Summary Background Occupational asthma is an avoidable form of asthma. In Finland, the diagnosis of occupational asthma entitles substantial compensation to the employee. The diagnostics are based on symptoms, exposure assessment, allergologic investigations, follow‐up of peak expiratory flow (PEF) at work and at home and, in many cases, specific challenge tests. Objective To study the causative agents of occupational asthma in Finland. Methods The causative agents and the numbers of new occupational asthma cases notified to the Finnish Register of Occupational Diseases (FROD) during 1986–2002 are reported. Results The number of occupational asthma cases increased from 1986 until 1995, after which a downward trend, stabilizing during the last few years, has been observed. The majority of the cases (59%) in the beginning of the period (1986–1990) were associated with agriculture, but the percentage has fallen thereafter (42% of the cases in 1998–2002) along with the fall in the total number of cases. Since 1995, indoor moulds from water‐damaged buildings have caused an increasing number of cases and have become the most important causative agents (0.5% cases, in 1986–1990 and 18% of the cases in 1998–2002). Chemicals have caused 10–30% of the cases, a decreasing number since 1990. The most important chemicals causing occupational asthma have been diisocyanates and welding fumes, followed by hairdressing chemicals and formaldehyde. Conclusions The number of occupational asthma cases in Finland reached its height in the mid‐1990s. The decrease in the number of total cases is because of the decrease in agriculture‐associated cases, reflecting the number of employees in agriculture‐associated occupations, which has greatly decreased since Finland joined the EU in 1995. An epidemic of mould‐induced asthma, affecting mostly white‐collar employees working in moisture‐damaged buildings, has taken place since 1995.
Toskala, Elina MD, PhD; Piipari, Ritva MD; Aalto-Korte, Kristiina MD, PhD; Tuppurainen, Matti MD; Kuuliala, Outi MSc; Keskinen, Helena MD Author Information
Objectives. The authors assessed the effects of environmental tobacco smoke (ETS) on the development of asthma in adults. Methods. In the Pirkanmaa district of South Finland, all 21- to 63-year-old adults with new cases of asthma diagnosed during a 2.5-year period (n = 521 case patients, out of 441 000 inhabitants) and a random sample of control subjects from the source population (932 control subjects) participated in a population-based incident case–control study. Results. Risk of asthma was related to workplace ETS exposure (adjusted odds ratio [OR] = 2.16; 95% confidence interval [CI] = 1.26, 3.72) and home exposure (OR = 4.77; 95% CI = 1.29, 17.7) in the past year. Cumulative ETS exposure over a lifetime at work and at home increased the risk. Conclusions. This study indicates for the first time that both cumulative lifetime and recent ETS exposures increase the risk of adult-onset asthma.
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.
To the Editor: Welding is associated with respiratory effects such as metal fume fever, chronic bronchitis, lung function abnormalities, and occupational asthma (OA).1 Previous studies have described OA in workers exposed to welding fumes from stainless steel2,3 and aluminum.4 Stellite is a metal alloy with both cobalt and chromium.5 The amount of cobalt is usually about 60% and of chromium about 30%. It also contains tungsten and a small amount of carbon. Stellite alloys are resistant to corrosion and also retain their hardness at elevated temperatures. They are used in wear-related applications such as in the manufacture of components of gas turbine and jet engines, and in cutting tools. Previously, respiratory symptoms including cough, dyspnea, and wheezing have been described in saw filers exposed to stellite,6 and in workers maintaining hard metal and stellite blades.7 However, to the best of our knowledge, OA associated with exposure to welding fumes from stellite has not been described. We report here on such a worker. A 42-year-old man, working since age 18 for the same employer manufacturing machines for the pulp and paper industry, had tasks including cutting mild or stainless steel for his first 6 years. Thereafter, he worked as a machinist; the material used was mild or stainless steel, and he also used metal working fluids. Very near his workplace, welding on stellite took place, but he himself did not take part. The patient had a history of perennial rhinitis, and had smoked for 4 years in his youth. He had been examined in a local central hospital for dyspnea 15 years before the examinations at the Finnish Institute of Occupational Health (FIOH), where bronchial asthma was diagnosed and asthma medication started. During one year prior to examinations at the FIOH, the patient had started to experience worsening of his asthma symptoms. This worsening was clearly related to exposure to stellite welding fumes, and his use of short-acting inhaled bronchodilating medication was therefore increased. Before this, his asthma has been in good balance with moderate use of regular inhaled budenoside combined with sodium chromoglycate. Because of asthma exacerbation, the patient contacted his occupational health physician, and workplace peak expiratory flow (PEF) monitoring was scheduled. The results were suggestive of OA: PEF values were 540–620 L/min when he was not in his workplace or when he was not exposed to welding fumes from stellite; on one working day with stellite welding, his PEF value fell to 480 L/min, but rose after short-acting bronchodilatating medication to 590 L/min. The patient was referred to FIOH for further examination. At the FIOH, auscultation of his chest was normal. Total serum immunoglobulin (Ig)E was 281 kU/L. Spirometry was normal, but the histamine challenge test revealed mild bronchial hyperresponsiveness (PD15 1.20 mg). His diurnal PEF and forced expiratory volume in 1 second (FEV1) values were within normal limits. Skin prick tests for common allergens showed allergy to pollens of grass, mugwort, alder, and dandelion, to