Print
Details: Category: reuse | Published: 18 August 2014 | Hits: 3898

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