Occupational health physicians as users of electronic health records.

BACKGROUND: Electronic health records (EHRs)' purpose is to facilitate the documentation of patient data and to improve the exchange of information between the professionals involved in a patient's care. AIMS: To investigate occupational health (OH) physicians' experiences of EHRs and the factors hampering work. METHODS: An electronic questionnaire was sent to physicians working in OH services in April 2017 and a total of 342 OH physicians participated in the study. The results were reported as quantities and percentages. The survey text was analysed using data-driven content analysis. RESULTS: The respondents considered their EHR stable in terms of technical features but the routine tasks with EHR were not straightforward. Also, the documentation of patient data for statistical purposes took an unreasonable amount of time and the access to patient data from other organizations was poor. Instead, a well-functioning feature of EHRs were electronic prescriptions. The factors, which hampered respondents' work, were constant or frequent time pressure, too little time to do their job properly and a stress caused by uncompleted tasks. CONCLUSIONS: This study showed that the usability problems of EHRs were the slowness, unexpected downtimes and difficulties in obtaining patient data. Also, respondents felt very often a lack of time in their work. OH physicians' work is best supported by EHRs that consider their specific role in healthcare, i.e. the assessment of work ability, the co-ordination of care and rehabilitation and support for return to work.

Airborne occupational allergic contact dermatitis from triglycidyl-p-aminophenol and tetraglycidyl-4,4'-methylene dianiline in preimpregnated epoxy products in the aircraft industry.

BACKGROUND: Very little is known about allergic contact dermatitis (ACD) from preimpregnated epoxy products (prepregs). OBJECTIVE: To describe a patient with occupational ACD from prepregs, and report new quantitative data on the content of prepregs. METHODS AND RESULTS: A laminator developed work-related vesicular hand dermatitis. He worked in an aircraft plant assembling aircraft parts, being exposed to preimpregnated carbon fiber and fiberglass sheets (prepregs), and epoxy adhesive tapes and foams. Triglycidyl-p-aminophenol (TGPAP; 1-0.25%, 2+; 0.05%, 1+) and tetraglycidyl-4,4'-methylene dianiline (TGMDA; 1%, 3+; 0.5-0.05%, 2+) provoked allergic patch test reactions, whereas o-diglycidyl phthalate was negative (1-0.05% pet) and standard epoxy provoked a weak (?+) reaction. Six prepreg products provoking allergic patch test reactions were analyzed for their TGPAP, TGMDA and diglycidyl ether of bisphenol A (DGEBA) content using gas and liquid chromatographic methods, showing up to 10% of TGPAP, 19% of TGMDA and 5% of DGEBA in the prepregs. An epoxy primer contained 61% of TGPAP. CONCLUSION: TGPAP and TGMDA caused occupational ACD. These chemicals need to be used when patch testing patients are exposed to prepregs, because patch testing with DGEBA may be negative.

Cellulase allergy and challenge tests with cellulase using immunologic assessment.

OBJECTIVES: This study attempted to develop and evaluate a challenge test for diagnosing allergic asthma and rhinitis due to cellulase. METHODS: Challenge tests in a chamber were performed on 11 persons sensitized to cellulase. Four different enzyme-lactose mixtures, starting from a 0.03% mixture, were used. The enzyme dust was generated from a dry enzyme preparation mixed with lactose powder, using pressurized air. The cellulase concentration in the air was measured with an immunochemical method. RESULTS: Nasal, pharyngeal, or bronchial symptoms could be elicited at cellulase air concentrations of 1 to 1300 microg/m3. A dose-response relationship was observed for symptoms in repeated challenge tests with increasing concentrations of cellulase. For 2 persons skin symptoms could also be reproduced. CONCLUSION: The challenge method proved to be a practical means with which to simulate conditions at the worksite and elicit the specific respiratory symptoms of the patients.

Occupational dermatoses from exposure to epoxy resin compounds in a ski factory.

Of 22 workers in a ski factory, occupational allergic contact dermatitis was found in 8. 6 were sensitive to epoxy resin compounds, i.e., epoxy resins, hardeners or diluents, 1 to cobalt in glass-fiber reinforcements, and 1 to formaldehyde in a urea-formaldehyde glue and a lacquer. 4 workers had irritant contact dermatitis from epoxy resin compounds, lacquers, sanding dust, or glass-fiber dust. 3 had contact allergy from a new sensitizer, diethyleneglycol diglycidyl ether, in a reactive diluent. Immediate transfer of workers sensitized to epoxy resin from epoxy exposure prevents aggravation of their dermatitis and broadening of the sensitization to epoxy hardeners, diluents and other compounds.

Occupational allergic contact dermatitis and contact urticaria caused by polyfunctional aziridine hardener.

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.

Analysis of patients with allergic patch test reactions to a plastics and glues series.

839 patients were patch tested with a series of 31 plastics and glues allergens at a dermatologic clinic over a period of 7 years. 52 (6%) had a positive patch test reaction to 1 or more such allergens. Clinic charts of 47 patients (out of 52) were available for the study. All but 3 patients had dermatitis on their hands: 17 had only hand dermatitis. 25 (53%) patients' test results were of present or past relevance to their skin diseases. 11 patients (68%) with occupational allergic contact dermatitis (ACD) and 14 (45%) with non-occupational dermatitis had relevant reactions. p-tertiary-butylphenol-formaldehyde resin was the most common allergen (9 cases). 7 patients reacted to diaminodiphenylmethane. 5 patients, who had colophony allergy, reacted to abietic acid and 4 to abitol. There was no reaction to 14 test substances. Special series, such as this plastics and glues series, reveal the cause of ACD less frequently than standard series. However, there is no other way to confirm allergy to these usually industrial allergens, which can also sensitize through non-occupational exposure during hobby working or through unpolymerized monomer left in the finished plastic product.

Immunologic contact urticaria due to airborne methylhexahydrophthalic and methyltetrahydrophthalic anhydrides.

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.

Nickel release from metals, and a case of allergic contact dermatitis from stainless steel.

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.

A single accidental exposure may result in a chemical burn, primary sensitization and allergic contact dermatitis.

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.

Epoxy dermatitis.

Dermatitis caused by exposure to epoxy resin compounds was observed in the 1950s, shortly after epoxy resins were introduced. Following a description of the chemistry and the use of epoxy compounds, the authors discuss delayed and immediate allergic epoxy dermatitis and irritant epoxy dermatitis as well as factors such as exposure and skin testing.

Concomitant sensitization to triglycidyl isocyanurate, diaminodiphenylmethane and 2-hydroxyethyl methacrylate from silk-screen printing coatings in the manufacture of circuit boards.

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.

Occupational allergic contact dermatitis due to coconut diethanolamide (cocamide DEA).

Coconut diethanolamide (CDEA), manufactured from coconut oil, is widely used as a surface-active agent in hand gels, hand-washing liquids, shampoos and dish-washing liquids. CDEA has rarely caused allergic contact dermatitis. During 1985-1992, we investigated 6 patients with occupational allergic contact dermatitis caused by CDEA. 2 became sensitized from a barrier cream, 3 from a hand-washing liquid, and 1 had been exposed both to a hand-washing liquid and to a metalworking fluid containing CDEA. Leave-on products (hand-protection foams) caused sensitization much more rapidly (2-3 months) than rinse-off products (hand-washing liquids; 5-7 years). Due to the extensive use of CDEA and the lack of proper declaration of products, it is difficult to avoid CDEA exposure. No contact allergy to another coconut-oil-derived sensitizer (cocamidopropyl betaine) was found in the patients.