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7 years experience of photopatch testing with sunscreen allergens in Sweden.

https://arctichealth.org/en/permalink/ahliterature33993
Source
Contact Dermatitis. 1998 Feb;38(2):61-4
Publication Type
Article
Date
Feb-1998
Author
B. Berne
A M Ros
Author Affiliation
Department of Dermatology, University Hospital, Uppsala, Sweden.
Source
Contact Dermatitis. 1998 Feb;38(2):61-4
Date
Feb-1998
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Aged
Aged, 80 and over
Allergens - administration & dosage - adverse effects
Child
Dermatitis, Allergic Contact - diagnosis - etiology
Dermatitis, Photoallergic - diagnosis - etiology
Female
Humans
Male
Middle Aged
Multicenter Studies
Patch Tests
Severity of Illness Index
Skin - drug effects - pathology - radiation effects
Sunscreening Agents - administration & dosage - adverse effects
Sweden
Ultraviolet Rays - adverse effects
Urticaria - chemically induced
Abstract
Since 1990 7 sunscreen allergens have been included in the standard photopatch protocol at 2 Swedish dermatology clinics. 355 consecutive patients with suspected photosensitivity were tested, and in 28 of these (7.9%), a total of 42 allergic reactions were found. 80% of the reactions were of photocontact origin. The most common allergen was benzophenone-3 (Eusolex 4360), with 15 photocontact and 1 contact allergic reactions, followed by isopropyl dibenzoylmethane (Eusolex 8020) (8 photocontact, 4 contact) and butyl methoxydibenzoylmethane (Parsol 1789), with 6 photocontact reactions. There were 2 cases of photocontact allergy to phenylbenzimidazole sulfonic acid (Eusolex 232), which has not been reported previously. 1 case of contact urticaria from benzophenone-3 was accidentally found. In addition, 21 + reactions of doubtful relevance were noted in 14 patients: 16 on irradiated and 5 on non-irradiated test sites. Among these, irritant and phototoxic reactions may be included. These results indicate that the inclusion of UV filters in the standard photopatch protocol is important. Immediate-type testing for urticaria could also be of value.
PubMed ID
9506215 View in PubMed
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[Activity of some carbohydrate-metabolizing enzymes in sheep skin]

https://arctichealth.org/en/permalink/ahliterature62510
Source
Ukr Biokhim Zh. 1976 Jan-Feb;48(1):27-9
Publication Type
Article
Author
S F Shvets'
I A Makar
L I Solodib
Source
Ukr Biokhim Zh. 1976 Jan-Feb;48(1):27-9
Language
Ukrainian
Publication Type
Article
Keywords
Animals
Diet
English Abstract
Glucokinase - metabolism
Glucosephosphate Dehydrogenase - metabolism
Hexokinase - metabolism
Insulin - pharmacology
Phosphofructokinase-1 - metabolism
Seasons
Skin - drug effects - enzymology
Sulfates - pharmacology
Vitamin A - pharmacology
Abstract
The activity of carbohydrate metabolism certain enzymes [hexokinase (EC 2.7.1.1.), glucokinase (EC 2.7.1.2), phosphofructokinase (EC 2.7.1.11.1), glucoso-6-phosphate-dehydrogenase (EC 1.1.1.49.)] was studied in the sheep skin when adding vitamin A, sodium sulphate and insulin to the basic ration. The activity of the studied enzymes in the skin was established to be rather high and depend to a considerable extent on feeding, seasonal and hormonal factors. In summer the activity of such enzymes as glucoso-6-phosphate-dehydrogenase and glucokinase decreases, and that of hexokinase, vice versa, increases. Vitamin A alone against a background of the basic ration almost has no effect on the activity of the enzymes, with the exception of phosphofructokinase in certain periods of the experiment. More noticeable shifts in the activity of the enzymes were observed in the case when vitamin A and sodium sulphate were added to the ration of sheep, and also with the injection of insulin. In such cases in the sheep skin there occurs first of all an increase in the activity of glucokinase and glucoso-6-phosphate-dehydrogenase.
PubMed ID
130704 View in PubMed
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Alternatives for skin sensitisation: Hazard identification and potency categorisation: Report from an EPAA/CEFIC LRI/Cosmetics Europe cross sector workshop, ECHA Helsinki, April 23rd and 24th 2015.

