Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0152030 (skin irritation)
 2,146 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

TAHT (1,3,5-triacryloylhexahydro-s-triazine), a reactive chemical coupling agent, was highly toxic following a single peroral dose of an aqueous suspension (10% w/v) to Wistar rats, or following application of TAHT in dichloromethane (DCM) solution (10% w/v) to covered skin of New Zealand rabbits. It was moderately toxic when applied dermally as an aqueous paste. Ocular contact with 25 mg of TAHT in a 5% aqueous suspension, or of 0.5 mg of TAHT in a 10% (w/v) solution in DCM, produced severe corneal damage, iritis and blepharo-conjunctivitis. A 30-min exposure of uncovered rabbit skin to 1 mg of TAHT in a 10% (w/v) aqueous suspension produced only slight skin irritation. However, 24-h exposures to TAHT on covered skin produced erythema, edema, ecchymoses, scabs, and death depending upon dosage and vehicle. In vitro genotoxicity studies revealed no positive effects upon gene mutations (HGPRT locus) or on sister chromatid exchanges (SCEs) of CHO cells exposed to TAHT with and without a rat-liver S9 metabolic activation system. TAHT did not increase the levels of [3H]thymidine incorporation in a test for unscheduled DNA synthesis with primary rat hepatocytes. In contrast, substantial increases in the number of chromosome breaks and rearrangements were observed in chromosome preparations used for the SCE analyses. The clastogenic activity of TAHT was confirmed in an in vitro chromosome aberration test with CHO cells. Treatment-related increases in chromosome breakage were observed at two independent sampling times and positive effects did not depend upon the presence or absence of a metabolic activation system. Clastogenic activity of TAHT was also demonstrated in vivo in a micronucleus test using mouse peripheral polychromatic erythrocytes. Significant, treatment-related increases in micronucleated polychromatic erythrocytes were obtained at two of three sampling times. The high degree of mammalian toxicity, severe eye irritancy and the in vitro and in vivo clastogenicity indicate that TAHT should be handled as a hazardous material using suitable caution and protective equipment.
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PMID:Studies on the acute toxicity primary irritancy and genotoxic potential of 1,3,5-triacryloylhexahydro-s-triazine (TAHT). 372 91

Aqueous solutions of > or =5% glutaraldehyde (GA) are of moderate acute peroral toxicity and those of < or =2% are of slight toxicity. By single sustained skin contact, aqueous GA solutions of > or =45% are of moderate acute percutaneous toxicity, those of 25% are of slight toxicity and those of </=15% do not present an acute percutaneous hazard. Vapor generated at ambient temperature may cause sensory irritant effects to the eye and respiratory tract, but not acute respiratory tract injury. The 50% decrease in respiratory rate (rd(50)) is 13.86 ppm. A 0.1% solution of GA is not irritating to the eye; the threshold for conjunctival irritation is 0.2% and for corneal injury it is 1.0%. Eye injury is moderate at 2% and severe at > or =5%. Primary skin irritation depends on the duration and contact site, occlusion and solvent. By sustained contact, the threshold for skin irritation is 1%, above which erythema and edema are dose related. With 45% and higher, skin corrosion may occur. There is a low incidence of skin sensitizing reactions, with an eliciting threshold of 0.5% aqueous GA. However, GA is neither phototoxic nor photosensitizing. Subchronic repeated exposure studies by the peroral route show only renal physiological compensatory effects, secondary to reduced water consumption. Repeated skin contact shows only minor skin irritant effects without systemic toxicity. By subchronic vapor exposure, effects are limited to the nasal mucosa at 1.0 ppm, with a no-effect concentration generally at 0.1 ppm. There is no evidence for systemic target organ or tissue toxicity by subchronic repeated exposure by any route. A chronic drinking water study showed an apparent increase, in females only, of large granular cell lymphocytic leukemia but this was not dosage related. This is most likely the result of a modifying effect on the factor(s) responsible for the expression of this commonly occurring rat neoplasm. A chronic (2-year) inhalation toxicity/oncogenicity study showed inflammatory changes in the anterior nasal cavity but no neoplasms or systemic toxicity. In vitro genotoxicity studies--bacterial mutagenicity, forward gene mutation (HGPRT and TK loci), sister chromatid exchange, chromosome aberration, UDS and DNA repair tests--have given variable results, ranging from no effect through to weak positive. In vivo genotoxicity studies--micronucleus, chromosome aberration, dominant lethal and Drosophila tests--generally have shown no activity but one mouse intraperitoneal study showed bone marrow cell chromosome aberrations. Developmental toxicity studies show GA not to be teratogenic, and a two-generation study showed no adverse reproductive effects. Percutaneous pharmacokinetic studies showed low skin penetration, with lowest values measured in vitro in rats and human skin. Overexposure of humans produces typical sensory irritant effects on the eye, skin and respiratory tract. Some reports have described an asthmatic-like reaction by overexposure to GA vapor. In most cases this resembles reactive airways dysfunction syndrome, and the role of immune mechanisms is uncertain. Local mucosal effects may occur if medical instruments or endoscopes are not adequately decontaminated. Protection of individuals from the potential adverse effects of GA exposure requires that there be adequate protection of the skin, eyes and respiratory tract. The airborne concentration of GA vapor should be kept below the recommended safe exposure level (e.g. the threshold limit value) by the use of engineering controls. Those who work with GA should, through a training program, be aware of the properties of GA, its potential adverse effects, how to handle the material safely and how to deal with accidental situations involving GA. If effects develop in exposed workers, the reasons should be determined immediately and corrective methods initiated. (c) 2001 John Wiley & Sons, Ltd.
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PMID:Toxicological, medical and industrial hygiene aspects of glutaraldehyde with particular reference to its biocidal use in cold sterilization procedures. 1128 36

