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Background: Several epidemiological studies have reported an increased risk of asthma among professional cleaners. To date, however, no analysis of large patient series from clinic of occupational medicine has been published., Aims: To describe the cases of occupational asthma (OA) diagnosed at the Finnish Institute of Occupational Health (FIOH) during the period 1994-2004 in workers employed in professional cleaning work., Methods: OA was diagnosed according to patient history, lung function examinations and specific challenge tests with measurements of the forced expiratory volume in 1 second and peak expiratory flow values., Results: Our series comprised 20 patients, all female, with a mean age of 48.8 years (range 27-60 years). The mean duration of cleaning work before the onset of the respiratory symptoms was 14.3 years (range 1-36 years), and the mean duration of cleaning work before the FIOH examinations was 18.6 years (range 3-38 years). OA was triggered by chemicals in 9 cases (45%) and by moulds in 11 cases (55%). The chemicals were cleaning chemicals (wax-removing substances containing ethanolamines in five cases and a cleaning agent containing chloramine-T in one case) and chemicals used in the industrial processes at workplaces (three cases). Of the moulds, the most frequently associated with OA was Aspergillus fumigatus (nine cases)., Conclusions: OA was attributed not only to cleaning chemicals but also to other chemicals used in work environments. Moulds are presented as a new cause of OA in cleaners.

Background: Cobalt has been shown to induce mainly asthma, allergic contact dermatitis and hard metal disease. The data on cobalt asthma are mainly based on case reports., Aims: To characterize all the cases of occupational cobalt asthma encountered in a cobalt plant at the time of diagnosis and 6 months later. We also evaluated the incidence of cobalt asthma in different departments on the basis of data on occupational exposures., Methods: We identified cases of cobalt asthma confirmed with specific bronchial challenge tests in the Kokkola cobalt plant in Finland where exposure levels have been regularly monitored., Results: Between 1967 and 2003, a total of 22 cases of cobalt asthma were diagnosed in the cobalt plant. On challenge tests, mostly late or dual asthmatic reactions were observed. The incidence of cobalt asthma was the highest in the departments with the highest cobalt exposure levels. All cases of cobalt asthma were encountered in departments where irritant gases were present in the ambient air in addition to cobalt. At the time of the follow-up examination 6 months later, non-specific hyperreactivity had mostly remained at the same level or increased., Conclusions: The incidence of cobalt asthma correlated with the exposure levels of cobalt in corresponding departments. An irritating effect of gaseous compounds may enhance the risk of cobalt asthma and even the smallest amounts of cobalt may be harmful to susceptible workers. Symptoms of asthma may continue despite the fact that occupational exposure to cobalt has ceased.

Chemicals that may cause allergy are being used in structure nails. In this case report two structure nail makers are described, who were diagnosed with occupational asthma in clinical studies. The studies included an inhalational exposure simulating the work. The causative agents of occupational asthma are apparently the acrylate compounds contained in the chemicals; use of these compounds has previously been linked with allergic contact dermatitis and asthma. Since the making of structure nails involves health risks, such work requires appropriate premises and personal protection.

Background: In recent decades, the use of artificial nails including methacrylates (MAs) has increased. This study presents the first two clinical cases of occupational asthma (OA) caused by sculptured nails containing MAs., Methods: In both cases, OA was diagnosed on the basis of a work simulation test combined with the patient's history of occupational exposure and respiratory symptoms., Results: Both patients developed work-related respiratory symptoms 4-5 years before the current examinations. Previously, the first patient (a 30-year-old female) was diagnosed as having allergic contact dermatitis (ACD) to MAs; the second patient (a 27-year-old female) had no skin symptoms. In both cases, a dual asthmatic reaction was observed in the bronchial provocation test, in which the patients simulated their work using their own products including MAs., Conclusions: Sculptured nails containing MAs can induce OA in nail technicians. Products not containing MAs should be used to prevent OA and ACD. If MAs are used, they should be handled with appropriate safety measures., (Copyright 2008 Wiley-Liss, Inc.)

The aim of the present study was to describe the cases of occupational asthma (OA) due to stainless steel welding fumes diagnosed at the Finnish Institute of Occupational Health during the period 1994-2003. OA was diagnosed according to patient history, lung function examinations and welding challenge tests with measurements of the forced expiratory volume in one second (FEV(1)) and peak expiratory flow (PEF) values. The present series comprised 34 patients, all male, with a mean age of 44.7 yrs (range 22-57), mainly working as welders. The mean duration of exposure was 22.4 yrs, and the mean duration of exposure before the onset of respiratory symptoms was 18 yrs. Dyspnoea was the most frequently reported work-related respiratory symptom. During the inhalation challenge tests, the mode of the asthmatic FEV(1)/PEF reaction was delayed in 16 (47%) patients, immediate in nine (26%) patients and dual (both immediate and delayed) in nine (26%) patients. In the follow-up assessment 6 months later, only six patients were considered able to continue performing welding tasks, whereas occupational injury pension was recommended for seven, and measures of vocational rehabilitation for 14 patients. In most cases, after the diagnosis of occupational asthma, the continuation of welding work was not possible.