https://arctichealth.org/en/permalink/ahliterature275417
Source
Regul Toxicol Pharmacol. 2015 Nov;73(2):660-6
Publication Type
Conference/Meeting Material
Date
Nov-2015
Author
David Basketter
Takao Ashikaga
Silvia Casati
Bruno Hubesch
Joanna Jaworska
Joop de Knecht
Robert Landsiedel
Irene Manou
Annette Mehling
Dirk Petersohn
Emiel Rorije
Laura H Rossi
Winfried Steiling
Silvia Teissier
Andrew Worth
Source
Regul Toxicol Pharmacol. 2015 Nov;73(2):660-6
Date
Nov-2015
Language
English
Publication Type
Conference/Meeting Material
Keywords
Animal Testing Alternatives - methods - trends
Animals
Cosmetics - administration & dosage - pharmacokinetics - toxicity
Dermatitis, Allergic Contact - metabolism - pathology
Education - methods - trends
Europe
Finland
Humans
Research Report - trends
Risk Assessment - methods - trends
Skin - drug effects - metabolism - pathology
Abstract
In the two years since the last workshop report, the environment surrounding the prediction of skin sensitisation hazards has experienced major change. Validated non-animal tests are now OECD Test Guidelines. Accordingly, the recent cross sector workshop focused on how to use in vitro data for regulatory decision-making. After a review of general approaches and six case studies, there was broad consensus that a simple, transparent stepwise process involving non-animal methods was an opportunity waiting to be seized. There was also strong feeling the approach should not be so rigidly defined that assay variations/additional tests are locked out. Neither should it preclude more complex integrated approaches being used for other purposes, e.g. potency estimation. All agreed the ultimate goal is a high level of protection of human health. Thus, experience in the population will be the final arbiter of whether toxicological predictions are fit for purpose. Central to this is the reflection that none of the existing animal assays is perfect; the non-animal methods should not be expected to be so either, but by integrated use of methods and all other relevant information, including clinical feedback, we have the opportunity to continue to improve toxicology whilst avoiding animal use.
PubMed ID
26456663 View in PubMed
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[Anti-inflammatory effect of N-stearoylethanolamine in experimental burn injury in rats]

https://arctichealth.org/en/permalink/ahliterature98804
Source
Ukr Biokhim Zh. 2009 Mar-Apr;81(2):107-16
Publication Type
Article
Author
N M Hula
A A Chumak
A H Berdyshev
O F Mehed'
T M Horid'ko
N L Kindruk
H V Kosiakova
O D Zhukov
Source
Ukr Biokhim Zh. 2009 Mar-Apr;81(2):107-16
Language
Ukrainian
Publication Type
Article
Keywords
Administration, Cutaneous
Administration, Oral
Animals
Anti-Inflammatory Agents - administration & dosage - pharmacology - therapeutic use
Antioxidants - administration & dosage - pharmacology - therapeutic use
Burns - drug therapy - enzymology - immunology - metabolism
Catalase - blood - metabolism
Disease Models, Animal
Erythrocytes - drug effects - enzymology - metabolism
Ethanolamines - administration & dosage - pharmacology - therapeutic use
Glutathione Reductase - blood - metabolism
Interleukin-6 - blood - immunology
Liver - drug effects - enzymology
Nitric Oxide Synthase - metabolism
Rats
Skin - drug effects - enzymology - injuries - metabolism
Spleen - drug effects - enzymology
Stearic Acids - administration & dosage - pharmacology - therapeutic use
Superoxide Dismutase - blood - metabolism
Tumor Necrosis Factor-alpha - blood - immunology
Wound Healing - drug effects
Abstract
The biochemical mechanisms of anti-inflammatory effect of endocannabinoid congener N-stearoylethanolamine (NSE) was studied on the model of experimental burn in rats. The animals after the thermal burn of the skin received per os during 7 days the water suspension of NSE in a doze 10 mg/kg of body weight. In the other groups of rats the suspension was applied to the wound (the concentration of NSE was 10 mg/ml). It was shown for the first time that NSE accelerated the process of burn wound healing by the inhibition of proinflammatory cytokines (TNFalpha, IL-6) production. NSE caused the normalization of the iNOS and cNOS activity and of nitrite content in plasma, erythrocytes, liver and spleen of rats. NSE also modified the antioxidant enzymes (catalase, superoxide dismutase and glutathione peroxidase) activity and diminished the level of lipid peroxidation. The discovered anti-inflammatory NSE properties suggest the possibility of its usage for burn treatment.
