 (May, 2000) *

*** SUBSTANCE IDENTIFICATION ***

HSDB CHEMICAL NAME : PERACETIC ACID
HSDB NUMBER : 1106
LAST REVISION DATE : 20000309
CAS REGISTRY NUMBER : 79-21-0
SYNONYMS:
ACETIC PEROXIDE ; ACETYL HYDROPEROXIDE ; ACIDE PERACETIQUE (FRENCH) ; Acide peroxyacetique (French) ; Acido peroxiacetico (Spanish) ; Caswell No. 644 ; DESOXON 1 ; EPA Pesticide Chemical Code 063201 ; Estosteril ; ETHANEPEROXOIC ACID ; HYDROPEROXIDE, ACETYL ; KYSELINA PEROXYOCTOVA (Czech) ; Monoperacetic acid ; OSBON AC ; PAA [REF-1, p.406]; PEROXOACETIC ACID ; PEROXYACETIC ACID ; Proxitane 4002
MOLECULAR FORMULA : C2-H4-O3
WISWESSER LINE NOTATION : QOV1 [REF-2, p.85/8507]
RTECS NUMBER : NIOSH/SD8750000
SHIPPING NUMBER/NAME:
UN 2131; Peroxyacetic acid, not more than 43% and not more than 6% hydrogen peroxide
NA 2131; Peracetic acid solution, not over 43% peracetic acid and not over 6% hydrogen peroxide
IMO 5.2; Peroxyacetic acid, not more than 43% and with not more than 6% hydrogen peroxide

*** DESCRIPTION AND WARNING PROPERTIES ***

COLOR/FORM:
Colorless liquid [REF-3]
ODOR:
Acrid [REF-4, p.1231]
SKIN, EYE, AND RESPIRATORY IRRITATIONS:
Vapor: Irritating to eyes, nose & throat. Liquid: Irritating to skin & eyes. [REF-5]
Strong skin and eye irritant. [REF-6, p.46]

*** SAFETY HAZARDS AND PROTECTION ***

DOT EMERGENCY GUIDELINES:
. Fire or explosion: May explode from heat or contamination. May ignite combustibles (wood, paper, oil, clothing, etc.). May be ignited by heat, sparks or flames. May burn rapidly with flare-burning effect. Containers may explode when heated. Runoff may create fire or explosion hazard. /Peracetic acid, solution/ [REF-7, p.G-147]
. Health: TOXIC; inhalation, ingestion or contact (skin, eyes) with vapors, dusts or substance may cause severe injury, burns, or death. Contact of vapor or substance with eyes may cause blindness within minutes. Fire may produce irritating, corrosive and/or toxic gases. Toxic fumes or dust may accumulate in confined areas (basement, tanks, hopper/tank cars, etc.). Runoff from fire control or dilution water may cause pollution. /Peracetic acid, solution/ [REF-7, p.G-147]
. Public safety: CALL Emergency Response Telephone Number on Shipping Paper first. If Shipping Paper not available or no answer, refer to appropriate telephone number listed on the inside back cover. Isolate spill or leak area immediately for at least 25 to 50 meters (80 to 160 feet) in all directions. Keep unauthorized personnel away. Stay upwind. Keep out of low areas. /Peracetic acid, solution/ [REF-7, p.G-147]
. Protective clothing: Wear positive pressure self-contained breathing apparatus (SCBA). Wear chemical protective clothing which is specifically recommended by the manufacturer. Structural firefighters' protective clothing is recommended for fire situations ONLY; it is not effective in spill situations. /Peracetic acid, solution/ [REF-7, p.G-147]
. Evacuation: Large spill: Consider initial evacuation for at least 250 meters (800 feet). Fire: If tank, rail car or tank truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions. /Peracetic acid, solution/ [REF-7, p.G-147]
. Fire: Small fires: Dry chemical, CO2, water spray or regular foam. Large fires: Flood fire area with water from a distance. Do not use straight streams. Move containers from fire area if you can do it without risk. Do not move cargo or vehicle if cargo has been exposed to heat. Fight fire from maximum distance or use unmanned hose holders or monitor nozzles. Cool containers with flooding quantities of water until well after fire is out. ALWAYS stay away from the ends of tanks. For massive fire, use unmanned hose holders or monitor nozzles; if this is impossible, withdraw from area and let fire burn. /Peracetic acid, solution/ [REF-7, p.G-147]
. Spill or leak: ELIMINATE all ignition sources (no smoking, flares, sparks or flames in immediate area). Keep combustibles (wood, paper, oil, etc.) away from spilled material. Do not touch damaged containers or spilled material unless wearing appropriate protective clothing. Keep substance wet using water spray. Stop leak if you can do it without risk. Small spills: Take up with inert, damp, noncombustible material using clean non-sparking tools and place into loosely covered plastic containers for later disposal. Large spills: Wet down with water and dike for later disposal. Prevent entry into waterways, sewers, basements or confined areas. DO NOT CLEAN-UP OR DISPOSE OF, EXCEPT UNDER SUPERVISION OF A SPECIALIST. /Peracetic acid, solution/ [REF-7, p.G-147]
. First aid: Move victim to fresh air. Call emergency medical care. Apply artificial respiration if victim is not breathing. Administer oxygen if breathing is difficult. Remove and isolate contaminated clothing and shoes. Remove material from skin immediately. In case of contact with substance, immediately flush skin or eyes with running water for at least 20 minutes. Keep victim warm and quiet. Ensure that medical personnel are aware of the material(s) involved, and take precautions to protect themselves. /Peracetic acid, solution/ [REF-7, p.G-147]

