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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., Methods: The clinical and occupational history was based on the information kindly provided by the Occupational Unit of the National Health Service and on the case history of a hospital admittance in 2001, when the patient underwent surgery for lung cancer., Results: The patient worked for 6 years in an asbestos manufacturing industry where she was exposed to high concentrations of asbestos, and then worked for 14 years in a sugar refinery only during the summer. She had benign pleural effusion, pleural plaques, asbestosis and lung cancer., Conclusions: We concluded that a six-year exposure to high doses of asbestos may induce lung cancer and asbestosis in a female non-smoker.

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. nonimmunologic OA, which occurs after single or multiple exposures to high concentrations of irritants; 3. work-aggravated asthma, which is pre-existing or concurrent asthma exacerbated by workplace exposures; and 4. variant syndromes. OA is important to recognize clinically, because it has serious medical and socioeconomic consequences. Diagnosis of OA should be confirmed by objective testing early after its onset. Removal of the worker from exposure to the causal agent and early treatment with anti-inflammatory drugs lead to a better outcome. Assessment of the work environment and identification of host factors may provide us with useful information about the mechanisms involved in OA. Another issue concerns strategies for preventing OA which should be implemented.

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. Evidence for cell-mediated immunity in OA induced by isocyanates has been provided by bronchoalveolar lavage, bronchial biopsy and induced sputum studies. The pathology of this type of asthma is similar to that of nonoccupational asthma, with cells such as eosinophils and T lymphocytes that exhibit signs of activation, and with thickening of the reticular layer of the basement membrane. Animal studies have shown that isocyanate asthma is driven primarily by CD4+ T cells and is dependent upon the expression of Th2 cytokines. However, animal models are not always reflective of human responses. OA induced by isocyanates similarly to nonoccupational asthma, is a multifactorial condition, and it is likely that complex gene-environment interactions play a role. Better understanding of these interactions is important for affected workers, and also has potential relevance for nonoccupational asthma.