Biomedical subjects

Piera Boschetto

Publications and source records attributed to Piera Boschetto.

8 recordsLinked to original sources

PubMed2006

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. Specific settings and agents are quoted which have been indicated or confirmed as linked to COPD. Coal miners, hard-rock miners, tunnel workers, concrete-manufacturing workers, nonmining industrial workers have been shown to be at highest risk for developing COPD. Further evidence that occupational agents are capable of inducing COPD comes from experimental studies, particularly in animal models. In conclusion, occupational exposure to dusts, chemicals, gases should be considered an established, or supported by good evidence, risk factor for developing COPD. The implications of this substantial occupational contribution to COPD must be considered in research planning, in public policy decision-making, and in clinical practice.

Journal Article↗

PubMed2005

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. Assessment of the work environment has improved, making it possible to measure concentrations of several high- and low-molecular-weight agents in the workplace. The identification of host factors, polymorphisms, and candidate genes associated with OA is in progress and may improve our understanding of mechanisms involved in OA. A reliable diagnosis of OA should be confirmed by objective testing early after its onset. Removal of the worker from exposure to the causal agent and treatment with inhaled glucocorticoids lead to a better outcome. Finally, strategies for preventing OA should be implemented and their cost-effectiveness examined.

Adult↗

PubMed2005

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. Patients with COPD exacerbations had a lower sputum content of substance P compared with the other 3 groups (p<0.05). No differences were found between patients with stable COPD, smokers with normal lung function, and nonsmokers. Sputum levels of neurokinin A were trending in the same direction of substance P, but the significant difference was reached for the paired sputum samples collected from the same COPD patients (n=8) during exacerbation and in stable condition. COPD exacerbations are associated with a reduced sputum content of substance P and neurokinin A. These tackykinins might be involved in COPD exacerbations.

Aged↗

PubMed2005

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. 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.

Animals↗

PubMed2002

Airway inflammation in severe chronic obstructive pulmonary disease: relationship with lung function and radiologic emphysema.

The lung pathology of severe chronic obstructive pulmonary disease (COPD) has been poorly investigated. We examined surgical specimens obtained from patients with severe (forced expiratory volume in 1 second [FEV(1)] = 29 +/- 3% predicted, n = 9) or mild/no airflow limitation (FEV(1) = 86 +/- 5% predicted, n = 9) and similar smoking history. With histochemical and immunohistochemical methods we quantified the structural changes and the inflammatory cells in small airways and in muscular pulmonary arteries. As compared with smokers with mild/no COPD, smokers with severe COPD had an increased number of leukocytes in the small airways, which showed a positive correlation with the radiologic score of emphysema and with the value of residual volume, and a negative correlation with the values of FEV(1) and carbon monoxide diffusing capacity. The inflammatory process was characterized by an increase in CD8(+) and CD4(+) T-lymphocytes in the airway wall and by an increase in macrophages in the airway epithelium. When all smokers were considered together, the smoking history was correlated with both the airway wall and smooth muscle thickness, suggesting that smoking itself may play a role in the development of structural changes. No structural and cellular differences were observed in pulmonary arteries between smokers with severe COPD and smokers with mild/no COPD. In conclusion, in the small airways of smokers with severe COPD, there is an increased number of leukocytes, which is correlated with reduced expiratory flow, lung hyperinflation, carbon monoxide diffusion impairment, and radiologic emphysema, suggesting a role for this inflammatory response in the clinical progression of the disease.

Case-Control Studies↗

PubMed2002

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. The phenotype of the disease was characterized by using detailed clinical history, lung volumes, airway responsiveness to methacholine, and airway responsiveness to TDI. GST genotypes were determined by using PCR-based assays. RESULTS: In patients exposed to TDI for 10 or more years, the frequency of the GSTP1 Val/Val genotype was lower in subjects who had asthma (odds ratio, 0.23; 95% confidence interval, 0.05-1.13; P =.074). Similarly, the frequency of this genotype was significantly lower in subjects with evidence of moderate-to-severe airway hyperresponsiveness to methacholine compared with the frequency in subjects with normal or mild hyperresponsiveness (P =.033). CONCLUSION: These data suggest that homozygosity for the GSTP1*Val allele confers protection against TDI-induced asthma and airway hyperresponsiveness. This view is supported by the finding that the protective effect increases in proportion to the duration of exposure to TDI.

Adult↗

PubMedDate not supplied

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. 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.

Allergens↗

PubMedDate not supplied

[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. 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.

Asbestos↗