PubMed ID
19873884 View in PubMed
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The antimicrobial effectiveness of operative-site preparative agents: a microbiological and clinical study.

https://arctichealth.org/en/permalink/ahliterature245644
Source
J Bone Joint Surg Am. 1980 Jul;62(5):826-8
Publication Type
Article
Date
Jul-1980
Author
M A Ritter
M L French
H E Eitzen
T J Gioe
Source
J Bone Joint Surg Am. 1980 Jul;62(5):826-8
Date
Jul-1980
Language
English
Publication Type
Article
Keywords
Anti-Infective Agents, Local - pharmacology
Bacteria - isolation & purification
Disinfection
Hexachlorophene - pharmacology
Hip Joint - surgery
Humans
Iodine - pharmacology
Iodophors - pharmacology
Preoperative Care
Skin - drug effects - microbiology
Sterilization
Surgical Wound Infection - prevention & control
Triclosan - pharmacology
Abstract
Eight wound preparative agents (one triclosan compound, one hexachlorophene compound, and six iodophors) were evaluated under actual operating-room conditions for efficacy in de-germing the operative site prior to the performance of 310 total hip arthroplasties. All of the preparations tested achieved a significant reduction (p less than or equal to 0.001) of indigenous skin microflora compared with the pre-scrub level in both the post-scrub and the postoperative cultures. Two iodophors, when applied as sprays, demonstrated excellent bactericidal action, were less time-consuming and easier to use than the compounds that were applied as scrubs, and did not alter the low (0.42 per cent) infection rate that we have recorded over a period of four years.
PubMed ID
7391106 View in PubMed
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Biological monitoring of dermal and air exposure to cobalt at a Swedish hard metal production plant: does dermal exposure contribute to uptake?

https://arctichealth.org/en/permalink/ahliterature291746
Source
Contact Dermatitis. 2017 Oct; 77(4):201-207
Publication Type
Journal Article
Date
Oct-2017
Author
Maria Klasson
Magnus Lindberg
Ing-Liss Bryngelsson
Helena Arvidsson
Carin Pettersson
Bente Husby
Håkan Westberg
Author Affiliation
Department of Occupational and Environmental Medicine, Örebro University, 701 85, Örebro, Sweden.
Source
Contact Dermatitis. 2017 Oct; 77(4):201-207
Date
Oct-2017
Language
English
Publication Type
Journal Article
Keywords
Air Pollutants, Occupational - analysis - toxicity
Cobalt - analysis - blood - toxicity
Dermatitis, Allergic Contact - epidemiology
Humans
Occupational Exposure - adverse effects
Skin - drug effects - metabolism
Sweden
Abstract
Occupational exposure to cobalt is well established in hard metal manufacture. Cobalt is known to cause contact allergy, asthma, hard metal lung disease, and lung cancer. The relationship between skin exposure and uptake determined in blood has not been extensively investigated.
To examine whether skin and inhalable air exposure to cobalt contributes to uptake, determined as cobalt in blood, in a hard metal manufacturing factory.
The amount of cobalt on the skin found with an acid wash technique, the air concentrations of inhalable cobalt and cobalt blood concentrations were determined and correlated in exposed workers.
We found a significant rank correlation for cobalt concentrations on the skin, in inhalable air, and in blood (0.376-0.498). Multiple linear regression showed significant regression coefficients for cobalt skin exposure and blood (B?=?0.01, p?
