Methyl acrylate: a new sensitizer in nail lacquer.
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Biomedical subjects
Publications and source records attributed to T Estlander.
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Acid anhydrides are low-molecular-weight chemicals known to cause respiratory irritancy and allergy. Skin allergy has on rare occasions been reported. 2 workers contracted hives and itching on uncovered skin after 2 months exposure to methyltetrahydrophthalic anhydride (MTHPA) and methylhexahydrophthalic anhydride (MHHPA), to which they had airborne exposure. Later, the patients also developed conjunctivitis, rhinitis, sore throat, cough or asthma. In addition to MTHPA, 1 worker was also exposed to unsaturated polyester resin (UP). Both patients' immediate allergy to MTHPA and MHHPA was verified by positive prick tests to MTHPA and MHHPA, conjugated with human serum albumin (HSA), and positive radioallergosorbent tests (RASTs) to these anhydrides. On prick testing, both patients also reacted to a phthalic anhydride (PA)-HSA-conjugate and 1 of the patients to UP-HSA-conjugate. Specific immediate allergy to UP was shown by RAST. RAST inhibition with MTHPA, MHHPA and UP-resin conjugates confirmed IgE-mediated allergy and cross-reactivity between anhydrides. Our patients had developed airborne contact urticaria caused by phthalic anhydrides, in addition to respiratory allergy. Phthalic anhydride contained in the UP resin was possibly responsible for the immediate reaction of the skin.
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Polyfunctional aziridine (PFA) is increasingly used as a water-based cross-linker in 2-component paints, paint primers, lacquers, topcoats and other protective coatings. The cross-linker (PFA hardener) is made by reacting multifunctional acrylic monomer with a highly reactive aziridine compound. During 1992-1993, we came across 2 patients with allergic patch test reactions provoked by PFA hardener. One of the patients was a parquet layer, and the other a printer. Allergic contact dermatitis (ACD) was diagnosed by positive allergic patch test reactions to PFA hardener in a dilution series in pet.:0.3%-1% gave ++ to allergic reactions in both patients, whereas 0.1% gave a weak (+) or questionable reaction (?+), respectively. The methacrylate patch test series was negative in both patients, although gas chromatography/mass spectrometry analysis showed that PFA hardener contained 0.3% of trimethylolpropane triacrylate (TMPTA), a multifunctional acrylic monomer. One of the patients also had symptoms of contact urticaria, and a prick test with PFA hardener (1% aq.) induced a histamine-sized prick test reaction. The positive reactions with the PFA hardener and the negative reactions with the starting chemicals and additives in PFA, namely acrylates, propyleneimine and dimethylethanolamine, indicate that PFA caused ACD. This is in accordance with our previous observations, but differs from the reports of others, whose patients had been sensitized to acrylates present as remnants in the PFA hardener. As test substance, 0.5% PFA hardener in pet. is recommended for patch testing. Testing should be performed in patients with contact dermatitis if exposure to PFA has occurred. Skin prick tests may be of help to detect contact urticaria.
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A 48-year-old female silk-screen printer had worked in the manufacture of circuit boards for 12 years before she got the first symptoms of dermatitis on her wrists and lower arms. On the 1st patch test session, epoxy resin and the remainder of the standard series were negative, while a plastics and glues series gave an allergic reaction to 4,4'-diaminodiphenylmethane (DDM). The 2nd test session revealed allergic reactions to several acrylics, several epoxy compounds and 3 ink components. According to the material safety data sheets, 1 ink hardener contained DDM, but the causative agent in 1 ink and 1 ink hardener remained uncertain. The manufacturers of the 2 inks kindly provided us with their components for further patch tests. 2 of these components gave allergic reactions: triglycidyl isocyanurate (TGIC) and 2-hydroxyethyl methacrylate (2-HEMA). Our case report shows that the manufacture of circuit boards involves exposure to highly sensitizing chemicals. DDM, TGIC and 2-HEMA should be remembered as silk-screen printers' potential contact sensitizers in the manufacture of circuit boards.
It is known from experimental studies that antigenic potency and the concentration of antigen determine whether exposure to an antigen will result in sensitization. A single accidental exposure to concentrated antigen may therefore induce primary sensitization. The purpose of this report was to collect clinical cases in which a single exposure had resulted in contact dermatitis suspected to be allergic. Only patients without previous relevant skin symptoms were included. Patch testing was used to demonstrate sensitization. 6 patients developed occupational allergic contact dermatitis from accidental exposure. Patch testing revealed allergy to diglycidylether of bisphenol A epoxy resin, polyfunctional aziridine hardener, methyl acrylate, phenol-formaldehyde resin, and methylchloroisothiazolinone/methylisothiazolinone (Kathon LX), respectively. Furthermore, 2 patients developed allergic contact dermatitis from their first exposure to tear gas chemicals, namely omega-chloroacetophenone and ortho-chlorobenzylidene malonitrile. A single exposure can therefore induce both sensitization and subsequent allergic contact dermatitis without further exposure. The allergens described must be considered strong allergens. The skin should immediately be cleaned if an accidental splash with such an allergen has taken place.