Occupational asthma (OA) can be induced by fumes of manual metal-arc welding on stainless steel. In recent years, the use of special stainless steels (SSS) with high chromium content has increased. This study presents two cases of OA caused by manual metal-arc welding on SSS. In both cases, the diagnosis of OA was based on respiratory symptoms, occupational exposure and positive findings in the specific challenge tests. In the first case, a 46-yr-old welder had experienced severe dyspnoea while welding SSS (SMO steel), but not in other situations. Challenge tests with both mild steel and stainless steel using a common electrode were negative. Welding SSS with a special electrode caused a delayed 37% drop in forced expiratory volume in one second (FEV1). In the second case, a 34-yr-old male had started to experience dyspnoea during the past few years, while welding especially SSS (Duplex steel). The workplace peak expiratory flow monitoring was suggestive of OA. Challenge tests with both mild steel and stainless steel using a common electrode did not cause bronchial obstruction. Welding SSS with a special electrode caused a delayed 31% drop in FEV1. In conclusion, exposure to manual metal-arc welding fumes of special stainless steel should be considered as a new cause of occupational asthma.

Occupational asthma has been found to be associated with lowered socio-economic outcomes, an increased unemployment rate and a decreased quality of life. The compensation of occupational diseases is comparatively favourable in Finland. Our aim was to follow-up the working status and life satisfaction of patients with diisocyanate-induced asthma in 245 cases diagnosed during 1976-1992. A questionnaire was sent out on average 10 (3-19) yr after the diagnosis to the surviving 235 patients. The questionnaire was validated by re-examining 91 of them clinically, and with spirometry, histamine challenge test and peak flow surveillance. Of the 213 responding patients, 14% were unemployed, and for 50% of them unemployment was caused by asthma. Unemployment was associated with nocturnal asthma symptoms (OR 10.93; CI 2.69-44.452), increased PEF variability (OR 8.46; CI 1.52-46.97) and with the use of short-acting beta-sympathomimetic medication (p=0.045). Satisfaction with life was associated with present working (OR 3.50; CI 1.73-7.06) and with good condition of asthma as assessed by the use of asthma medication (OR 0.49; CI 0.27-0.89) and objective measurements of the asthma condition, e.g. PEF variability (OR 0.21; CI 0.08-0.59). As a conclusion, unemployment was remarkably low as compared with earlier reports and related to the period of simultaneous economic recession. Unemployment, as well as dissatisfaction with life were associated with poor conditions of asthma. Unemployment was associated with improper asthma care favouring the use of short-acting beta-sympathomimetic medication. Proper follow-up of asthma is essential for minimizing the social complaints of occupational asthma, as well as for enhancing life satisfaction.

Exhaled nitric oxide (NO) is a marker of eosinophilic inflammation of the airway mucosa accompanying changes in the clinical condition of asthma. Allergen exposure has been associated with delayed elevation of exhaled NO. The aim of this study was to assess the asthmatic airway inflammation with exhaled NO measurements during specific bronchial challenge tests with occupational agents. Forty patients with suspected occupational asthma were investigated. Specific bronchial challenge tests were performed with forced expiratory volume in one second or peak expiratory flow follow-up, supplemented by exhaled NO measurements before and 24 h after challenge tests. In active challenges, which induced bronchoconstriction, a significant mean increase of exhaled NO concentration was noted. In patients with a normal or slightly increased (<14.5 parts per billion (ppb)) basal NO level and a late bronchoconstriction, a significant increase in exhaled NO was seen. Patients with a high basal NO level (>14.5 ppb) and a significant bronchoconstriction did not show a significant NO elevation. Challenge tests without bronchoconstriction were not associated with a significant elevation of exhaled NO. Exhaled nitric oxide measurements can be used to indicate the development of airway inflammation accompanying late asthmatic reaction after bronchial challenge tests in patients with a normal or slightly increased basal nitric oxide concentration.

In 1976-1992 245 new cases of asthma induced by diisocyanates were diagnosed, caused by hexamethylene diisocyanate (HDI) in 39%, diphenylmethane diisocyanate (MDI) in 39%, and toluene diisocyanate (TDI) in 17% of the cases. Our aim was to study the clinical outcome of diisocyanate-induced asthma. A questionnaire was sent to the 235 patients alive in 1995, and validated by reexamining clinically 91 of them. The study was carried out on average 10 () yr after the diagnosis. Of the patients 82% experienced symptoms of asthma, 34% used no medication, and 35% were on regular medication. The patients having displayed immunoglobulin E (IgE) antibodies to isocyanates used less medication (OR 0.273; CI 0.098, 0.758) and had fewer symptoms of asthma (OR 0.329; CI 0.124, 0.875) than the IgE-negative ones. They also had a significantly shorter duration of symptoms (p = 0.0025), latency period (p = 0.0249), and duration of exposure (p = 0.0008) than the IgE-negative patients. This did not, however, entirely explain the more favourable outcome of the IgE-positive patients. Patients with HDI-induced asthma used less medication (OR 0.412; CI 0.229, 0.739) than patients with MDI- and TDI-induced asthma. The results confirm the generally rather poor medical outcome of diisocyanate-induced asthma; the persistence of symptoms and unspecific bronchial reactivity were pronounced in TDI-induced asthma. A more favourable outcome was associated with IgE mediation and HDI inducement.