** FIRE AND REACTIVITY **

FIRE POTENTIAL:
. Flammable liquid. [REF-8, p.2611]
. Dangerous fire hazard by chemical reaction with reducing agents or exposure to heat. /Organic peroxides/ [REF-8, p.2611]

NFPA HAZARD CLASSIFICATION:
. Health: 3. 3= Materials that, on short exposure, could cause serious temporary or residual injury, including those requiring protection from all bodily contact. Fire fighters may enter the area only if they are protected from all contact with the material. Full protective clothing, including self-contained breathing apparatus, coat, pants, gloves, boots and bands around legs, arms, and waist, should be provided. No skin surface should be exposed. /Peracetic acid diluted with 60% acetic acid/ [REF-9, p.325M-77]
. Flammability: 2. 2= Includes materials that must be moderately heated before ignition will occur and includes Class II and IIIA combustible liquids and solids and semi-solids that readily give off ignitible vapors. Water spray may be used to extinguish fires in these materials because the materials can be cooled below their flash points. /Peracetic acid diluted with 60% acetic acid/ [REF-9, p.325M-77]
. Reactivity: 4. 4= Includes materials that, in themselves, are readily capable of detonation, explosive decomposition, or explosive reaction at normal temperatures and pressures. This includes materials that are sensitive to local mechanical or thermal shock. If a material having this Reactivity Hazard Rating is involved in an advanced or massive fire, the area should be immediately evacuated. /Peracetic acid diluted with 60% acetic acid/ [REF-9, p.325M-77]

FLASH POINT:
40.6 deg C (Open cup) [REF-10, p.400]

AUTOIGNITION TEMPERATURE:
392 deg F (200 deg C) /Peracetic acid (less than 40%)/ [REF-9, p.49-134]

FIRE FIGHTING PROCEDURES:
. Use flooding quantities of water. Use water spray to keep fire-exposed containers cool. Fight fire from protected location or maximum possible distance. Approach fire from upwind to avoid hazardous vapors and toxic decomposition products. /Peracetic acid (less than 40%)/ [REF-9, p.49-133]
. To fight fire, use water, foam, CO2. [REF-8, p.2611]

EXPLOSIVE LIMITS AND POTENTIAL:
. Liquid will detonate if concn rises above 56% because of evaporation of acetic acid. [REF-5]
. SPONTANEOUS CHEMICAL REACTION, IGNITION OR EXPLOSION MAY OCCUR IF MIXED WITH READILY OXIDIZABLE, ORGANIC OR FLAMMABLE MATERIALS OR CHEMICAL ACCELERANTS. [REF-9, p.49-134]
. Severe explosion hazard when exposed to heat or by spontaneous chemical reaction. Explodes violently at 110 deg C. [REF-8, p.2611]
. It is insensitive to impact but explodes violently at 110 deg C. The solid acid has exploded at -20 deg C. [REF-11]

REACTIVITIES AND INCOMPATIBILITIES:
. Explosive reaction with acetic anhydride; 5-p-chlorophenyl-2,2-dimethyl-3-hexanone. Violent reaction with ether solvents (e.g., tetrahydrofuran; diethyl ether); metal chloride solutions (e.g., calcium chloride; potassium chloride; sodium chloride); olefins; organic matter. [REF-8, p.2611]
. Upon contact with reducing materials, such as organic matter or thiocyanates, an explosion can occur. /Organic peroxides/ [REF-8, p.2611]

DECOMPOSITION:
. DECOMPOSES VIOLENTLY @ 230 DEG F (110 DEG C) /PERACETIC ACID DILUTED WITH 60% ACETIC ACID/ [REF-9, p.325M-77]
. When heated to decomposition it emits acrid smoke and irritating fumes. [REF-8, p.2611]

OTHER HAZARDOUS REACTIONS:
. Shock- and friction-sensitive when concentrated above 56%. /Peracetic acid (less than 40%)/ [REF-9, p.49-134]

** PROTECTIVE EQUIPMENT AND CONTROLS **

PROTECTIVE EQUIPMENT AND CLOTHING:

. Self-contained breathing apparatus; full protective clothing (goggles, rubber gloves, etc) [REF-5]

OTHER PREVENTATIVE MEASURES:

. METHODS ARE ADOPTED FOR HANDLING PERACETIC ACID IN AIR-CONDITIONED LAB FOR GERM-FREE ANIMALS TO MINIMIZE AMT OF FREE ACID VAPOR CIRCULATING. TECHNIQUES HELPED TO CONFINE & NEUTRALIZE PERACETIC ACID VAPOR. [REF-12]
. SRP: The scientific literature for the use of contact lenses in industry is conflicting. The benefit or detrimental effects of wearing contact lenses depend not only upon the substance, but also on factors including the form of the substance, characteristics and duration of the exposure, the uses of other eye protection equipment, and the hygiene of the lenses. However, there may be individual substances whose irritating or corrosive properties are such that the wearing of contact lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In any event, the usual eye protection equipment should be worn even when contact lenses are in place.

** STORAGE, CLEANUP AND DISPOSAL **

STABILITY/SHELF LIFE:
. Thermally unstable. [REF-9, p.49-133]
. After 30 days the specific formulations Peracetic Acid 20 g/l, Peracetic Acid N 20 g/l (with wetting agent), and Peracetic Acid Spirit show a loss of peracetic acid of 25, 35, 22%, respectively, with storage at 2-5 degrees. [REF-13]

STORAGE CONDITIONS:
. Store in a cool, dry, well-ventilated location. Separate from acids, alkalies, organic materials, heavy metals. Normally kept refrigerated outside or detached storage is preferred. /Peracetic acid (less than 40%)/ [REF-9, p.49-134]

CLEANUP METHODS:
. Cover with weak reducing agents such as hypo, bisulfites or ferrous salts. Bisulfites or ferrous salts need additional promoter of some 3M sulfuric acid for rapid reaction. Transfer the slurry (or sludge) into a large container of water and neutralize with soda ash. ... [REF-10, p.400]
. Eliminate all ignition sources. Use water spray to cool and disperse vapors; protect personnel, and dilute spills to form nonflammable mixtures. Absorb in noncombustile material for proper disposal. ... /Peracetic acid (less than 40%)/ [REF-9, p.49-133]

DISPOSAL METHODS:
. /SRP: For laboratory scale quantities/: Destruction procedure: Add 5 ml or 5 g of the compound to 100 ml of 10% (w/v) sodium metabisulfite solution and stir the mixture at room temp. Test for completeness of destruction by adding a few drops of the reaction mixture to an equal volume of 10% (w/v) potassium iodide soln, acidifying with 1 M hydrochloric acid soln, and adding a drop of starch as an indicator. A deep blue color indicates the presence of excess oxidant. If destruction is complete, discard the mixture. If destruction is not complete, add more sodium metabisulfite soln until a negative test is obtained. /Peracids/ [REF-14, p.329]
. SRP: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.

*** HEALTH HAZARDS AND TOXIC EFFECTS ***

HUMAN TOXICITY EXCERPTS:

SYMPTOMATOLOGY (... INGESTION OR SKIN CONTACT): 1. CORROSION OF MUCOUS MEMBRANES OF MOUTH, THROAT AND ESOPHAGUS, WITH IMMEDIATE PAIN AND DYSPHAGIA. NECROTIC AREAS ... GRAYISH WHITE BUT SOON ACQUIRE A BLACKISH DISCOLORATION (YELLOW IN CASE OF NITRIC ACID) & SOMETIMES SHRUNKEN OR WRINKLED TEXTURE ... 2. EPIGASTRIC PAIN ... MAY BE ASSOC WITH NAUSEA & VOMITING ... AT TIMES, GASTRIC HEMORRHAGE MAY BE INTENSE, AND VOMITUS THEN CONTAINS FRESH BLOOD. PROFOUND THIRST. 3. ULCERATION OF ALL MEMBRANES AND TISSUES WITH WHICH THE ACID COMES IN CONTACT. AFTER THE INGESTION OF CONCN MINERAL ACID, THIS CORROSION MAY LEAD WITHIN A FEW HR OR A FEW DAYS TO GASTRIC PERFORATION AND PERITONITIS. 4. CIRCULATORY COLLAPSE WITH CLAMMY SKIN, WEAK & RAPID PULSE, SHALLOW RESP, AND SCANTY URINE. CIRCULATORY SHOCK IS OFTEN IMMEDIATE CAUSE OF DEATH. 6. LATE ESOPHAGEAL, GASTRIC & PYLORIC STRICTURES & STENOSES, WHICH MAY REQUIRE MAJOR SURGICAL REPAIR, SHOULD BE ANTICIPATED. SIGNS OF OBSTRUCTION COMMONLY A!
PPEAR WITHIN A FEW WK BUT MAY BE DELAYED FOR MONTHS AND EVEN YEARS. PERMANENT SCARS MAY ALSO APPEAR IN THE CORNEA, SKIN AND OROPHARYNX. 7. UNCORRECTED CIRCULATORY COLLAPSE OF SEVERAL HR ... MAY LEAD TO RENAL FAILURE & ISCHEMIC LESIONS IN LIVER & HEART. /ACIDS/ [REF-15, p.III-10]