Thiourea compounds are mainly used as accelerators in the rubber industry, but also in other industries, e.g., as antioxidants in the graphics industry. Thiourea compounds may provoke allergic contact dermatitis, although the number of reported cases is relatively low. During 1985-1991, we had 5 patients with allergic patch test reactions caused by thiourea compounds. 1 of our patients had to use a knee brace after an occupational accident. He developed allergic contact dermatitis caused by the knee brace, probably because he had become sensitized to diethylthiourea. 2 patients were probably sensitized by diphenylthiourea in neoprene gloves. A florist had an allergic patch test reaction to diphenylthiourea and might have been sensitized by fungicides or pesticides, which break down into thioureas. It is often difficult, however, to detect the source of thiourea compound sensitization. If the patient has contact dermatitis and has been exposed to products that may contain thiourea compounds (or compounds that break down into thiourea compounds), such as rubber, PVC plastic or adhesive, diazo paper, paints or glue remover, anticorrosive agents, fungicides or pesticides, patch testing with a series of thiourea compounds needs to be performed. If patch testing with thiourea compounds is not performed, allergic contact dermatitis caused by thiourea compounds is not likely to be diagnosed.
The prevalence of allergic contact dermatitis (ACD) caused by nickel is increasing. The probable cause is the increased use of nickel-containing metals in intimate contact with the skin. The critical factor is the amount of nickel released from these metals (bioavailable nickel) onto the skin. In the present study, we determined, with flame atomic absorbtion spectrometry, the amount of nickel released into synthetic sweat from metal samples. The results of this method were compared with the results of the dimethylglyoxime (DMG) test, which is considered to be a reliable means of identifying whether nickel-containing metals may cause allergy symptoms in sensitive individuals. Out of 10 samples studied, only small amounts (< 0.5 microgram/cm2/week) were released from 2 samples, and the DMG test was negative. From 5 samples, more than 0.5 microgram/cm2/week was released, and the DMG test was positive. For 3 samples, however, the DMG test was negative, though the flame atomic absorption spectrometry test showed considerable release of nickel. Therefore, although the DMG test can be used as a first line test for determining nickel release, some DMG-negative metal materials probably induce nickel sensitization, and should by no means be advertised as safe in this respect. We also report a nickel-allergic patient who developed ACD from stainless steel, indicating that some types of stainless steel release enough nickel to elicit allergic symptoms.
Dental personnel are exposed to a high number of sensitizing chemicals such as acrylics, metals, anesthetics, fragrances, and antimicrobials. Although these chemicals usually cause allergic contact dermatitis, they also may cause immediate contact reactions. Usually the diagnostics involve patch testing, but prick testing needs to be performed to confirm immediate allergy. This article reviews the important causes and diagnostics of skin allergy in dental personnel. Special attention is given to the acrylates and methacrylates.
A 27-year-old woman had for 2 years performed manual grinding of metal castings that contained nickel. She had previously had allergic contact dermatitis from nickel but started to get contact urticaria, rhinitis and asthmatic attacks at work. The symptoms disappeared at weekends and on holiday. Scratch chamber tests, open tests, specific IgE determinations (RAST), and RAST-inhibition test indicated that she had developed an IgE-mediated allergy to nickel; the bronchial provocation reaction with NiSO4 was, however, a late one. Patch tests confirmed her allergic contact dermatitis to be caused by nickel. This is the first patient, to the best of our knowledge, reported to have developed allergic contact dermatitis, allergic contact urticaria, rhinitis and asthma from nickel.
Occupational allergic contact dermatitis from metallic mercury is rare. Here we present the only 2 patients with relevant occupational mercury allergy detected at our clinic since 1974. The first patient was a dental nurse who became sensitized to metallic mercury from amalgam when handling uncured amalgam without protective gloves. The second patient had previously been sensitized to mercury from topical medicaments and developed work-related dermatitis when a mercury thermometer was broken at her place of work. Both patients had a positive patch test reaction to metallic mercury.
