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Biomedical subjects

H Keskinen

Publications and source records attributed to H Keskinen.

At least 37 records · Page 2Linked to original sources
PubMed1997

Rhinitis caused by ninhydrin develops into occupational asthma.

Ninhydrin (2,2-dihydroxy-1,3-indanedione or 1,2,3-triketo-hydrindene hydrate) is a chemical used in the detection of free amino and carboxyl groups in proteins and peptides. Allergic, immunoglobulin E (IgE)-mediated rhinitis caused by ninhydrin was diagnosed earlier in a 41 yr old woman working as a laboratory technician in a forensic laboratory. Despite handling ninhydrin only in a flow cabinet, symptoms of dyspnoea developed 6 months later. Peak flow was found to vary by 20% during working days. In the specific inhalation challenge it was shown that occupational asthma had also developed due to continuing slight exposure to ninhydrin. The titre of ninhydrin-specific IgE also increased from 0.6 to 1.1 kU x L(-1) in the follow-up. This case stresses the importance of cessation of allergen exposure in occupational allergic rhinitis, in order to prevent asthma.

Adult↗
PubMed1997

Allergic alveolitis following exposure to epoxy polyester powder paint containing low amounts (<1%) of acid anhydrides.

Only one case report concerning allergic alveolitis caused by polyester powder paint has been published previously. The aim of this study was to determine whether phthalic anhydride (PA) or trimellitic anhydride (TMA) is the alveolitis-causing agent in such paint. A 61 year old woman showed recurrent symptoms of chills, cough, and fever whilst at work. She was working in a plant where epoxy polyester powder paints were used to paint metal. The paint was found to contain low (<1%) amounts of TMA and PA. The patient showed shadowing on chest radiographs. In bronchoalveolar lavage, lymphocytosis (67%) and a low T-helper/T-suppressor ratio (0.2) were found. Transfer factor was within normal limits, but a slight reduction was verified after re-exposure to the paint. The symptoms, exposure, reduction in transfer factor, findings on chest radiographs and bronchoalveolar lavage were consistent with allergic alveolitis. In conclusion, the polyester powder paint used in the plant caused allergic alve olitis in this patient. Of the constituents in the paint, trimellitic anhydride and phthalic anhydride were the possible causative agents.

Air Pollutants, Occupational↗
PubMed1997

Occupational asthma caused by triglycidyl isocyanurate (TGIC).

BACKGROUND: Polyester powder paints are extensively used in metal painting. Triglycidyl isocyanurate (TGIC), an epoxy compound, is often used as a hardener. Several cases of allergic eczema from occupational exposure to TGIC have been reported in the literature. OBJECTIVE: We examined a 36-year-old non-smoking man who worked mainly as a spray painter, using a polyester powder paint containing 4% TGIC. During painting he used protective clothing and a motorized breathing protector. After 4 years he developed eczema on his hands, face and body, and an occupational allergic eczema caused by TGIC was diagnosed. He also suffered from powder-paint-related asthmatic symptoms. METHODS: Occupational asthma was diagnosed in accordance with the accepted guidelines. Inhalation challenge tests were performed with the paint and TGIC. RESULTS: Spirometry showed slight obstruction; the blood eosinophils and serum IgE value were elevated. Skin-prick tests with common environmental allergens were negative. The challenge test with lactose powder was also negative. A challenge test with a paint containing TGIC (4%) induced a dual reaction in PEF and a late 23% fall in FEV1. A test with TGIC (4%) mixed with lactose induced a dual PEF reaction, and also dual changes in spirometry. The PD15 in the histamine challenge test decreased significantly after the challenge tests. CONCLUSIONS: To our knowledge this is the first diagnosed case of occupational asthma caused by TGIC. This case report emphasizes the importance of protecting both the skin and respiratory tract of workers against chemicals such as TGIC, capable of causing skin and respiratory allergy.

Adult↗
PubMed1996

Pocket-sized spirometer for monitoring bronchial challenge procedures.