PERACETIC ACID HAS BEEN IDENTIFIED AS A CILIA TOXIC & MUCOUS COAGULATING AGENT IN URBAN AIR POLLUTION. [REF-16, p.339]

No adverse effects such as fever, chills, burning sensation of the shunt, headache, or bacteremia were seen after 80 dialyses with reprocessed dialyzers disinfected with peracetic acid, using dialyzers up to 6 times. [REF-17]

Patients receiving hemodialysis therapy risk exposure to both disinfectants and sterilants. Reuse of dialyzers has introduced the use of sterilants such as peracetic acid. The use of these sterilants is recognized as a potential risk, and residue tests are carried out for the presence of these sterilants at the ppm level. [REF-18]

When Renalin was used for reprocessing hemodialyzers, decreases in clearance of urea, creatinine, vitamin B-12 and a fall in KUF was observed. [REF-19]

NON-HUMAN TOXICITY EXCERPTS:

Virus inactivation by peracetic acid was observed in a municipal sewage effluent. [REF-20]

Mice and guinea pigs were exposed to peracetic acid aerosol (186 or 280 mg/cu m) 30 min twice daily for 90 days. Bronchopneumonia and liver granuloma were observed in most of the animals. Increased incidence of lung tumors and decreased leukocyte counts were observed in mice. [REF-21]

Topical application of a 0.12% solution of peroxyethanoic acid 2 times daily for either 28 or 90 days, with a regimen of 5 days of treatment followed by 2 days of no treatment, caused general systemic toxic effects in the /guinea pigs/; the effects were more pronounced with the 90 day treatment. [REF-22]

Guinea pigs exposed to inhalation of 1 or 3% solutions of peracetic acid for 3 days showed eye irritation and coughing, both in a concn-related manner. The mucosas of the respiratory tract of animals treated with a 3% solution showed histopathological alterations whereas the animals treated with 1% did not show such toxic effects. [REF-23]

Peracetic acid at 3% caused dermatitis on guinea pig skin with the dermatitis starting after 2 hr of direct contact. There was no dermatitis after 5 hr of direct contact with a 1% solution. [REF-24]

Peroxyacetic acid was assayed for induction of unscheduled DNA synthesis by liquid scintillation counting of hot acid extractable DNA and light microscope autoradiography. Peroxyacetic acid was also assayed for induction of DNA repair synthesis by differential density labeling ultracentrifugation. Conflicting results were obtained for peroxyacetic acid using the unscheduled DNA synthesis techniques. Negative results were consistently obtained, however, in 3 separate assays using 2 different peroxyacetic acid samples with the more definitive differential density DNA repair synthesis technique. Hydrogen peroxide was present as a contaminant in the peroxyacetic acid samples. Peroxyacetic acid does not induce DNA repair synthesis and the conflicting peroxyacetic acid results may be due to the presence of hydrogen peroxide in commercial samples of peroxyacetic acid. [REF-25]

Peracetic acid at a concentration of 0.1% in water has been found to be ... irritating to rabbit's eyes. However, 10% solution causes ulceration and perforation of the cornea and formation of symblepharon, despite prompt irrigation with water after application to the rabbit's eye. [REF-26, p.708]

Four chemicals were evaluated for their efficacy against Fusarium oxysporum. Peratol, a hydrogen peroxide and peracetic acid containing formulation, gave 100% kill after 80 min at a concentration of 0.5%. [REF-27]

There is no release of evaporable toxic substances into the air after disinfection with the exception of products based on peracetic acid. Cell cultures are chosen as indicators for the toxicity of evaporable substances. It is shown that the cells were able to propagate in the presence of active oxygen containing disinfectants as well as in the blanc test. However, there was no propagation of cells in the presence of formaldehyde, glutardialdehyde and peracetic acid. [REF-28]

In a long term experiment on rabbits, 0.2% peracetic acid (0.5% Wofasteril) was applied to the dorsal skin, the oral and the vaginal mucosa 3 times per week for 12 months. Each type of tissue received 153 individual doses. The histological examinations did not yield dysplasias in the sense of a carcinogenic action of peracetic acid. Despite the very high dose, the mucosal tissues under study showed neither inflammations nor scar formation after 12 months. A loss of minute accessory hairs on the dorsal skin was observed. [REF-29]

