The asthma syndrome: inciters, inducers, and host characteristics.

M Me ec ch ha an ni is sm ms s a an nd d p pa at th ho ol lo og gy y o of f o oc cc cu up pa at ti io on na al l a as st th hm ma a More than one mechanism may be operative in occupational asthma. Among the mechanisms proposed, immunological mechanisms and airway inflammation play an important role. There is evidence to confirm that T-lymphocyte activation and local accumulation in the bronchial wall of activated eosinophils occurs in asthma of diverse aetiology, i.e. immunoglobulin E (IgE)-mediated, occupational and intrinsic.Neurogenic pathways should be further investigated as a potential mechanism of modulation and amplification of airway inflammation in occupational asthma.

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Section: Mechanismsmentioning

confidence: 99%

Mechanisms and pathology of occupational asthma

Mapp

Saetta²,

Maestrelli³

et al. 1994

Eur Respir J

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“…It has been reported that exposure to fumes and vapours can be related to airway hyperresponsiveness (AHR). Exposure to high levels of irritants may induce persistent AHR due to mucosal inflammation of the bronchus, whereas exposure to low levels of irritants may provoke an airway narrowing due to a direct effect on the bronchial irritant receptors [2][3][4][5][6]. It has not been investigated whether exposures to irritant gases or fumes at levels commonly found in occupational settings result in obstructive lung diseases [1,7].…”

mentioning

confidence: 99%

Airway hyperresponsiveness in workers exposed to low levels of irritants

Kremer¹,

Pal²,

Schouten³

et al. 1995

Eur Respir J

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A Ai ir rw wa ay y h hy yp pe er rr re es sp po on ns si iv ve en ne es ss s i in n w wo or rk ke er rs s e ex xp po os se ed d t to o l lo ow w l le ev ve el ls s o of f i ir rr ri it ta an nt ts s ABSTRACT: The purpose of this study was to assess the association between occupational exposure to low levels of airway irritants, and airway responsiveness to histamine. In 688 male workers, symptom prevalence was assessed according to the British Medical Research Council (BMRC) questionnaire. All subjects performed a 30 s tidal breathing challenge test. Airway hyperresponsiveness (AHR) was defined as a 20% fall in forced expiratory volume in one second (FEV 1 ) at ≤32 mg·ml -1 histamine. On the basis of job titles and working department, the exposure status of all workers was characterized into seven groups: 1) reference group; 2) white collars; 3) SO 2 , HCl, SO 4 2-; 4) polyester vapour; 5) oil mist and oil vapour; 6) polyamide and polyester vapour; and 7) multiple exposures.Using multiple logistic regression, no association was found between the exposure groups and a higher prevalence of AHR. A higher prevalence was significantly associated with a low FEV 1 , a history of allergy, and the presence of chronic respiratory symptoms. Subjects in the SO 2 group and the oil mist group with ≤5 exposure years had a lower prevalence of AHR, probably due to pre-employment selection procedures. There was some trend for subjects with more than 5 yrs exposure to polyester vapour and to oil mist and to oil vapour to have a higher prevalence of AHR. Analyses using the dose-response slope according to O'Connor, revealed similar results and provides no additional information.We conclude that no association could be demonstrated between low grade exposure to airway irritants and airway hyperresponsiveness, and that further research is needed to elucidate this relationship.

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“…causing reversible airway bronchoconstriction associated with long-lasting airway hyperresponsiveness to nonspecific and/or specific agents) or as "inciter" (i.e. triggering asthma attacks) [36]. Among the mechanisms proposed in the pathogenesis of occupational asthma, the immunological one plays a key role [35].…”

Section: Mechanismmentioning

confidence: 99%