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Dive into the research topics where Henrik Nordman is active.

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Featured researches published by Henrik Nordman.


American Journal of Industrial Medicine | 2000

Incidence of occupational asthma by occupation and industry in Finland.

Antti Karjalainen; Kari Kurppa; Simo Virtanen; Helena Keskinen; Henrik Nordman

BACKGROUNDnSystematic research on occupation or industry-specific incidence of occupational asthma (OA) is sparse. We calculated the incidence of notified OA by occupation, industry and causative agent in Finland for the years 1989-95.nnnMETHODSnThe numbers of cases of reported OA were retrieved from the Finnish Registry of Occupational Diseases for the population between 20 and 64 years of age. The numbers of employed workers were retrieved from Statistics Finland. Incidence rates were calculated for each occupation, industry and the total workforce.nnnRESULTSnAltogether 2602 cases of OA were notified and the mean annual incidence rate was 17.4 cases/100,000 employed workers. The incidence rate was the highest in bakers, other painters and lacquerers, veterinary surgeons, chemical workers, farmers, animal husbandry workers, other food manufacturing workers, welders, plastic product workers, butchers and sausage makers, and floor layers. Cases caused by animal epithelia, hairs and secretions or flours, grains, and fodders accounted for 60% of the total.nnnCONCLUSIONSnEstimation of occupation and industry-specific incidence rates forms the basis for successful prevention of OA, but necessitates collection of data over several years from well-established surveillance systems.


The Journal of Allergy and Clinical Immunology | 1985

Formaldehyde asthma--rare or overlooked?

Henrik Nordman; Helena Keskinen; Matti Tuppurainen

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.


Pharmacogenetics | 2002

N-acetyltransferase genotypes as modifiers of diisocyanate exposure-associated asthma risk

Harriet Wikman; Päivi Piirilä; Christina Rosenberg; Ritva Luukkonen; Katja Kääriä; Henrik Nordman; Hannu Norppa; Ari Hirvonen

We observed previously that polymorphisms in glutathione S-transferase (GST) genes modified allergic responses to diisocyanate exposure. Here, we extended the study to examine the possible role of N-acetyltransferase (NAT) genotypes in the development of diisocyanate-induced ill effects, both separately and in combination with the previously examined GSTM1, GSTM3, GSTP1 and GSTT1 genotypes. The study population comprised 182 diisocyanate-exposed workers, 109 of whom were diagnosed with diisocyanate-induced asthma and 73 of whom had no symptoms of asthma. The diisocyanates to which the workers had been exposed to were diphenylmethane diisocyanate (MDI), hexamethylene diisocyanate (HDI) and toluene diisocyanate (TDI). The NAT2 genotype did not have any significant effect on the risk of developing asthma, but the putative slow acetylator NAT1 genotypes posed a 2.54-fold risk of diisocyanate-induced asthma (95% confidence interval [CI] 1.32 to 4.91). The effect of the NAT1 genotype was especially marked for workers exposed to TDI, among whom the NAT1 slow acetylator genotypes posed a 7.77-fold risk of asthma (95% CI 1.18 to 51.6). Statistically significant increases in asthma risk were also observed among the whole study population for the concurrent presence of the GSTM1 null genotype and either NAT1 (odds ratio [OR] 4.53, 95% CI 1.76 to 11.6) or NAT2 (OR 3.12, 95% CI 1.11 to 8.78) slow acetylator genotypes, and of NAT1 and NAT2 slow acetylator genotypes (OR 4.20, 95% CI 1.51 to 11.6). The results suggest for the first time that in addition to GSTs, the NATs play an important role in inception of asthmatic reactions related to occupational exposure to diisocyanates.


Clinical & Experimental Allergy | 1988

Experiences of specific IgE in asthma due to diisocyanates

Helena Keskinen; Outi Tupasela; Ulla Tiikkainen; Henrik Nordman

The specific IgE antibodies were studied with the Phadebas® RAST technique in 35 patients with asthma due to diisocyanates. Two had been sensitized to toluene diisocyanate (TDI), 17 to methylene diisocyanate (MDI) and 16 to hexamethylene diisocyanate (HDI). In each case the diagnosis was confirmed with a bronchial provocation test (BPT). The asthmatic reaction was immediate in 17 cases, of which three had also a late reaction (dual). Eighteen patients reacted only with a late reaction. Seven (20%) had specific IgE to diisocyanates. All RAST‐positive patients had an immediate asthmatic reaction. None of the late reactors and referents had positive RASTs. RAST inhibition tests with 94–100% inhibition confirmed the specificity of the method. There was cross‐reactivity between different diisocyanates, however. The patients with positive RAST to diisocyanates had a higher level of total IgE than the RAST negative group and the referents.