6 men contracted occupational allergic contact dermatitis from unsaturated polyester (UP) cements. 4 of the men were employed in car repair painting and the remaining 2 in mold manufacturing. The exposure time to UP cements ranged from 6 to 32 years before onset of skin symptoms. All patients had eczema on their hands; in addition, 4 had skin symptoms on airborne areas, i.e., wrists, neck and face. All 6 patients developed allergic reactions when patch tested with UP resin at 0.5-10% in petrolatum (pet.). None of the tested patients reacted to auxiliary or cross-linking chemicals of the cements. Diethylene glycol maleate (DGM) was purified and identified from the UP resin of a cement. 1 patient reacting to UP resin was also patch test positive to DGM and he produced an allergic reaction to DGM down to a concentration of 0.0032% pet. DGM was found in both uncured and cured UP resin. None of the patients could continue their work with UP cements after their sensitization.
Between 1974 and 1992, we were consulted by 4 patients (an orthodontist, 2 dental technicians and a dental worker trained in-house) who had developed occupational allergic contact dermatitis from working with dental prostheses. All patients had positive allergic patch test reactions to methyl methacrylate (MMA), the acrylate which is the most widely used in work with prostheses. All but the orthodontist also reacted to dimethacrylates, which are used in cross-linked dental prostheses. The last patient, investigated in 1992, had been exposed mainly to light-cured acrylics, which are similar in composition to dental composite resins. These acrylics, only recently introduced into prosthetic work, contain more potent acrylic sensitizers than MMA. Accordingly, dental personnel working with prostheses may face a higher risk of sensitization than previously. To detect cases of occupational allergic contact dermatitis, we suggest that patients working with dental prostheses should be patch tested with MMA, 2-hydroxyethyl methacrylate, dimethacrylates, epoxy acrylates and urethane acrylates.
Allergic contact dermatitis caused by gold is rare, and only isolated cases have been reported. Patch testing with gold may cause a long-lasting reaction. The purpose of this study is to describe a well-studied case of gold allergy caused by dental gold crowns. A gold-sensitized patient and a non-sensitized control subject were examined using patch tests, immunohistochemistry, electron microscopy and blast transformation reactions. Sodium thiosulfate, auranofin and sodium thiomalate gave positive patch test reactions. Immunohistochemistry and electron microscopy were performed from biopsies taken from allergic patch test reactions caused by gold sodium thiosulfate 1 day and 17 days after applying the patches, from normal skin and from a 17-day-old allergic patch test reaction caused by ammonium persulfate. Down-regulation had taken place by 17 days in the allergic ammonium persulfate reaction, but not in the 17-day allergic gold test reaction. The patient reacted to all but one of the gold-induced blast transformation tests, sodium chloroaurate being non-inductive. The non-sensitized control subject did not exhibit any reactions. In conclusion, gold sodium thiosulfate, gold sodium thiomalate and auranofin can be used as patch test substances for gold allergy, though long-lasting allergic patch test reactions may develop. In vitro gold salt induced blast transformation is an alternative test for gold allergy. The slow down-regulation of the allergic patch test reactions needs to be studied further.
A total of 100 workers, 86 from the glass-fibre-reinforced plastics (GRP) industry, 11 from polystyrene production and 3 from polyester resin coating manufacture, were examined for occupational skin hazards and for evaluation of skin protection. The workers had been exposed to many chemicals. Those working in the GRP industry had also been exposed to glass fibre and to dust produced by finishing work. 94% used protective gloves. 22 workers, all employed in the GRP industry, had contracted occupational skin disorders. 6 had allergic and 12 irritant contact dermatitis. 4 workers had an accidental injury caused by a peroxide catalyst, fire, hot air and constant mechanical friction. Allergic dermatoses were due to natural rubber (latex) (4 cases) in protective gloves, phenol-formaldehyde resin (1 case) and cobalt naphthenate (1 case). Irritant hand dermatoses (5 cases) were caused by the combined hazardous effect of unsaturated polyester or vinyl ester resins, organic solvents, glass fibre and dust from finishing work on the skin. Other cases of irritant dermatoses (7 cases) were due to the dust, promoted by mechanical friction of clothes. Skin disorders in the GRP industry were common (26%) but the symptoms were mild and only 3 patients had been on sick leave because of occupational skin disease.
Carbonless copy paper, or 'no carbon required' (NCR) paper, has often been implicated as the cause of skin, respiratory, or general symptoms, but allergy has been verified in only a few cases. A 43-year-old machinist whose work involved the manufacture of NCR paper developed occupational dermatitis on the hands. On patch testing, both the NCR paper and 1 of the chemicals used to produce the microcapsules of the NCR paper, namely diethylenetriamine (DETA), provoked an allergic reaction. Analysis of the paper showed that it contained enough DETA to induce allergic contact dermatitis. People who handle NCR paper and develop symptoms of contact dermatitis should be patch tested with DETA.