epithelia of cow, and to Pityrosporum ovale, but for metals they were negative.8 The concentrations of the tested metals in water solutions were nickel sulfate 10 mg NiSO4/mL, potassium dichromate 1 mg Cr6+/mL, chromium chloride 1 mg Cr3+/mL, and cobalt chloride 1 mg Co2+/mL.3 Diagnosis of OA was made according to the European guidelines.9 Bronchial challenge tests were performed in a special welding exposure chamber. The referent test was by a diluent (ALK-Abello A/S, Copenhagen, Denmark). Cobalt and chromium challenge tests comprised solutions of cobalt chloride (0.1–10 mg Co2+/mL) and potassium dichromate (0.01—1 mg Cr6+/mL). Stellite welding was done by welding (30 minutes) on mild steel with a special stellite electrode (Soudostel HR21, Soudometal SA, Belgium), which consisted of about 65% cobalt, 28% chromium, 4.5% molybdenum, 2.5% nickel, and 0.25% carbon. After challenge tests, the patient was followed up for 24 hours. Lung function measurements (FEV1 and PEF) were done with a portable, pocket-size spirometer (One Flow, STI MEDICAL, Saint-Romans, France). A drop of 20% in PEF or FEV1 was regarded as significant compared with both starting level and control test. Clinical symptoms and lung auscultation findings were also recorded. In our patient, the referent inhalation challenge test did not indicate any adverse reactions, nor did the tests with both cobalt and chromium solutions. Welding mild steel with the specific electrode for stellite, however, caused an immediate asthmatic reaction, with a 21% drop in PEF measurements, and a suggestive delayed reaction, with a 15% drop. FEV1 values did not show a significant drop (maximal drop was –10% immediately). In association with the significant PEF drop, lung auscultation revealed wheezing in forced expirium. To confirm the diagnosis of OA, a workplace challenge test with PEF monitoring was performed. This showed a variation in PEF values of 560–630 L/min without exposure to stellite welding fumes, but after a 3-hour work exposure to stellite welding, PEF values dropped to 480 L/min and returned to the starting level in 19 hours. Based on work-related respiratory symptoms, occupational exposure, suggestive workplace PEF monitoring, positive findings in the specific welding challenge test, and the positive workplace challenge test, the diagnosis was OA. Avoidance of working near stellite welding was recommended, and regular inhaled budesonide medication was continued, with salbutamol on demand. Our patient's asthmatic reaction was specifically related to stellite welding, since specific challenge tests with either cobalt or chromium solutions did not indicate any adverse reactions. The rationale for first performing challenge tests to chromium and cobalt solutions was that these metals might have been responsible, because stellite contains them and because these agents have earlier been associated with OA.10,11 In line with this, we used a diluent as a referent challenge. Because these active challenge tests did not indicate any adverse reactions and the patient's OA was clearly associated with stellite welding fumes, we performed this challenge test, as well, using welding on mild steel with a special stellite electrode. This was reasonable, because most of the welding fumes are generated from the electrode, with the welded material playing a minor role. In our patient, the pathophysiological mechanism responsible for the induction of OA remains unknown. Although some studies concerning OA related to metals have proposed an IgE-mediated mechanism, skin reactivity to metal salts has not been consistently demonstrated in subjects with OA caused by these agents.12 Our patient showed no immediate skin reactivity to chromium or cobalt in skin-prick tests, and the specific challenge tests with these metal solutions did not indicate any adverse reactions. Tungsten was not skin prick tested. The literature has one case study reporting tungsten- induced OA with positive scratch test to this metal; in that case, however, the diagnosis of OA was based only on symptoms, with no lung function examinations or specific challenge tests.13 Unfortunately, we could not determine the concentrations of the welding aerosols during specific challenge tests to possibly further elucidate the pathophysiological mechanism. In conclusion, exposure to welding fumes from stellite should be included among etiological factors capable of inducing OA. Where there is doubt about the diagnosis, specific challenge tests remain the only method to confirm OA caused by welding fumes at an individual level. Timo Hannu, MD, PhD Ritva Piipari, MD Matti Tuppurainen, MD Timo Tuomi, PhD Finnish Institute of Occupational Health, Occupational medicine Helsinki, Finland
SUMMARY Immunoglobulin G (IgG) antibodies against microbes related to indoor dampness problems have been used as potential biomarkers of fungal exposure in clinical investigations. There is limited information on their relation to asthma. We conducted a population-based incident case–control study to assess the risk of asthma in relation to specific IgG antibodies to eight dampness-related microbes: Aspergillus fumigatus, A. versicolor, Cladosporium cladosporioides, Fusarium oxysporum, Sporobolomyces salmonicolor, Stachybotrys chartarum, Streptomyces albus and Trichoderma citrinoviride. We recruited systematically all new cases of asthma during a 2·5-year study period and randomly selected controls from a source population of adults 21–63 years of age living in the Pirkanmaa Hospital District, South Finland. The clinically diagnosed case series consisted of 521 adults with newly diagnosed asthma and the control series of 932 controls selected randomly from the source population. IgG antibodies were analysed with ELISA. An increased risk of developing asthma in adulthood was significantly related to IgG antibodies to T. citrinoviride, but not to the other moulds. There was no evidence of a dose–response relation between the IgG antibody level and the risk of asthma. T. citrinoviride may play a role in the aetiology of adult-onset asthma or serve as an indicator of other causal factors.