Notes
Cites: Ann Occup Hyg. 2000 Oct;44(7):519-22 PMID 11042253
Cites: Contact Dermatitis. 1983 May;9(3):195-200 PMID 6222874
Cites: Int Arch Occup Environ Health. 1997;69(3):193-200 PMID 9049670
Cites: Occup Environ Med. 1994 Jul;51(7):447-50 PMID 8044242
Cites: Br J Ind Med. 1986 Jul;43(7):474-85 PMID 3718895
Cites: Contact Dermatitis. 2011 Sep;65(3):125-37 PMID 21692808
Cites: Lancet. 1981 Feb 21;1(8217):412-4 PMID 6110042
Cites: Int Arch Occup Environ Health. 2007 May;80(6):527-31 PMID 17136408
Cites: Chest. 1989 Jan;95(1):29-37 PMID 2909353
Cites: Contact Dermatitis. 2008 Jun;58(6):347-54 PMID 18503684
Cites: Am Rev Respir Dis. 1990 May;141(5 Pt 1):1373-8 PMID 2160215
Cites: Sci Total Environ. 1994 Jun 30;150(1-3):141-4 PMID 7939587
Cites: Ann Occup Hyg. 2010 Apr;54(3):340-50 PMID 20150401
Cites: Int Arch Occup Environ Health. 1985;57(1):19-26 PMID 4077278
Cites: Ann Occup Hyg. 2016 Jul;60(6):684-99 PMID 27143598
Cites: Am Ind Hyg Assoc J. 1996 Apr;57(4):365-9 PMID 8901238
Cites: Ind Health. 1989;27(4):155-63 PMID 2613559
Cites: Acta Derm Venereol. 1967;47(5):287-92 PMID 4168784
Cites: Int Arch Occup Environ Health. 2004 Feb;77(2):85-9 PMID 12819972
Cites: Br Heart J. 1972 Jan;34(1):113-6 PMID 4258223
Cites: Contact Dermatitis. 2006 May;54(5):233-8 PMID 16689805
Cites: Contact Dermatitis. 2014 Jun;70(6):361-8 PMID 24617983
Cites: Occup Environ Med. 1999 Nov;56(11):765-73 PMID 10658563
Cites: Ann Occup Hyg. 2002 Mar;46(2):209-17 PMID 12074030
Cites: Toxicol Lett. 2007 Apr 5;170(1):49-56 PMID 17382494
Cites: Int Arch Occup Environ Health. 1985;55(4):269-76 PMID 4008051
Cites: Contact Dermatitis. 1978 Jun;4(3):128-32 PMID 668342
Cites: Ann Occup Hyg. 2012 Nov;56(9):1000-12 PMID 22805749
Cites: Scand J Work Environ Health. 1996 Feb;22(1):62-5 PMID 8685677
Cites: J Environ Monit. 2010 Oct 6;12(10):1815-22 PMID 20730217
Cites: Thorax. 1983 Feb;38(2):119-28 PMID 6857569
Cites: Int Arch Occup Environ Health. 2010 Feb;83(2):173-81 PMID 19495786
Cites: J Am Acad Dermatol. 1986 Jul;15(1):1-10 PMID 2941461
Cites: Occup Environ Med. 2001 Oct;58(10):631-4 PMID 11555683
Cites: IARC Monogr Eval Carcinog Risks Hum. 2006;86:1-294 PMID 16906675
PubMed ID
28675438 View in PubMed
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Bisphenol A exposure via thermal paper receipts.

https://arctichealth.org/en/permalink/ahliterature258746
Source
Toxicol Lett. 2014 Nov 4;230(3):413-20
Publication Type
Article
Date
Nov-4-2014
Author
Simo P Porras
Milla Heinälä
Tiina Santonen
Source
Toxicol Lett. 2014 Nov 4;230(3):413-20
Date
Nov-4-2014
Language
English
Publication Type
Article
Keywords
Adult
Aged
Benzhydryl Compounds - urine
Environmental Exposure - analysis
European Continental Ancestry Group
Female
Finland
Gas Chromatography-Mass Spectrometry
Healthy Volunteers
Humans
Male
Middle Aged
Occupational Exposure - analysis
Paper
Phenols - urine
Reference Values
Reproducibility of Results
Skin - drug effects
Young Adult
Abstract
Bisphenol A (BPA) has one of the highest production volumes of all chemicals worldwide. It has been widely studied because of its endocrine modulating activity. In addition to dietary intake, absorption of BPA via the skin from handling thermal papers is believed to be a relevant route of exposure. We studied BPA exposure via thermal paper receipts in simulation experiments performed by three volunteers, and examined urinary excretion of BPA. We also evaluated background BPA excretion among the Finnish working-age population. The geometric mean BPA excretion among non-occupationally exposed working-age Finns (n=121) was 2.6 µg/l, the range being 0.8-18.9 µg/l. The 95th percentile of the non-occupationally exposed people was 8 µg/l, and this was set as the reference limit for the non-occupationally exposed population. In the first simulation experiment, which was conducted under conditions representing the most likely exposure, i.e., the work of a cashier in a supermarket, BPA excretion remained below the reference limit in all participants. In the second simulation experiment, with more intensive, short-time handling of thermal paper (three times 5 min), urinary excretion also remained at or below background levels (highest value being 10.3 µg/l). The calculated maximum BPA excretion per day after handling thermal paper was less than 0.2 µg/kg of body weight, suggesting a total daily intake over 25 times lower than the European Food Safety Authority's (EFSA's) proposal for a temporary tolerable daily intake (temporary TDI) (5 µg/kg/day).
