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Query: UMLS:C0242379 (lung cancer)
 71,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This review deals with some of the emerging events that are assuming increasing relevance as work-related respiratory diseases (indoor air pollution and sick building syndrome, respiratory toxicity of formaldehyde, pollutant-induced asthma, dental technician lung diseases, lung cancer from diesel exhaust, environmental silicosis). The industrial hygienist's role in recognition, evaluation, and control of health hazards is stressed as an essential contribution to both prevention and diagnosis of occupational lung disease.
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PMID:New trends in occupational and environmental diseases: the role of the occupational hygienist in recognizing lung diseases. 808 23

Exposure to environmental tobacco smoke (ETS) is widespread in European countries, the most serious exposures occurring at home and in the workplace. Epidemiological studies have, essentially, addressed the association between ETS exposure and respiratory health in children, and increased risk of lung cancer among adult nonsmokers. Relatively few studies have been reported on ETS and adult non-neoplastic respiratory diseases. On the basis of the available data, no definite conclusion (excluding the acute irritating effect of ETS on respiratory mucous membranes) can be drawn. Although biologically plausible, it remains controversial whether ETS exposure is associated with chronic respiratory symptoms and occurrence of chronic obstructive pulmonary disease, including asthma. Most of the studies that have used the most sensitive indicators of pulmonary function have suggested a negative impact of ETS exposure. However, if really present, the physiological significance of such small changes is unclear, and the relationship to long-term changes in lung function is not established. Moreover, the possibility of bias and confounding factors must be taken into account. Thus, there is a need for further epidemiological studies on ETS exposure and adult non-neoplastic respiratory disorders.
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PMID:Exposure to environmental tobacco smoke and adult non-neoplastic respiratory diseases. 814 19

The risk of cancer was evaluated among 77,952 asthma patients with bronchial asthma. The series was obtained through linkage of two registers: the Finnish Social Insurance Institution's file of asthma patients and the Finnish Cancer Registry. There was a significant excess risk of lung cancer in both sexes, the standardized incidence ratio (SIR) being 1.32 among men and 1.66 among women. In women, the risk of cancer of the rectum was significantly increased (SIR 1.42), whereas the risks of cancer of the corpus uteri and multiple myeloma were lower than expected (SIR 0.76 and 0.53, respectively). In men, the incidence of cancer of the larynx was significantly reduced (SIR 0.63) and that of the bladder increased (SIR 1.25). When both sexes were combined, cancers of the colon (SIR 1.17) and rectum (SIR 1.28) also showed a significantly elevated risk. A reduction in risk was seen in stomach cancer (SIR 0.88) and lymphatic leukaemia (SIR 0.55). The increased lung cancer risk may be due to local inflammatory changes. It is possible that differences in the immune system, e.g. natural killer cell activity, explain some of the reduced cancer risks.
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PMID:Cancer incidence among 78,000 asthmatic patients. 814 10

Each antigen (Ag)-driven immune reaction begins with Ag recognition by T-lymphocytes through a surface molecular structure and T-cell antigen receptor (TCR). TCR is a proteid heterodimer, composed of an alpha and a beta chain (alpha beta+ T-cells) or of a gamma and a delta chain (gamma delta+ T-cells); each TCR chain is composed of two subunits the constant (C) region and the variable (V) region, whose combination is responsible, at least in part, for Ag specificity of each T-cell. Immune reactions toward known (e.g. tuberculosis) or unknown (e.g. sarcoidosis). Ags play an important role in the pathogenesis of many pulmonary disorders. The study of TCR may be performed at DNA, RNA and protein levels, applying molecular biology techniques. Using this molecular approach, it has been demonstrated, for example, that subgroups of patients have increased proportions of lung and/or blood T-cells bearing TCR with certain V regions of the alpha beta+ T-cells or of the gamma delta+ T-cells, suggesting that these cells were reacting toward antigenic stimuli. Similar results were obtained in tuberculosis, where an increase in gamma delta+ T-cells have been observed in peripheral blood of some patients. In asthma and in lung cancer a characterisation of TCRs of T-cells reacting to the involved allergens or to the tumour-associated Ags is still lacking, although animal studies show a selection of allergen-specific TCRs among the airway T-cells, and the ability of tumour-infiltrating gamma delta+ T-cells to kill cancer cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The T-cell antigen receptor: methods of study and relevance in the pathogenesis of pulmonary disorders. 819 19

Bronchial asthma itself or the treatment of asthma may modify the immunological response to cancer. The survival of lung cancer patients with a preceding diagnosis of bronchial asthma was compared with that of non-asthmatic lung cancer patients in Finland during 1970-1989. This was accomplished by linking two nation-wide data registers, the medication reimbursement register and the cancer registry. For 921 out of the 926 asthmatic patients with lung cancer diagnosed after the diagnosis of bronchial asthma, a non-asthmatic referent patient, matching with respect to sex, anatomical site, and histological type of tumour, as well as to age and year of lung cancer diagnosis, was successfully found in the files of the Cancer Registry. Another referent group was formed by using the stage of lung cancer at diagnosis as an extra matching criterion; this search was successful for 895 asthmatic lung cancer patients. The corrected 5-year survival rate of asthmatic lung cancer patients was 8.4% and that of the referent patients, not matched for stage, 9.6%. When stage was included as matching criterion the corresponding rates were 8.5% and 8.1% respectively. None of these differences were significant. The prognosis of asthmatic and non-asthmatic lung cancer patients thus seemed to be similar.
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PMID:Survival rates in lung cancer patients with and without bronchial asthma. 821 35