... The characterization of the skin tolerance to several disinfectants /was studied/. ... Guinea pig epidermis was treated for 1, 7 and 14 days with conventional working dilution of peracetic acid ... disinfectant. ... The exposure to the disinfectant caused a disappearance of histochemically detectable Langerhans cells in treated epidermis. .... [REF-30]

Histological investigations were made on uteri of 61 cattle (27 of them after intrauterine treatment). The response activated by 0.2% peracetic acid in the bovine endometrium was a primary inflammatory process, however, necrotizing within clearly pronounced limits. Degenerative alterations were the major histological findings 35 min from application of 0.2% peracetic acid. They were recordable from the epithelium but at that point in time could easily affect the entire cellular stratum. Histopathological phenomena on the fourth day from application of 0.2% peracetic acid were clearly less strongly pronounced than on the third day. Histiocyte infiltrates of moderate and rarely high intensity reflected incr phagocytosis in the process of endometrial regeneration. [REF-31]

** EMERGENCY TREATMENT **

ANTIDOTE AND EMERGENCY TREATMENT:

For immediate first aid: Ensure that adequate decontamination has been carried out. If victim is not breathing, start artificial respiration, preferably with a demand-valve resuscitator, bag-valve-mask device, or pocket mask as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep victim quiet and maintain normal body temperature. Obtain medical attention. /Organic peroxides/ [REF-32, p.134]

For basic treatment: Establish a patent airway. Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if necessary. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... Monitor for shock and treat if necessary ... Anticipate seizures and treat if necessary ... For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with normal saline during transport ... Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool. Do not attempt to neutralize because of exothermic reaction. Cover skin burns with dry, sterile dressings after decontamination ... . /Organic peroxides/ [REF-32, p.135]

*** METABOLISM AND PHARMACOLOGY ***

MECHANISM OF ACTION:

To explore possible mechanisms of the arachidonic acid deficiency of the RBC membrane in alcoholics, the effect of ethanol and its oxidized products, acetaldehyde and peracetic acid, with other peroxides on the accumulation of 14(C)arachidonate into RBC membrane lipids in vitro was compared. Incubation of erythrocytes with 50 mM ethanol or 3 mM acetaldehyde had no effect on arachidonate incorporation. Pretreatment of erythrocytes with 10 mM hydrogen peroxide, 0.1 mM cumene hydroperoxide or 0.1 mM t-butyl hydroperoxide had little effect on 14(C)arachidonate incorporation in the absence of azide. However, pretreatment of cells with N-ethylmaleimide, 0.1 mM peracetic acid or performic acid, with or without azide, inhibited arachidonate incorporation into phospholipids but not neutral lipids. In chase experiments, peracetate also inhibited transfer of arachidonate from neutral lipids to phospholipids. To investigate a possible site of this inhibition of arachidonate transfer!
into phospholipids by percarboxylic acids, a repair enzyme, arachidonoyl CoA: 1-palmitoyl-sn-glycero-3-phosphocholine acyl transferase was assayed. As in intact cells, phospholipid biosynthesis was inhibited more by N-ethylmalemide and peracetic acid than by hydrogen peroxide, cumene hydroperoxide, and t-butyl hydroperoxide. Peracetic acid was the only active inhibitor among ethanol and its oxidized products studied and may deserve further examination in ethanol toxicity. [REF-33]

*** ENVIRONMENTAL FATE AND EXPOSURE POTENTIAL ***

ENVIRONMENTAL FATE/EXPOSURE SUMMARY:

Peracetic acid's production and use as a bleaching agent, fungicide and bactericide may result in its release to the environment through various waste streams. It is also formed naturally in the environment through a series of photochemical reactions involving formaldehyde and photo-oxidant radicals. Based on an experimental vapor pressure of 14.5 mm Hg at 25 deg C, peracetic acid is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase peracetic acid is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals with an estimated atmospheric half-life of about 4 days. Due to its high water solubility, it can dissolve in clouds and rainwater and has been identified as a constituent of acid rain. Peracetic acid is expected to have very high mobility in soils based on an estimated Koc value of 4. Volatilization from dry soil surfaces is expected based upon the vapor pressure of this compound. Volatilization from moist soil su!
rfaces is also expected based upon the measured Henry's Law constant of 2.14X10-6 atm-cu m/mol. This compound has been shown to biodegrade under aerobic conditions. In water, peracetic acid is not expected to adsorb to suspended solids or sediment based upon its estimated Koc value. A measured pKa value of 8.2 indicates that peracetic acid is expected to dissociate somewhat at environmental pH values. This compound is also expected to slowly hydrolyze to acetic acid and hydrogen peroxide. Volatilization from water surfaces is expected to occur slowly given its measured Henry's Law constant. Estimated half-lives for a model river and model lake are 15 and 112 days, respectively. Bioconcentration in aquatic organisms is considered low based upon an estimated BCF value of 1. Occupational exposure may be through inhalation and dermal contact with this compound at workplaces where peracetic acid is produced or used. (SRC)