TEG is a liquid higher glycol of very low vapor pressure with uses that are primarily industrial. It has a very low order of acute toxicity by i.v., i.p., peroral, percutaneous and inhalation (vapor and aerosol) routes of exposure. It does not produce primary skin irritation. Acute eye contact with the liquid causes mild local transient irritation (conjunctival hyperemia and slight chemosis) but does not induce corneal injury. Animal maximization and human volunteer repeated insult patch tests studies have shown that TEG does not cause skin sensitization. A study with Swiss-Webster mice demonstrated that TEG aerosol has properties of a peripheral chemosensory irritant material and caused a depression of breathing rate with an RD(50) of 5140 mg m(-3). Continuous subchronic peroral dosing of TEG in the diet of rats did not produce any systemic cumulative or long-term toxicity. The effects seen were dose-related increased relative kidney weight, increased urine volume and decreased urine pH, probably a result of the renal excretion of TEG and metabolites following the absorption of large doses of TEG. There was also decreased hemoglobin concentration, decreased hematocrit and increased mean corpuscular volume, probably due to hemodilution following absorption of TEG. The NOAEL was 20 000 ppm TEG in diet. Short-term repeated aerosol exposure studies in the rat demonstrated that, by nose-only exposure, the threshold for effects by respiratory tract exposure was 1036 mg m(-3). Neither high dosage acute nor repeated exposures to TEG produce hepatorenal injury characteristic of that caused by the lower glycol homologues. Elimination studies with acute peroral doses of TEG given to rats and rabbits showed high recoveries (91-98% over 5 days), with the major fraction appearing in urine (84-94%) and only 1% as CO(2). TEG in urine is present in unchanged and oxidized forms, but only negligible amounts as oxalic acid. Developmental toxicity studies with undiluted TEG given by gavage produced maternal toxicity in rats (body weight, food consumption, water consumption, and relative kidney weight) with a NOEL of 1126 mg kg(-1) day(-1), and mice (relative kidney weight) with a NOEL of 5630 mg kg(-1) day(-1). Developmental toxicity, expressed as fetotoxicity, had a NOEL of 5630 mg kg(-1) day(-1) with the rat and 563 mg kg(-1) day(-1) with mice. Neither species showed any evidence of embryotoxicity or teratogenicity. There was no evidence for reproductive toxicity with mice given up to 3% TEG in drinking water in a continuous breeding study. TEG did not produce mutagenic or clastogenic effects in the following in vitro genetic toxicology studies: Salmonella typhimurium reverse mutation test, SOS-chromotest in E. coli, CHO forward gene mutation test (HGPRT locus), CHO sister chromatid exchange test, and a chromosome aberration test with CHO cells. The use patterns suggest that exposure to TEG is mainly occupational, with limited exposures by consumers. Exposure is normally by skin and eye contact. Local and systemic adverse health effects by cutaneous exposure are likely not to occur, and eye contact will produce transient irritation without corneal injury. The very low vapor pressure of TEG makes it unlikely that significant vapor exposure will occur. Aerosol exposure is not a usual exposure mode, and acute aerosol exposures are unlikely to be harmful, although a peripheral sensory irritant effect may develop. However, repeated exposures to a TEG aerosol may result in respiratory tract irritation, with cough, shortness of breath and tightness of the chest. Recommended protective and precautionary measures include protective gloves, goggles or safety glasses and mechanical room ventilation. LC(50) data to various fish, aquatic invertebrates and algae, indicate that TEG is essentially nontoxic to aquatic organisms. Also, sustained exposure studies have demonstrated that TEG is of a low order of chronic aquatic toxicity. The bioconcentration potential, environmental hydrolysis, and photolysis rates are low, and soil mobility high. In the atmosphere TEG is degraded by reacting with photochemically produced hydroxyl radicals. These considerations indicate that the potential for ecotoxicological effects with TEG is low.
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PMID:Triethylene glycol HO(CH2CH2O)3H. 1729 11