The biological effect of exposure to wood dust depends on its composition and the content of microorganisms which are an inherent element of the dust. The irritant and allergic effects of wood dust have been recognised for a long time. The allergic effect is caused by the wood dust of subtropical trees, e.g. western red cedar (Thuja plicata), redwood (Sequoia sempervirens), obeche (Triplochiton scleroxylon), cocabolla (Dalbergia retusa) and others. Trees growing in the European climate such as: larch (Larix), walnut (Juglans regia), oak (Quercus), beech (Fagus), pine (Pinus) cause a little less pronounced allergic effect. Occupational exposure to irritative or allergic wood dust may lead to bronchial asthma, rhinitis, alveolitis allergica, DDTS (Organic dust toxic syndrome), bronchitis, allergic dermatitis, conjunctivitis. An increased risk of adenocarcinoma of the sinonasal cavity is an important and serious problem associated with occupational exposure to wood dust. Adenocarcinoma constitutes about half of the total number of cancers induced by wood dust. An increased incidence of the squamous cell cancers can also be observed. The highest risk of cancer applies to workers of the furniture industry, particularly those dealing with machine wood processing, cabinet making and carpentry. The cancer of the upper respiratory tract develops after exposure to many kinds of wood dust. However, the wood dust of oak and beech seems to be most carcinogenic. It is assumed that exposure to wood dust can cause an increased incidence of other cancers, especially lung cancer and Hodgkin's disease. The adverse effects of microorganisms, mainly mould fungi and their metabolic products are manifested by alveolitis allergica and ODTS. These microorganisms can induce aspergillomycosis, bronchial asthma, rhinitis and allergic dermatitis.
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PMID:[Biological effect of wood dust]. 823 99

Thrombosis-inducing activity (TIA) is a factor which was recently identified in plasma from patients with advanced lung cancer and acute respiratory tract infection. In the present study, TIA was measured during periods of attack and nonattack in patients with the allergic and nonallergic type of asthma and pulmonary emphysema with an asthmatic component. In the allergic type of asthma, the attack was accompanied by the appearance of TIA, but when the attack ended it disappeared from plasma. In the nonallergic type of asthma and emphysema with an asthmatic component, TIA remained negative even during the attack. These observations indicate that TIA has some correlations with allergic asthma.
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PMID:Thrombosis-inducing activity--a factor which appears in plasma of patients with allergic asthma during attack. 824 3

We conducted a clinical study on asthmatic patients who were readmitted within three months of discharge. During twelve years (1979-1991), the number of patients who were readmitted within three months was 139 cases (209 episodes) in our department. Patients with respiratory diseases made up 53% of the subjects. Among patients with pulmonary disease who were readmitted within three months, the number of patients with lung cancer was 25 cases and that with bronchial asthma 24 cases. Within a month period, the number of readmitted patients with bronchial asthma was the largest 59% (19 cases) and the number of patients with lung cancer came second (4 cases). As for the characteristics of these asthmatic patients, the intrinsic type (15 cases), those with a history of over one year of the disease (20 cases), and those with steroid dependency (10 cases) were most commonly observed. Readmission occurred frequently between October and April. Readmission occurred frequently because of asthmatic attacks due to infection of reduction of steroid. Among asthmatic patients who were readmitted within one month, the disease severity was mild to moderate in 11 out of 19 patients, but there was a tendency for this to become intractable thereafter. It is impossible to prevent all patients from seeling readmission within a short period of discharge. However, we think the doctor's careful education of the patients is an important factor to reduce the early readmission rate of asthmatic patients.
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PMID:[A clinical study on asthmatic patients who were readmitted after a short period of discharge]. 828 39

Environmental tobacco smoke is a complex mixture of many chemical substances. The term passive smoking is used when a person breathes in air contaminated by tobacco smoke. Active and passive smoking expose an individual to the same substances, but the relative concentrations of the various substances differ. Thus, under conditions where individuals are exposed to an amount of nicotine corresponding to their smoking 1/2 a cigarette, they will be exposed to an amount of nitrosodimethylamine corresponding to their smoking about five cigarettes. Exposure of children to environmental tobacco smoke is associated with increased risk of lower respiratory tract infections, middle ear infections and asthma. Accumulating evidence points to passive smoking as a risk factor for the sudden infant death syndrome. Long term exposure to environmental tobacco smoke increases risk of lung cancer and heart disease. It is estimated that in Norway, 50 non-smokers die of lung cancer and 300-500 of heart disease annually, as a result of long term exposure to environmental tobacco smoke.
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PMID:[Health damages from passive smoking]. 865 89

Female lung cancer death rates increased by more than 550 percent between 1950 and 1991. In 1986 lung cancer surpassed breast cancer to become the leading cause of cancer death in women in the United States. The lung cancer epidemic is primarily attributable to cigarette smoking, which is responsible for at least 80% of the disease in women. There are gender differences in the distribution of lung cancer by histologic type, even controlling for smoking, and some data suggest greater female than male susceptibility to lung cancer at a given level of smoking. Exposure to environmental tobacco smoke increases risk of lung cancer in nonsmoking women. Family history of lung cancer, personal history of lung disease (e.g. asthma, chronic bronchitis, pneumonia, or tuberculosis), and a history of radiotherapy also appear to be associated with increased risk. Data specific to women on the role of household radon exposures or of specific occupational or environmental exposures are relatively sparse and inconsistent. Finally, many studies have reported a decreased risk of lung cancer in individuals who consume high levels of fruits and vegetables; however, clinical trials fail to support a beneficial effect of beta-carotene supplementation. Since cigarette smoking accounts for the vast majority of lung cancer cases in women, efforts to prevent adolescent girls from starting to smoke and to encourage cessation among established smokers have the greatest potential for reducing the female lung cancer burden.
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PMID:Female lung cancer. 872 18


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