PubMed ID
25175590 View in PubMed
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Characterization of a potential animal model of an idiosyncratic drug reaction: nevirapine-induced skin rash in the rat.

https://arctichealth.org/en/permalink/ahliterature7276
Source
Chem Res Toxicol. 2003 Sep;16(9):1078-89
Publication Type
Article
Date
Sep-2003
Author
Jacintha M Shenton
Munehiro Teranishi
Mones S Abu-Asab
Julie A Yager
Jack P Uetrecht
Author Affiliation
Faculty of Pharmacy, University of Toronto, Toronto, Ontario, Canada.
Source
Chem Res Toxicol. 2003 Sep;16(9):1078-89
Date
Sep-2003
Language
English
Publication Type
Article
Keywords
Administration, Oral
Animals
CD4 Lymphocyte Count
CD8-Positive T-Lymphocytes - immunology
Disease Models, Animal
Dose-Response Relationship, Drug
Drug Eruptions - etiology
Drug Evaluation, Preclinical - methods
Exanthema - chemically induced - pathology - physiopathology
Female
Food
Forecasting
Hepatomegaly - chemically induced - complications - pathology
Liver - drug effects - pathology - ultrastructure
Macrophages - immunology
Male
Mice
Mice, Inbred Strains
Nevirapine - administration & dosage - adverse effects
Rats
Rats, Inbred Lew
Rats, Sprague-Dawley
Research Support, Non-U.S. Gov't
Skin - drug effects - pathology - ultrastructure
Spleen - cytology - physiopathology - transplantation
Time Factors
Abstract
Idiosyncratic drug reactions are difficult to study in humans due to their unpredictability. Unfortunately, this characteristic also hinders the development of animal models needed for mechanistic studies. Nevirapine, used to treat human immunodeficiency virus (HIV) infections, results in a severe idiosyncratic skin rash in some patients. We found that nevirapine can also cause a significant rash in some strains of rats. At a dose of 150 mg/kg/day, the incidence in female Sprague-Dawley rats was 6/28 (21%), in female Brown Norway rats 32/32 (100%), and in female Lewis rats 0/6 (0%) while no male Sprague-Dawley or Brown Norway rats developed a rash. Female SJL mice 0/7 also did not develop nevirapine-induced skin lesions. The first sign of a reaction in Brown Norway rats was red ears at days 7-10 followed by a rash with scabbing mainly on the back; this was a shorter time to onset than in Sprague-Dawley rats. Light microscopy of the skin revealed a primarily mononuclear inflammatory infiltrate and lesions typical of self-trauma. Immunohistochemistry results suggest that the infiltrate was composed of CD4 and CD8 T cells as well as macrophages. A lower dose of either 40 or 75 mg/kg/day did not lead to a rash and, in fact, 2 weeks of the lower doses induced tolerance to the 150 mg/kg/day dose in female Brown Norway rats. A dose of 100 mg/kg/day resulted in rash in 2/4 (50%) of female Brown Norway rats. Rechallenge of Brown Norway rats that had been allowed to recuperate after a nevirapine-induced rash led to red ears in less than 24 h followed by hair loss and occasional skin lesions. Although the skin rash was less evident on rechallenge, microscopically, the cellular infiltrate was more prominent, especially surrounding the hair follicles. Moreover, there were lesions of interface dermatitis with apoptosis and satellitosis, indicative of a cell-mediated immune attack on the epidermis. While systemic signs of illness did not accompany the rash on primary exposure, on rechallenge, the animals appeared generally unwell and this forced sacrifice after 2 weeks or less of treatment. Importantly, splenocytes isolated from rechallenged animals were able to transfer susceptibility to nevirapine-induced skin rash to naïve female Brown Norway recipients, which was illustrated by a faster time to onset of rash in the recipients. The characteristics of this adverse reaction are similar to that seen in humans; that is, it is idiosyncratic in that it only occurs in some strains of animals, is delayed in onset, is more common in females, is dose-dependent, and appears to be immune-mediated. Therefore, it may represent a good animal model for the study of idiosyncratic drug reactions.
PubMed ID
12971795 View in PubMed
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49 records – page 1 of 5.