Aluminium potroom asthma: the Norwegian experience

Kongerud, Johny; J, Bøe; Søyseth, Vidar; Naalsund, Anne; Magnus, Per

doi:10.1183/09031936.94.07010165

Cited by 78 publications

(63 citation statements)

References 33 publications

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“…Bronchial biopsy studies in smoking asthmatics are lacking, apart from the current authors9 previous study of occupational nonatopic asthma in aluminium potroom workers [7], who were exposed to a complex mixture of particulates and gases [8]. Even though smoking and nonsmoking asthmatics had parallel increases in reticular basement membrane thickness, the smoking asthmatics had no increase in subepithelial total leukocyte density (CD45+ cells).…”

mentioning

confidence: 86%

Reduced bronchial CD4+ T-cell density in smokers with occupational asthma

Sjåheim¹,

Kongerud²,

Bjørtuft³

et al. 2006

Eur Respir J

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Cigarette smoking may alter bronchial inflammation in asthma. Multicolour immunohistofluorescent examination on bronchial cryosections was used to examine bronchial inflammatory cell infiltrate in patients with occupational asthma. Monoclonal antibodies to CD3, CD4, CD8, T-cell receptor-d1, CD68 and human leukocyte antigen-DR were combined to identify Tcell subsets and macrophages in bronchial biopsies from 20 workers with occupational asthma (12 smokers and eight nonsmokers), 15 healthy workers (seven smokers and eight nonsmokers) and 10 nonsmoking, nonexposed controls.The increased subepithelial CD4+ T-cell density in nonsmoking asthmatics was not present in smoking asthmatics, who had the lowest CD4+ T-cell density of all groups. The decreased subepithelial CD4+ and CD8+ T-cell density correlated with a reduction in lung function, as measured by percentage predicted forced expiratory volume in one second, in smoking asthmatics only. Although smoking asthmatics had a significantly increased number of intraepithelial CD8+ T-cells and macrophages compared with nonsmoking asthmatics, the proportion of cd-T-cells was significantly decreased in both asthmatic groups.Smoking asthmatics had a distinctly different distribution of T-cell subsets compared with nonsmoking asthmatics. The accumulation of subepithelial CD4+ T-cells, which was observed in nonsmoking asthmatics, appeared to be inhibited in smoking asthmatics, suggesting a smokinginduced bronchial immune modulation, at least in occupational asthma in the aluminium industry.

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mentioning

confidence: 86%

Reduced bronchial CD4+ T-cell density in smokers with occupational asthma

Sjåheim¹,

Kongerud²,

Bjørtuft³

et al. 2006

Eur Respir J

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“…Some studies also show conflicting results for mortality from obstructive lung disease, although most indicate an elevated risk (2)(3)(4)(5)(6)(7)(8). A Norwegian longitudinal morbidity study has, however, provided evidence of airway obstruction among potroom workers (9,10). Asthma-like symptoms ("potroom asthma") have been among the most important health problems in this industry for several decades and have been reported in Norway since 1937 (1 1,12).…”

Section: Bons Potroom Emission Primary Aluminum Smeltersmentioning

confidence: 99%

“…Cross-sectional studies may therefore have failed to detect work-related effects. Variations in the definition of occupational obstructive lung disease may also explain some of the inconsistencies between the morbidity studies (10).…”

Section: Respiratory Diseasementioning

confidence: 99%

Nonmalignant mortality among workers in six Norwegian aluminum plants

Romundstad¹,

Andersen²,

Haldorsen

2000

Scand J Work Environ Health

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Objectives This study investigated the associations between exposure to fluorides and polycyclic aromatic hydrocarbons (PAH) and mortality from nonmalignant diseases among workers in the Norwegian primary aluminum industly. Methods Mortality among 10 857 men, employed for more than 3 years in 1 of 6 aluminum plants, was investigated from 1962 to 1996, giving 239 246 person-years during follow-up. A job-exposure matrix covering all 6 plants was used to estimate the individual exposure to total fluorides and particulate PAH. The observed causespecific deaths were compared with expected figures calculated from national rates. Dose-response relations were investigated by internal colnparisons using Poisson regression and by stratified analyses for standardized mortality ratio. Potential confounding by smoking was investigated in subanalyses restricted to 3 of the plants for which information on smoking habits was accessible. Results Mortality from circulatory disease was slightly lower than expected [SMR 0.95,95% confidence interval (95%CI) 0.9-1.01, while there was an increased mortality from asthma, emphysema, and chronic bronchitis combined, SMR 1.2 (95% CI 1.0-1.5). Mortality from these diseases was associated with cumulative exposure to fluorides. The rate ratio in the internal analysis rose steadily to 2.5 (95% CI 1.5-4.3) for the upper exposure category. No association was observed between cumulative fluoride exposure or PAH exposure and circulatory mortality. C O~C~U S~O~S The study showed an association between exposure to potroom emissions measured by fluorides and mortality from asthma, emphysema, and chronic bronchitis combined.

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“…The term "potroom asthma" refers to the occurrence of work-related asthma symptoms among those employed in the production of aluminium from alumina into electrolytic cells ("pot") [37]. Different mechanisms could be involved in the development of these symptoms, including an irritant effect resulting from exposure to pollutants (i.e.…”

Section: Variant Syndromesmentioning

confidence: 99%

Definitions and types of work-related asthma: a nosological approach

Vandenplas¹,

Jl²

2003

Eur Respir J

111

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The workplace can trigger or induce asthma and cause the onset of different types of work-related asthma. Analysis of previous definitions of occupational asthma (OA) led to the conclusion that evidence of a direct causal relationship between workplace exposure and the development of asthma remains the key element for defining OA.Based on clinical features and pathophysiological mechanisms, the following conditions should be distinguished in the spectrum of work-related asthma: 1) immunological OA characterised by a latency period necessary to acquire immunologically induced sensitisation; 2) nonimmunological OA characterised by the rapid onset of asthma following single or multiple exposures to high concentrations of irritant compounds; 3) work-related asthma defined by exacerbation of symptoms in workers with pre-existing or coincident asthma; and 4) variant syndromes including eosinophilic bronchitis, potroom asthma, and asthma-like disorders caused by organic dusts.The issues and controversies relating to this approach are critically reviewed in order to stimulate the consensus development of operational definitions of work-related asthma. Eur Respir J 2003; 21: 706-712.

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Aluminium potroom asthma: the Norwegian experience

Cited by 78 publications

References 33 publications

Reduced bronchial CD4+ T-cell density in smokers with occupational asthma

Reduced bronchial CD4+ T-cell density in smokers with occupational asthma

Nonmalignant mortality among workers in six Norwegian aluminum plants

Definitions and types of work-related asthma: a nosological approach

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