Mechanisms of occupational asthma.

Inhalation of agents in the workplace can induce asthma in a relatively small proportion of exposed workers. Like nonoccupational asthma, occupational asthma is probably the result of multiple genetic, environmental, and behavioral influences. It is important that occupational asthma be recognized clinically because it has serious medical and socioeconomic consequences.

Decreased heme-oxygenase (HO)-1 in the macrophages of non-small cell lung cancer.

Reactive oxygen species (ROS) are important in the initiation and promotion of cells to neoplastic growth. Heme-oxygenase (HO)-1, the inducible form of heme-oxygenase, is a cytoprotective enzyme that plays a central role in the defence against oxidative stress and is implicated in the protection of lung tissue against exogenous oxidant exposure. We investigated whether the expression of HO-1 would be decreased in lung tumour as compared with tumour-free adjacent lung tissues.

[Lung cancer in a female non-smoker with occupational exposure to asbestos: a case report].

Background: Until recently, asbestos was widely used in a variety of industrial processes. Workers exposed to asbestos may develop lung and pleural diseases such as asbestosis, lung cancer, benign pleural effusion, pleural plaques and mesothelioma.

Objective: To describe a clinical case of lung cancer in a female non-smoker with occupational exposure to asbestos.

Occupational asthma.

Occupational asthma (OA) is one of the most common forms of occupational lung disease in many industrialized countries, having been implicated in 9 to 15% of adult-onset asthma. Work-related asthma includes: 1. immunologic OA, characterized by a latency period before the onset of symptoms; 2.

Chronic obstructive pulmonary disease (COPD) and occupational exposures.

Chronic obstructive pulmonary disease (COPD) is one of the leading causes of morbidity and mortality in both industrialized and developing countries. Cigarette smoking is the major risk factor for COPD. However, relevant information from the literature published within the last years, either on general population samples or on workplaces, indicate that about 15% of all cases of COPD is work-related.

Asthma induced by isocyanates: a model of IgE-independent asthma.

Developments in the understanding of causes and natural history of asthma induced by isocyanates may allow improved preventive strategies for occupational asthma (OA), and may also lead to improved understanding of mechanisms involved in IgE-independent nonoccupational asthma. Studies of genetic markers in OA induced by isocyanates suggest that HLA class II genes, glutathione S-transferase and NAT1 genotypes may predispose to development of this type of OA. Specific IgE antibodies against isocyanates are not always found in subjects with OA caused by isocyanates, leading most researchers to consider this type of OA, as a model of IgE-independent asthma.

Occupational asthma.

Substantial epidemiologic and clinical evidence indicates that agents inhaled at work can induce asthma. In industrialized countries, occupational factors have been implicated in 9 to 15% of all cases of adult asthma. Work-related asthma includes (1) immunologic occupational asthma (OA), characterized by a latency period before the onset of symptoms; (2) nonimmunologic OA, which occurs after single or multiple exposures to high concentrations of irritant materials; (3) work-aggravated asthma, which is preexisting or concurrent asthma exacerbated by workplace exposures; and (4) variant syndromes.

Genetics and the occupational environment.

Purpose Of Review: This article will focus on the role of risk factors including genetic factors in the development of sensitization and occupational asthma.

Recent Findings: We will review the recent literature published on the genetics of occupational asthma, especially on genes coding for class II human leukocyte antigen and on respiratory antioxidant mechanisms. We will also discuss published work on non-occupational asthma and on allergic rhinitis because this information may contribute to a better understanding of the mechanisms involved in occupational asthma and serve to confirm data obtained on the disease.

Defective production of soluble HLA-G molecules by peripheral blood monocytes in patients with asthma.

Background: HLA-G, a human nonclassic MHC class I molecule, is responsible for complex immunoinhibitory functions. HLA-G is expressed as membrane-bound and is secreted as soluble molecules by the peripheral blood CD14+ monocytes activated by IL-10.

Objective: It has been reported that LPS stimulation induces IL-10 production by PBMCs and that IL-10 levels are reduced in patients with severe asthma compared with patients with mild asthma and healthy subjects.

Sputum substance P and neurokinin A are reduced during exacerbations of chronic obstructive pulmonary disease.

Involvement of tachykinins in airway inflammation has been demonstrated in animal models, but evidence in humans is sparse. The aim of this study was to quantify the levels of substance P and neurokinin A in induced sputum of patients with chronic obstructive pulmonary disease (COPD) and to compare them with the levels in smokers with normal lung function and healthy nonsmokers. Content of tackykinins was measured in 12 sputum samples collected during stable condition and nine sputum samples collected during exacerbations from 13 COPD patients, in eight sputum samples from smokers with normal lung function and in nine from healthy nonsmokers.

Glutathione S-transferase GSTP1 is a susceptibility gene for occupational asthma induced by isocyanates.

Background: Polymorphism at the pi class glutathione-S-transferase locus (GSTP1) is associated with allergen-induced asthma and related phenotypes.

Objective: We sought to determine whether GSTP1 polymorphism influences susceptibility to asthma induced by toluene diisocyanate (TDI).

Methods: The role of GSTP1 was assessed in 131 workers exposed to TDI, 92 with TDI-induced asthma and 39 asymptomatic subjects.