Aluminiumindustriens
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Work related effects/resp. organs

The project Work related effects in respiratory regions was finalised by defence of the thesis for the medical doctor’s degree on June 13, 2008. 
Tone Sjåheim defended her thesis
Immunopathology of occupational asthma in aluminium potroom workers.
Conclusions

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CLINICAL AND IMMUNOLOGICAL STUDIES OF OCCUPATIONAL ASTHMA AT PRIMARY ALUMINIUM SMELTERS
The clinical provocative mechanism causing occupational asthma among operators at primary aluminium smelters is not known and has never earlier been tested.  The symptoms of asthma show an inflammation in the mucous membranes that are on the inside of the respiratory passages.  New data show that the irritation in respiratory organs or air pollution can by itself stimulate the immunity and induce changes in the inflammation.  The aim of this project is to survey and study in detail the changes of inflammation, which break out in the respiratory mucous membranes among  operators with occupational asthma in the potrooms.

METHOD
Bronchial biopsies and cleaning fluid from the lungs are examined by immune histochemical methods to estimate the cell compound, activity degree and signal  substances.  With our methods we hope to identify which part of the immunity that is central in the development of illness and in that way be able to document the causal relations.  It is of great importance to prevention, treatment and prognosis to clarity whether the inflammation changes of occupational asthma differ from asthma of other causes.

FINANCES
The study is financed by the Norwegian Research Board, NHO - Conferderation of Norwegian Enterprise and AMS (Nordic Aluminium Industry's Secretariat for Health, Environment and Safety) and is a collaboration project between Professor Johny Kongerud, Department of Thoracic Medicine, Rikshospitalet, and Dr. med. Trond Halstensen, University of Oslo.

PUBLICATIONS (last update 27.06.2008)

Immunopathology of occupational asthma in aluminium potroom workers
Tone Sjåheim’s thesis defended for the medical doctor’s degree June 13, 2008

Conclusions
This was the first time that pathological changes in the airways of workers with potroom asthma were examined.  The studies revealed that potroom asthma is associated with inflammatory changes in peripheral blood and bronchial mucosa, and that changes in non-smokers are similar to those previously reported in non-occupational and other occupational asthma. Smoking appeared to inhibit the asthma associated mucosal leukocyte accumulation in the asthmatic workers, suggesting an immunomodulating effect of smoking on the asthmatic reaction.  The studies revealed further several novel phenotypic characteristics of bronchial T-cells in asthma, in particular regulatory T-cells and T-cell proliferation.

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Airway inflammation in aluminium potroom asthma
T. Sjåheim, T. S. Halstensen, M. B. Lund, Ø. Bjørtuft, P. A. Drabløs, D. Malterud,
J. Kongerud
Occup. Environ. Med. 2004;61:779-785

Conclusions
Airway inflammation is a central feature of potroom asthma and exposure to potroom emissions induces pathological alterations similar to those described in other types of asthma.  Cigarette smoking seems to affect the underlying mechanisms involved in asthma, as the cellular composition of airway mucosa appears different in asthmatic smokers and non-smokers.
 

Blood Eosinophils in Workers With Aluminum Potroom Asthma Are Increased to Higher Levels in Non-Smokers Than in Smokers
T. Sjåheim, J. Kongerud, T. Søyseth
Am. J. Ind. Med. 2007;50:443–448

Conklusions
This study aimed to investigate the association between blood eosinophils and potroom asthma (PA). The prevalence of PA was positively associated with blood eosinophils. An attenuation of the blood eosinophil increase was observed in smoking asthmatics, suggesting an immune-modulating effect of smoking.
 

Reduced bronchial CD4+ T-cell density in smokers with occupational asthma
T. Sjåheim, J. Kongerud, Ø, Bjørtuft, P. A. Drabløs, D. Malterud, T. S. Halstensen
Eur. Respir. J. 2006;28:1138-1144

Conclusions
T-lymphocytes in the bronchial mucosa in workers with potroom asthma are affected by cigarette smoking.
Nonsmokers with potroom asthma have an increase in the T-cell subset CD4+, in common with nonsmokers with traditional asthma. However, smokers with potroom asthma have no increase in CD4+ T-cells.  The accumulation of subepithelial CD4+ T-cells, which was observed in the non-smoking asthmatics, appeared to be inhibited in smoking asthmatics.  This suggests a smoking-induced bronchial immune modulation, at least in occupational asthma in the aluminium industry.

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