Occupational and Environmental Medicine | 1997

Self reported respiratory symptoms and diseases among hairdressers.

Timo Leino; Lauri Tammilehto; Ritva Luukkonen; Henrik Nordman

OBJECTIVES: Hairdressers are exposed to many irritative and allergenic substances capable of causing occupational respiratory symptoms and diseases. The self reported prevalence of respiratory symptoms and diseases was studied, and the risks among hairdressers compared with saleswomen was estimated. METHODS: A cross sectional prevalence study of respiratory symptoms and diseases was carried out among hairdressers and supermarket saleswomen, with a computer assisted telephone interview method (CATI). The study population comprised all the female hairdressers and supermarket saleswomen aged 15-54 years in the Helsinki metropolitan area, Finland. Disproportionate random samples of female hairdressers and sales-women were drawn from the trade union membership registers. The interviews were carried out between February and April 1994. A response rate of 80.5% (355/440) was obtained for hairdressers and 82.2% (583/709) for saleswomen. Atopy, smoking, chronic illnesses, type of work, working hours, working conditions, personal and professional use of hair products, and the use of personal protective devices were assessed. The outcome variables were self reported symptoms of the upper and lower respiratory tract. These were used to define chronic bronchitis, and asthma, laryngitis, and allergic rhinitis diagnosed by a physician. RESULTS: There was a considerable difference in the prevalence of chronic bronchitis; 6.8% in hairdressers versus 1.9% in saleswomen. The odds ratio (OR) adjusted for age, smoking, and atopy for chronic bronchitis indicated an increased risk of chronic bronchitis (OR 4.8, 95% confidence interval (95% CI) 2.2 to 10.1). No association was found between work as a hairdresser and asthma, laryngitis, and allergic rhinitis. Also the prevalence of rhinitis, rhinitis with eye symptoms, cough with phlegm, dyspnoea, and dyspnoea accompanied by cough was increased among hairdressers. The corresponding adjusted risk ORs were 1.7 (95% CI 1.3 to 2.3) for rhinitis, 1.9 (95% CI 1.4 to 2.6) for rhinitis with eye symptoms, 1.4 (CI 1.1 to 1.9) for cough with phlegm, 1.5 (95% CI 1.0 to 2.2) for dyspnoea, and 1.6 (95% CI 1.0 to 2.7) for dyspnoea with cough. CONCLUSIONS: Our results indicate an increased prevalence of upper and lower respiratory symptoms among hairdressers. Allergenic and irritative chemicals in hairdressing are likely candidates explaining the difference found between the hairdressers and controls. Work related reasons should be considered when a hairdresser presents with airway symptoms. Preventive actions are needed to improve the working conditions and personal protection.


Occupational and Environmental Medicine | 2000

Risk of enzyme allergy in the detergent industry

Markku Vanhanen; Timo Tuomi; Ulla Tiikkainen; Outi Tupasela; Risto Voutilainen; Henrik Nordman

OBJECTIVES To assess the prevalence of enzyme sensitisation in the detergent industry. METHODS A cross sectional study was conducted in a detergent factory. Sensitisation to enzymes was examined by skin prick and radioallergosorbent (RAST) tests. 76 Workers were tested; 40 in manufacturing, packing, and maintenance, and 36 non-exposed people in management and sales departments. The workers were interviewed for work related respiratory and skin symptoms. Total dust concentrations were measured by a gravimetric method, and the concentration of protease in air by a catalytic method. RESULTS Nine workers (22%) were sensitised to enzymes in the exposed group of 40, whereas none were sensitised in the non-exposed group. All the sensitised people had symptoms at work; all had rhinitis and one had asthma. Protease concentrations were generally <20 ng/m3, but occasional peak values up to 80 ng/m3 were detected in the packing and maintenance tasks, and high values of >1 μg/m3 in the mixing area. CONCLUSION Despite the use of encapsulated enzyme preparations, high enzyme concentrations in workplace air are possible, resulting in a higher risk of sensitisation than expected.


Occupational and Environmental Medicine | 1996

Enzyme exposure and enzyme sensitisation in the baking industry.