Diagnosis of occupational asthma is verified by inhalation challenge testing when frequent monitoring of peak expiratory flow (PEF) or forced expiratory volume in 1 s (FEV1) is needed. FEV1 measurements also allow frequent monitoring of changes in small airways. For the follow-up of lung function of suspected occupational asthma, a reliable, personal and mobile device is needed. We studied the accuracy of a pocket-sized spirometer, Micro Plus Spirometer (MP), compared with our former combination of two devices, i.e. the values of forced expiratory volume in 1 s (FEV1) with those measured with the Vitalograph bellow spirometer (V); and the peak expiratory flow (PEF) values with the values obtained with a Wright PEF meter (W). In healthy control subjects, the values of FEV1 obtained with Micro Plus correspond well to those obtained using a bellow spirometer (R = 0.97) and the mean difference (MP-V) was -0.06 1 irrespective of the mean FEV1 value. W gives smaller PEF values than the MP; the mean difference in PEF (MP-W) was 44 1 min-1, but the values increased linearly with increasing flow. The poor relation between PEF values might be based on the low reliability of the Wright device. In patient follow-up, the FEV1 values measured with MP and V showed a good correlation (R = 0.99). The PEF values in patients increase linearly measured with W vs. MP with increasing flow values. In conclusion, we found the pocket-sized spirometer a handy and useful device for monitoring bronchial challenge procedures in patients with suspected occupational asthma. The number of exhalations during the challenge test follow-up is lessened when FEV1 and peak expiratory flow (PEF) can be measured simultaneously.

Adult↗
PubMed1995

Occupational respiratory and skin sensitization caused by polyfunctional aziridine hardener.

Polyfunctional aziridine (PFA) is increasingly used as a water-based crosslinker in two-component paints, paint primers, lacquers, topcoats and other protective coatings. The crosslinker is made by reacting multifunctional acrylic monomer with a highly reactive aziridine compound. Respiratory allergy or hypersensitivity from PFA has not been reported previously. During 1978-1991 we came across nine cases with hypersensitivity from PFA: two had allergic contact dermatitis (ACD), four had occupational asthma and three had both of them. Five of the patients were parquet layers, two were fibreboard painters, one was a spray painter and one was a salesman of PFA products. ACD was diagnosed by positive allergic patch test reactions with PFA in a dilution series in petrolatum: 0.32%-0.5% gave a 2(+)-3+ allergic reaction in the five cases with ACD but 0.1% gave only a weak reaction in one case, whereas the methacrylate patch test series was negative. The diagnosis of seven cases of occupational asthma due to PFA hardener was based on symptoms related to exposure to PFA hardener at work, and on positive provocation tests with PFA hardener. One had an immediate type reaction, one a had a dual reaction, and the others had late reactions. The positive reactions with the PFA hardener and the negative reactions with the acrylate compounds indicate that PFA caused ACD which is different from the previous reports in which acrylates present as impurities in the PFA hardener caused the sensitization.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Occupational asthma caused by decorative flowers: review and case reports.

Occupational respiratory symptoms caused by decorative flowers are seldom reported in the literature. In the years 1985-1993 four such cases of occupational asthma were diagnosed at the Institute of Occupational Health of Finland. Occupational asthma was caused by freesias (n = 1), chrysanthemums (n = 1), and tulips (n = 2). The diagnoses were based on work-related respiratory symptoms during flower handling in the patients' histories, specific challenge tests, and allergologic examinations. Flower allergy is rare but can even develop into occupational asthma. It usually leads to a change of profession.

Asthma↗
PubMed1994

Occupational asthma caused by ethanolamines.

Amino alcohols are used in various industries, often as minor constituents of compounds to modify the properties of the compound. Generally, they are considered to be safe, but they have been known to cause local skin irritation at higher concentrations in solutions. We report on three cases of occupational asthma caused by ethanolamines: two metal workers exposed to a cutting fluid containing triethanolamine, and one cleaner exposed to a detergent containing monoethanolamine. The diagnosis was based on work-related symptoms and on a chamber challenge with the suspected agent. Persistence of the symptoms after exposure ended was a common feature of the three cases.

Adult↗
PubMed1994

Pharyngeal edema caused by occupational exposure to cellulase enzyme.

Enzymes can cause allergic asthma and rhinitis. Although patients sometimes complain of symptoms in their throat, we have not been able to find any published report of pharyngeal edema caused by exposure to enzymes. We present the case of a maintenance foreman who worked in a factory producing enzymes, and who had pharyngeal edema, asthma, and rhinitis at work. Prick tests for cellulase enzyme and cellulase RAST were positive. The causal association between his pharyngeal symptoms and cellulase was demonstrated with inhalation provocation tests in an exposure chamber.

Bronchial Provocation Tests↗
PubMed1993

Immediate and delayed allergy to nickel with contact urticaria, rhinitis, asthma and contact dermatitis.

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.

Adult↗
PubMed1993

Occupational respiratory disease caused by acrylates.