ENVIRONMENTAL FATE:

. TERRESTRIAL FATE: Based on a recommended classification scheme(1), an estimated Koc value of 4(SRC), determined from a structure estimation method(2), indicates that peracetic acid is expected to have very high mobility in soil(SRC). Volatilization of peracetic acid from dry soil surfaces is expected based upon the measured vapor pressure of 14.5 mm Hg at 25 deg C(3,SRC). Volatilization of peracetic acid from moist soil surfaces(SRC) is also expected given a measured Henry's Law constant of 2.14X10-6 atm-cu m/mole at 25 deg C(4). Peracetic acid is expected to biodegrade in soils as indicated by an aerobic screening test(5). [REF-34]
. AQUATIC FATE: Based on a recommended classification scheme(1), an estimated Koc value of 4(SRC), determined from a structure estimation method(2), indicates that peracetic acid is not expected to adsorb to suspended solids and sediment in water(SRC). Peracetic acid will volatilize slowly from water surfaces(3,SRC) based on a measured Henry's Law constant of 2.14X10-6 atm-cu m/mole at 25 deg C(4). Estimated half-lives for a model river and model lake are 15 and 112 days, respectively(3,SRC). A measured pKa value of 8.2 indicates that peracetic acid is expected to dissociate somewhat at environmental pH values(4,SRC). Peracetic acid is expected to hydrolyze slowly to acetic acid and hydrogen peroxide in water(5). According to a classification scheme(6), an estimated BCF value of 1(3,SRC), from an estimated log Kow of -1.09(7,SRC), suggests that bioconcentration in aquatic organisms is low(SRC). Peracetic acid is expected to biodegrade as indicated by an aerobic screening t!
est(8). [REF-35]
. ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), peracetic acid, which has an experimental vapor pressure of 14.5 mm Hg at 25 deg C(2), will exist solely as a vapor in the ambient atmosphere. Vapor-phase peracetic acid is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be about 4 days(3,SRC). This compounds high water solubility enables it to be removed from the atmosphere by wet deposition and become a constituent in acid rain(4). [REF-36]

BIODEGRADATION:

. Using a standard BOD dilution technique and a sewage inoculum, a theoretical BOD of greater than 70% was observed for peracetic acid over an unspecified time frame(1). [REF-37]

ABIOTIC DEGRADATION:

. The rate constant for the vapor-phase reaction of peracetic acid with photochemically-produced hydroxyl radicals has been estimated as 4.04X10-12 cu cm/molecule-sec at 25 deg C(1). This corresponds to an atmospheric half-life of about 4 days at an atmospheric concentration of 5.0X10+5 hydroxyl radicals per cu cm(1,SRC). A measured pKa value of 8.2 indicates that peracetic acid is expected to dissociate somewhat at environmental pH values(2,SRC). Peracetic acid is expected to hydrolyze slowly to acetic acid and hydrogen peroxide in water(3). [REF-38]

BIOCONCENTRATION:

. An estimated BCF value of 1 was calculated for peracetic acid(SRC), using an estimated log Kow of -1.09(1,SRC) and a recommended regression-derived equation(2). According to a classification scheme(3), this BCF value suggests that bioconcentration in aquatic organisms is low(SRC). [REF-39]

SOIL ADSORPTION/MOBILITY:

. Using a structure estimation method based on molecular connectivity indices(1), the Koc for peracetic acid can be estimated to be about 4(SRC). According to a recommended classification scheme(2), this estimated Koc value suggests that peracetic acid is expected to have high mobility in soil(SRC). [REF-40]

VOLATILIZATION FROM WATER/SOIL:

. The Henry's Law constant for peracetic acid is measured as 2.14X10-6 atm-cu m/mole(SRC) at 25 deg C(1). This value indicates that peracetic acid will volatilize slowly from water surfaces(2,SRC). Based on this Henry's Law constant, the volatilization half-life from a model river (1 m deep, flowing 1 m/sec, wind velocity of 3 m/sec) is estimated as approximately 15 days(2,SRC). The volatilization half-life from a model lake (1 m deep, flowing 0.05 m/sec, wind velocity of 0.5 m/sec) is estimated as approximately 112 days(2,SRC). Peracetic acid is expected to volatilize from dry soil surfaces given its experimental vapor pressure of 14.5 mm Hg at 25 deg C(3,SRC). [REF-41]

** SOURCES AND CONCENTRATIONS **

NATURAL OCCURRING SOURCES:
. Peracetic acid is formed naturally in the environment through a series of photochemical reactions involving formaldehyde and photo-oxidant radicals(1). This compound's high water solubility enables it to become a constituent in acid rain(1). [REF-42]

ARTIFICIAL SOURCES:
. Peracetic acid's production and use as a bleaching agent, fungicide and bactericide(1) may result in its release to the environment through various waste streams(SRC). [REF-43]

