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Ocular lesions

Erythema and blisters developed within 24 hours on the trunk and legs of a worker exposed to residues of 1,2-dibromoethane in a pesticide tank (Letz et al. 1984). This patient, immediately after rescue, complained of burning eyes, but ocular lesions did not develop. [Pg.45]

Ocular lesions Ocular lesions such as optic neuritis or retinal thrombosis have been associated with the use of hormonal contraceptives. [Pg.216]

Skin and Eye Irritation The solvent should not be a skin or eye irritant. A product is considered to be a skin irritant if it has a mean score of 2 or more for either erythema and eschar formation or edema formation, based on the OECD dermal scoring system (OECD, TG 404). A product is classified as an eye irritant if it causes significant ocular lesions, in any type of ocular tissue (i.e., cornea, iris, or conjuncti-vae) within 72 hours after exposure and which persist for at least 24 hours. [Pg.127]

It is easily understood by intuition that acids, bases, oxidants, chelators, etc. express their reactivity with more or less intensity. Some are called a strong acid, a weak oxidant. In Sect. 3.4.3.1, we will study the importance of the applications of this theoretical approach for the understanding and the prediction of the importance of ocular lesions in case of corrosive projections. [Pg.25]

Cataract opacity of the lens. It is sometimes visible from the initial examination but, more often, it appears secondarily. It is the consequence of the intensity and the depth of the ocular lesions. It is an element revealing a very bad final prognosis for the burned eye. [Pg.101]

In 1993, the European Union revised its criteria for classification and labelling of substances and preparations based on their potential to cause ocular lesions [5] and in 1995 new experimental data on the irritation potential of surfactant raw materials became available. This led CESIO, once again, to review its guidance on classification and labelling of anionic and non-ionic surfactants. It resulted in the increase in several classification and labelling recommendations. These revisions, together with the classifications for quaternary ammonium compounds and fatty amines and derivatives which remained unchanged from the 1990 Report, are contained in the latest report published in January 2000 [6]. [Pg.248]

Characterized by subcutaneous nodules, a pruritic skin rash and ocular lesions often resuiting in biindness. [Pg.372]

According to Draize et al. (1944), injuries to the cornea, conjunctival and palpebral mucosae and the iris are scored separately. The severity of ocular lesions has been graded in a scale of weighted scores. [Pg.196]

The slow evolution of chronic bronchitis from air pollutants, the late ocular lesions following use of chloroquine, the accumulation of the tetracyclines in the fetus, and of course all the carcinogenic effects, are but a few of the countless objectionable results of new substances or technologies which appeared at first essentially safe. [Pg.49]

Dwivedi, P.C., Raizada, J.K., Saini, V.K., Mittal, P.C. (1985). Ocular lesions following methyl isocyanate contamination. Arch. Ophthalmol. 103 1627. [Pg.308]

Khurrum, M.A., Ahmad, H.S. (1987). Long-term follow up of ocular lesions of methyl isocyanate gas disaster in Bhopal. Indian J. Ophthalmol. 35 136-7. [Pg.309]

Amir, A., Turetz, J., Chapman, S., Fishbeine, E., Meshulam, J., Sahar, R., Liani, H., Gilat, E., Frishman, G., Kadar, T. (2000). Beneficial effects of topical anti-inflammatory drags against sulfur mustard-induced ocular lesions in rabbits. J. Appl. Toxicol. 20 (Suppl. 1) S109-14. [Pg.590]

Warthin, A.S., Weller, C.V. (1919). Chapter III The ocular lesions produced by dichlorethylsulphide (mustard gas). In The Medical Aspects of Mustard Gas Poisoning. C.V. Mosby, St Louis, MO. [Pg.593]

Therapy depends on etiology. In individuals who are suspected of having tuberculosis, diagnosis should make use of a purified protein derivative skin test, chest radiograph, and sputum cultures if necessary. These individuals should be referred for comanagement to their primary physician or to an infectious disease specialist. Though antituberculin agents are systemically administered, the ocular lesions are appropriately treated with topical steroids. In most instances, patients respond to 1% prednisolone acetate every 3 to 4 hours for the first day, subsequently tapered rapidly on the basis of the clinical response. [Pg.475]