Acrylates are compounds used in a variety of industrial fields and their use is increasing. They have many features which make them superior to formerly used chemicals, regarding both their industrial use and their possible health effects. Contact sensitization is, however, one of their well known adverse health effects but they may also cause respiratory symptoms. We report on 18 cases of respiratory disease, mainly asthma, caused by different acrylates, 10 cases caused by cyanoacrylates, four by methacrylates and two cases by other acrylates.

Acrylates↗
PubMed1992

Occupational dermatitis from exposure to polyurethane chemicals.

In addition to asthma, contact dermatitis may also develop from occupational contact with polyurethane (PU) chemicals. 6 cases of allergic contact dermatitis from exposure to PU chemicals were diagnosed in 1974-1990. The present paper summarizes the results and gives detailed descriptions of 3 such patients. 3 patients were allergic to 5 different diisocyanates (DICs), including 4,4'-diphenylmethane DIC (MDI), toluene DIC (TDI), 1,6-hexamethylene DIC (HID), and furthermore to diaminodiphenylmethane (MDA). 3 patients were sensitized by exposure to MDI. 2 of these reacted to MDI and MDA, and 1 to TDI in addition. 1 of the 3 patients reacted only to MDA, possibly formed by hydrolysis of MDI. Primary sensitization to MDA and cross-allergy to MDI could explain the reactions of the patients exposed to MDI, but separate sensitization may also be possible. Patch tests with fresh petrolatum (pet.) mixtures were first made and a 2% concentration was recommended for MDI and TDI. In order to determine the stability of DIC test substances, the last 2 patients were tested with old test substances. Tests with MDI 1.5% pet. and TDI 1.5% pet., 5.5 months and 15.5 months old, were positive. The results suggest that, when allergy to PU chemicals is suspected, patch tests should include, in addition to MDA, at least MDI and TDI 1.5-2% pet. They also suggest that test substances can be used for over a year, and that allergy to MDA may point to MDI exposure contained in PU chemicals.

Adult↗
PubMed1991

Allergy and toxicodermia from shiitake mushrooms.

Skin and respiratory symptoms developed within 2 months of exposure in a patient involved in the commercial production of shiitake mushrooms. A diagnosis of contact urticaria and allergic contact dermatitis from shiitake mushrooms was confirmed by prick and patch tests. The respiratory symptoms, their timing, the presence of precipitating IgG antibodies to shiitake spores and increased amounts of inflammatory cells and T lymphocytes in bronchoalveolar lavage indicated allergic alveolitis (mushroom worker's disease). A generalized exanthem developed in a second patient after eating raw shiitake mushrooms. Reactions to prick and patch tests with shiitake mushrooms were negative. The skin eruption in this patient corresponded to the previously reported shiitake-induced toxicodermia.

Adult↗
PubMed1991

Occupational urticaria from welding polyurethane.

An urticarial reaction associated with high fever developed in a welder on four occasions while he was welding steel profiles filled with polyurethane. The fumes emitted during pyrolysis of polyurethane and inhaled by the patient probably caused the urticarial reaction. Provocation tests with two pyrolysis products, 4,4-diphenylmethane diisocyanate and 4,4-diaminophenylmethane, were negative. This case demonstrates the difficulty in detecting the cause of urticaria induced by airborne chemicals.

Adult↗
PubMed1991

Allergy from cellulase and xylanase enzymes.

Modern biotechnical methods have enabled production of many new types of potentially allergenic proteins. Enzymes have long been known to be respiratory allergens, but relatively few cases of skin allergy have been reported. Here we describe four patients who developed occupational allergic respiratory symptoms, three with bronchial asthma and one with allergic rhinitis, caused by cellulase and/or xylanase enzymes. Each patient also had urticarial symptoms after skin contact with these enzymes. In addition, one of the patients had allergic contact dermatitis from cellulase, and one from xylanase. Allergic contact dermatitis was verified by positive patch tests with the enzymes, and the immediate allergy was revealed by skin prick tests, specific IgE determinations (RAST) and RAST-inhibition tests. All patients had positive RASTs to both cellulase and xylanase. In the RAST inhibition test 20 microliters of cellulase brought about a 94% inhibition, indicating the specificity of the RAST. Xylanase (20 microliters, 5% w/v) gave an 92% inhibition of cellulase RAST, indicating cross-reactivity between cellulase and xylanase. Three patients have been able to continue at their previous places of work, but at different worksites. One of the patients requires continuous medication for asthma and had to change her job because of persistent symptoms.

Adult↗