WATER CONCENTRATIONS:
. RAIN/SNOW: Acidic precipitation contains peracetic acid at nanomolar to low micromolar concentrations(1). [REF-42]

** HUMAN ENVIRONMENTAL EXPOSURE **

PROBABLE ROUTES OF HUMAN EXPOSURE:
. Occupational exposure to peracetic acid can occur through dermal contact and inhalation of vapor(1,SRC); personal protective equipment, including eye protection equipment, should be worn by persons handling the material(1). [REF-44, p.44-5]
. NIOSH (NOES Survey 1981-1983) has statistically estimated that 1,729 workers (92 of these are female) are potentially exposed to peracetic acid in the US(1). Occupational exposure may be through inhalation and dermal contact with this compound at workplaces where peracetic acid is produced or used(SRC). [REF-45]

*** STANDARDS AND REGULATIONS ***

TRANSPORT METHODS AND REGULATIONS:
. No person may /transport,/ offer or accept a hazardous material for transportation in commerce unless that person is registered in conformance ... and the hazardous material is properly classed, described, packaged, marked, labeled, and in condition for shipment as required or authorized by ... /the hazardous materials regulations (49 CFR 171-177)./ [REF-46]
. The International Maritime Dangerous Goods Code lays down basic principles for transporting hazardous chemicals. Detailed recommendations for individual substances and a number of recommendations for good practice are included in the classes dealing with such substances. A general index of technical names has also been compiled. This index should always be consulted when attempting to locate the appropriate procedures to be used when shipping any substance or article. [REF-47, p.5198-2, 5198-3]

CERCLA REPORTABLE QUANTITIES:
. Releases of CERCLA hazardous substances are subject to the release reporting requirement of CERCLA section 103, codified at 40 CFR part 302, in addition to the requirements of 40 CFR part 355. Peracetic acid is an extremely hazardous substance (EHS) subject to reporting requirements when stored in amounts in excess of its threshold planning quantity (TPQ) of 500 lbs. [QR] [REF-48]

FIFRA REQUIREMENTS:
. As the federal pesticide law FIFRA directs, EPA is conducting a comprehensive review of older pesticides to consider their health and environmental effects and make decisions about their future use. Under this pesticide reregistration program, EPA examines health and safety data for pesticide active ingredients initially registered before November 1, 1984, and determines whether they are eligible for reregistration. In addition, all pesticides must meet the new safety standard of the Food Quality Protection Act of 1996. Pesticides for which EPA had not issued Registration Standards prior to the effective date of FIFRA, as amended in 1988, were divided into three lists based upon their potential for human exposure and other factors, with List B containing pesticides of greater concern and List D pesticides of less concern. Peroxyacetic acid is found on List D. Case No: 4072; Pesticide type: Fungicide, Herbicide, Rodenticide, Antimicrobial; Case Status: RED Approved 12/93;!
OPP has made a decision that some/all uses of the pesticide are eligible for reregistration, as reflected in a Reregistration Eligibility Decision (RED) document.; Active ingredient (AI): Peroxyacetic acid; AI Status: OPP has completed a Reregistration Eligibility Decision (RED) document for the case/AI. [QR] [REF-49, p.331]

*** MONITORING AND ANALYSIS METHODS ***

ANALYTIC LABORATORY METHODS:

. Peracetic acid was determined in disinfectant containing hydrogen peroxide by mixing 20 ml disinfectant with 1 g sodium fluoride and titrating with 0.1 N potassium iodide until the pink color remains. The solution is then mixed with potassium iodide, and the iodide formed is titrated with 0.1 N sodium thiosulfate with starch indicator. [REF-50]
. Rapid photometric method to determine the contents of active chlorine and peracetic acid in soln of disinfectants. [REF-51]

*** MANUFACTURING AND USE INFORMATION ***

METHODS OF MANUFACTURING:
. [SRI] REACTION OF HYDROGEN PEROXIDE AND GLACIAL ACETIC ACID IN THE PRESENCE OF SULFURIC ACID CATALYST.
. PREPARED FROM ACETALDEHYDE AND OXYGEN IN PRESENCE OF COBALT ACETATE. BY THE AUTO-OXIDN OF ACETALDEHYDE. A 50% SOLN MAY BE OBTAINED FROM ACETIC ANHYDRIDE, HYDROGEN PEROXIDE, & SULFURIC ACID. [REF-4, p.1231]
. COMMERCIALLY, OZONE IS USED AS A CATALYST BELOW 15 deg C IN THE PRODUCTION OF PERACETIC ACID FROM ACETALDEHYDE AND OZONE [REF-52, p.V16 687]

FORMULATIONS/PREPARATIONS:
. 40% peracetic acid, 40% acetic acid, 5% hydrogen peroxide, 13% water, 500 ppm stabilizer [REF-5]
. Grade: technical [REF-3]
. Commercially available as a 40% solution in acetic acid. [REF-15, p.II-108]