Ankyloblepharon (adherence of the eyelids resulting in narrowing of palpebral apertures) was reported in a 59-year-old man during fluorouracil therapy for metastatic adenocarcinoma of the stomach (74). It appeared that bilateral conjunctival ulcers, secondary to fluorouracil and ulcerative blepharitis, resulted in ankyloblepharon. Withdrawal of chemotherapy resulted in improvement and re-initiation of therapy resulted in recurrence of ocular lesions. [Pg.1410]

A 13-year-old non-atopic girl with a 1-year history of recurrent itchy eyelid inflammation and conjunctivitis in both eyes had been fitted with a removable orthodontic appliance 14 months before (11). The metal wires of the orthodontic appliance were made of steel containing 10-13% nickel and 16-19% chromium. Patch-testing confirmed allergy to nickel. A low nickel diet improved the dermatitis, but it did not clear. She was advised to stop wearing the orthodontic appliance, and the ocular lesions cleared within 2 weeks. [Pg.2503]

Allopurinol (4-hydroxypyrazolo [3, 4-d] pyrimidine) is an inhibitor of xanthine oxidase that was successfully introduced in the treatment of primary gout about 45 years ago [171]. Allopurinol continues to be accepted as standard therapy in the treatment of primary and secondary hyperuricemia. Adverse reactions occur in about 10% of patients treated with allopurinol and are relatively mild and self-limited [171,172]. A mild maculopapular eruption or gastrointestinal disorders are usually noted, which promptly regress with cessation of therapy. Isolated instances of allopecia [173], bone marrow depression [174], ocular lesions [175], acute cholangitis [176], various types of hepatic injuries [177,178] temporal arthritis [179], and xanthine stones [180] have been reported. Recently, LaRosa et al [180a] have reported a case of xanthine nephropathy during treatment of childhood T-cell ALL. [Pg.469]

Key to toxicological effects C = Carcinogenic H = Hepatotoxic RT = Renal toxic G = Genotoxic D = Developmental M = Mutagenic MD = Metabolic disturbance N = Neurotoxic OL = Ocular lesions A = Aspermatogenesis HPP = Hepatic peroxisome proliferation F = Fetotoxic TP = Tumor promoter Cl = clastogenic. [Pg.389]

Table 1 Scale of weighted scores for grading the severity of ocular lesions... Table 1 Scale of weighted scores for grading the severity of ocular lesions...
Maumenee, A. E., Scholz, R. O. (1948). The histopathology of the ocular lesions produced by sulfur and nitrogen mustards. Bulletin Johns Hopkins Hospital, 82, 121—147. [Pg.75]

Mice exposed continuously to 4,000 ppm 1,1,1 -trichloroethane for 4 days exhibited eye irritation during exposure (Evans and Balster 1993). All of the above effects, however, were probably due to direct contact of the chemical in the air with the eye (see Section 2.2.3.2). Intermittent exposure of rats or mice to 2,000 ppm 1,1,1-trichloroethane for 90 days (Calhoun et al. 1981) or to 1,500 ppm for 2 years (Quast et al. 1988) had no effect on the incidence of ocular lesions. NOAEL and LOAEL values derived from these studies are recorded in Table 2-1 and plotted in Figure 2-1. [Pg.48]


See other pages where Ocular lesions is mentioned: [Pg.151]    [Pg.62]    [Pg.123]    [Pg.82]    [Pg.74]    [Pg.83]    [Pg.221]    [Pg.117]    [Pg.33]    [Pg.46]    [Pg.56]    [Pg.576]    [Pg.905]    [Pg.912]    [Pg.455]    [Pg.1116]    [Pg.54]    [Pg.514]    [Pg.580]    [Pg.581]    [Pg.1590]    [Pg.173]    [Pg.186]   


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Lesion

Ocular toxicity lesions

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