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.

Background: We report on IgE-mediated asthma, rhinoconjunctivitis, and contact urticaria to two Liliaceae plants, tulip and Easter lily (Lilium longiflorum), diagnosed in a floral shop worker., Methods: Occupational asthma was diagnosed according to patient history, PEF monitoring, and a work-simulating provocation test. Flower-specific IgE was studied, and RAST inhibition tests were performed., Results: Skin prick testing showed positive reactions to tulip, Easter lily, and chrysanthemum. Total IgE was 180 kU/I, and specific IgE to tulip was 2.6 and to Easter lily 6.5 kU/I. In the RAST-inhibition test, no cross-reactivity was found. Occupational asthma was diagnosed by peak flow monitoring at work and at home, as well as specific inhalation challenge with Easter lily, with an immediate 18% reduction in PEF. In addition, contact urticaria and conjunctivitis were diagnosed. After a 9-year follow-up without exposure to lilies, the skin prick tests to L. longiflorum and tulip were still positive, but the specific IgE had disappeared., Conclusions: A case of IgE-mediated occupational asthma, rhinoconjunctivitis, and contact urticaria caused by L. longiflorum and tulip is presented. RAST inhibition tests indicated concomitant sensitization to the two Liliaceae plants.

Background: Amino alcohols are low molecular weight chemicals used widely in industrial processes, often as minor constituents. They have been found to cause allergic contact dermatitis. Marked exposure through airways is uncommon in other than occupational settings where chemicals containing amino alcohols may be heated or vaporized, liberating free amino alcohols into the ambient air. A few cases of asthma and allergic rhinitis have been reported, but the amounts inducing the airway reactions have not been defined., Objective: To further characterize ethanolamine-induced asthma and define the concentration inducing the asthmatic reaction, a case of diethanolamine-induced occupational asthma in a patient handling diethanolamine containing cutting fluid is reported., Methods: Suspicion of work related asthma was raised by symptoms and peak expiratory flow monitorings at work and at home. Specific bronchial provocation tests with the cutting fluid containing DEA and with DEA aerosol at two different concentration below the American Conference of Governmental Industrial Hygienists threshold limit value of DEA (2.0 mg/m3) were done., Results: DEA caused asthmatic airway obstruction at two different concentrations below the ACGIH TLV. A slight dose-response relationship was observed. Specific IgE-antibodies against DEA could not be found., Conclusions: DEA is able to induce occupational asthma by a sensitization mechanism, the exact pathophysiological mechanism of which is not known.

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.

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.

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.

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.

A total of 230 persons who had been exposed to formaldehyde and suffered from asthma-like respiratory symptoms were examined between January 1, 1977, and May 31, 1983. All the subjects had a bronchial provocation test with formaldehyde. On the basis of the medical and occupational history of the patients, the specific bronchial provocation test, and other test results, 12 cases were considered to be caused by specific sensitization to formaldehyde. All subjects had been exposed occupationally. An exposure period of between 1 mo and 19 yr preceded the onset of symptoms. Three persons displayed no bronchial hyperreactivity as assessed with a histamine or metacholine provocation test. Eleven of the 12 reactions were triggered by about 2.5 mg/m3 and one reaction by about 1.2 mg/m3 of formaldehyde. The late reaction in 1 patient was completely blocked by the inhalation of 100 micrograms of beclomethasone di-isoproprionate before the challenge with formaldehyde. Seventy-one of the 218 subjects who did not react when they were challenged with formaldehyde demonstrated bronchial hyperreactivity. We conclude that formaldehyde asthma, although apparently a rare disease, is under reported. Removal from exposure has a favorable effect on the symptoms. Low domestic exposures, however, may maintain the symptoms in individuals already sensitized.

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 PEA 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 fibre-board 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 PEA 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 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 PEA caused ACD which is different from the previous reports in which acrylates present as impurities in the PFA hardener caused the sensitization. Patch testing with 05% PFA hardener should be performed in patients with contact dermatitis if exposure to PFA has occurred. PFA hardener may also cause occupational asthma. The cause-effect relationship can be verified with chamber challenge tests. The mechanism of the asthmatic reaction is obscure as with many other low molecular weight chemicals. The exposure to PFA hardener should be minimized at the workplaces to prevent sensitization. Careful protection of both the skin and the respiratory tract is mandatory. [ABSTRACT FROM AUTHOR]

Describes chlorendic anhydride allergy. Signs and symptoms; Anhydrides that cause immunoglobulin E-mediated allergies.