M Vanhanen; Timo Tuomi; H Hokkanen; O Tupasela; A Tuomainen; P C Holmberg; M Leisola; Henrik Nordman

OBJECTIVES: To assess the exposure to enzymes and prevalence of enzyme sensitisation in the baking industry. METHODS: A cross sectional study was conducted in four bakeries, one flour mill, and one crispbread factory. Sensitisation to enzymes, flours, and storage mites was examined by skin prick and radioallergosorbent (RAST) tests. 365 workers were tested. The workers were interviewed for work related respiratory and skin symptoms. Total dust concentrations were measured by a gravimetric method, and the concentration of alpha-amylase in air was measured by a catalytic method. An immunochemical method was used for measuring cellulase and xylanase in air. RESULTS: Total measured dust concentrations were from 0.1 to 18 mg/m3, with highest values in dough making areas of bakeries. The alpha-amylase concentrations generally followed the total dust concentrations and reached the highest values < 6.6 micrograms/m3 in the same areas. Cellulase and xylanase varied with concentrations < 180 ng/m3 and < 40 ng/m3, respectively, in the flour mill and the crispbread factory. No cellulase, but concentrations of 1-200 ng/m3 xylanase, were found in the bakeries, probably indicating the natural xylanase activity of wheat. 12 workers (8%) in the bakeries, three (5%) in the flour mill, and four (3%) in the crispbread factory were skin prick positive to enzymes. The corresponding percentages of positive reactions to flours were 12%, 5%, and 8%. CONCLUSIONS: The study confirmed that industrial enzymes in baking used as additives in a powdered form pose a risk of sensitisation. The no effect air concentrations for industrial enzymes are not known. Based on present knowledge, however, lowering exposures and eliminating short and high peaks by technical measures would lower the risk of sensitisation. This would be most effectively accomplished by shifting to non-dusty products.


Allergy | 2008

Inflammation and functional outcome in diisocyanate-induced asthma after cessation of exposure

Päivi Piirilä; Anna Meuronen; Marja-Leena Majuri; Ritva Luukkonen; T. Mäntylä; Henrik Wolff; Henrik Nordman; Harri Alenius; Annika Laitinen

Background:u2002 The clinical outcome of diisocyanate‐induced asthma has been found to be poor despite cessation of exposure. Our aim was to study the outcome of diisocyanate‐induced asthma after initiation of inhaled steroid treatment at a mean period of 7u2003months (range 2–60u2003months) after cessation of exposure by following up lung function and bronchial inflammation.


Clinical and Experimental Immunology | 2002

Immunoglobulin G antibodies against indoor dampness-related microbes and adult-onset asthma: a population-based incident case–control study

Maritta S. Jaakkola; S. Laitinen; Ritva Piipari; Jukka Uitti; Henrik Nordman; A.-M. Haapala; Jouni J. K. Jaakkola

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.


International Archives of Occupational and Environmental Health | 2010

New-onset adult asthma in relation to damp and moldy workplaces

Kirsi Karvala; Elina Toskala; Ritva Luukkonen; Sanna Lappalainen; Jukka Uitti; Henrik Nordman

ObjectiveDamp and moldy indoor environments aggravate pre-existing asthma. Recent meta-analyses suggest that exposure to such environments may also induce new-onset asthma. We assessed the probability of molds being the cause of asthma in a patient series examined because of respiratory symptoms in relation to workplace dampness and molds.MethodsAltogether 694 such patients had been clinically assessed between 1995 and 2004. According to their histories, they had all been exposed to molds at work and had suffered from work-related lower respiratory symptoms. The investigations had included specific inhalation challenge (SIC) tests with mold extracts and serial peak expiratory flow (PEF) recordings. Using internationally recommended diagnostic criteria for occupational asthma (OA), we categorized the patients into three groups: probable, possible, and unlikely OA (156, 45, and 475 patients, respectively). The clinical details of 258 patients were analyzed, and their levels of microbial exposure were evaluated.ResultsThe agreement between the serial PEF recordings and SIC tests (both being either positive or negative) was 56%. In the group of probable OA, mold sensitization was found in 20%. The level of exposure and sensitization to molds was associated with probable OA. At 6xa0months, the follow-up examinations of 136 patients with probable OA showed that the symptoms were persistent, and no improvement in spirometry was noted despite adequate treatment. Only 58% of the patients had returned to work.ConclusionsExposure to damp and moldy workplaces can induce new-onset adult asthma. IgE mediation is a rare mechanism, whereas other mechanisms are unknown.

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Päivi Piirilä

Finnish Institute of Occupational Health

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Lauri Tammilehto

Helsinki University Central Hospital

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A. I. Lauerma

Helsinki University Central Hospital

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