MANUFACTURERS:
. FMC Corporation, Hq, 200 E Randolph Dr, Chicago, IL 60601, (312) 861-6000; Chemical Products Group, 1735 Market St, Philadelphia, PA 19103; Peroxygen Chemical Div, River Rd and Sawyer Ave, PO Box 845, Buffalo, NY 14240; Production site: Buffalo, NY 14240 [REF-53, p.782]
. Union Carbide Corporation, Hq, Old Ridgeway Road, Danbury, CT 06817, (203) 794-2000; Subsidiary: Union Carbide Chemicals and Plastics Co, Inc; Solvents and Coatings Materials Div; Production site: Taft, LA 70057 [REF-53, p.782]

OTHER MANUFACTURING INFORMATION:
. A bioprosthesis sterilized with peracetic acid can be detoxified within 5 min by treatment with a sodium sulfite solution or by storing once in distilled water for 3 days. [REF-54]
. Storage of swine aortas in pH 5.6 buffered 1.332 M formaldehyde or 26.30 mM peracetic acid for 180 days gave no differences in mechanical strength and stability of the prostheses. [REF-55]
. Reprocessing of dialyzers using peracetic acid is an alternative to formaldehyde. [REF-17]

MAJOR USES:
. BACTERICIDE & FUNGICIDE, ESPECIALLY IN FOOD PROCESSING; REAGENT IN MAKING CAPROLACTAM; SYNTHETIC GLYCEROL [REF-3]
. BLEACHING TEXTILES, PAPER, OIL, WAXES, STARCH; POLYMERIZATION CATALYST; EPIOXIDATION OF FATTY ACID ESTERS AND EPOXY RESINS PRECURSORS [REF-3]
. Peracetic acid at a concentration of 0.1% in water has been found to be an effective disinfectant for Schiotz tonometers. ... [REF-26, p.708]
. POSTHARVEST SPRAY FOR BANANAS, CITRUS, BERRIES, OTHER FRUITS, VEGETABLES, AND CONTAINERS; WASH FOR EGGS; TREATMENT FOR CONTAINERS FOR HARVESTING CROPS. [REF-56, p.C-282]

U.S. PRODUCTION:
[SRI] (1972) PROBABLY GREATER THAN 1.08X10+10 G
[SRI] (1974) GREATER THAN 1.08X10+10 G

*** CHEMICAL AND PHYSICAL PROPERTIES ***

MOLECULAR WEIGHT : 76.05 [REF-4, p.1231]
MELTING POINT : -0.2 DEG C [REF-57, p.3-156]
BOILING POINT : 105 DEG C [REF-3]
DENSITY/SPECIFIC GRAVITY : 1.226 @ 15 DEG C/4 DEG C [REF-57, p.3-156]
VAPOR PRESSURE : 14.5 mm Hg at 25 deg C [REF-58]
CORROSIVITY : Corrosive to most metals, including aluminum [REF-5]
Highly corrosive [REF-15, p.II-108]
DISSOCIATION CONSTANTS:
pKa= 8.20 at 25 deg C [REF-59, p.5-53]
VISCOSITY : 3.280 cP @ 78 deg F [REF-5]

SOLUBILITIES:
. VERY SOL IN WATER, ETHER, SULFURIC ACID; SOL IN ETHANOL [REF-57, p.3-156]

SPECTRAL PROPERTIES:
. INDEX OF REFRACTION: 1.3974 @ 20 DEG C/D; MAX ABSORPTION (WATER): BELOW 240 NM (LOG E= GREATER THAN 1.4) [REF-60, p.C-96]
. UV: 3-4 (Organic Electronic Spectral Data, Phillips et al, John Wiley & Sons, New York) [REF-61, p.V2 37]

OTHER CHEMICAL/PHYSICAL:
. Oxidizing material dangerous in contact with organic materials, explodes at 110 deg C. [REF-3]
. Henry's Law constant: 2.08X10-6 atm cu m/mole at 25 deg C (experimental) [REF-62]

*** REFERENCES ***

SPECIAL REPORTS:

. Flemming HC; Peracetic Acid as Disinfectant--A Review Zentralbl Bakteriol Mikrobiol Hyg (B) 179 (2): 97-111 (1984). A review on peracetic acid as a disinfectant.
. USEPA; Chemical Profiles: Peracetic Acid (1985). Aspects covered in this data sheet: chemical identity; exposure limits; physicochemical properties; fire and explosion hazards; reactivity; health hazards; uses; handling of spills or releases.
. Lai DY, et al; J Environ Sci Hlth 14 (1, Pt C): 63-80 (1996). Carcinogenic potential of organic peroxides prediction based on structure activity relationships and mechanism based short term test.

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*** END OF RECORD ***
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