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Airways lung cancer

Aerosol size has an effect on the lung dose. Fine particles breathed through the mouth or the nose from lOOnm to 1,000 nm median size had 5-20 nGy per becquerel. Below 100 nm, this number more than doubled at 25-65 nGy per becquerel at 20 nm median size. Median sizes had an approximate geometric standard deviation of 2, so that the 95% confidence interval of particle sizes ranged from 0.25 to 4 times the stated median size. Very small particles deposited more efficiently in the airways. Lung cancer was related to radiation dose. These dose estimates are important determinants of lung cancer. [Pg.388]

Most lung cancers are derived from the epithelium of the airways and therefore are classified as carcinomas. There are... [Pg.1325]

Radiation therapy is the treatment of choice for chemotherapy-resistant tumors such as non-small cell lung cancer (NSCLC) or in chemotherapy-refractory patients with SVCS. Between 70% and 90% of patients will experience relief of symptoms. Radiation therapy also may be combined with chemotherapy for chemotherapy-sensitive tumors such as SCLC and lymphoma. In the rare emergency situations of airway obstruction or elevated intracranial pressure, empirical radiotherapy prior to tissue diagnosis should be used. In most patients, symptoms resolve within 1 to 3 weeks. [Pg.1475]

The histological types of lung cancer seen to excess in uranium miners reflect those in the population at large (Masse, 1984). These occur almost entirely in bronchial airways. Approximately 207 are adenocarcinomas which occur in peripheral bronchioles (Spencer, 1977) where there are no basal cells. Squamous cell cancers predominate in miners exposed early in life to relatively low concentrations of radon daughters (Saccomanno et aJL., 1982). These are considered likely to arise from the secretory small mucous granular cells which undergo cell division and extend to the epithelial surface (Masse, personal communication). Division of these cells is accelerated after irritation by toxicants such as cigarette smoke or infectious diseases (Trump et a L., 1978). [Pg.402]

It is reasonable to conclude that dose to cells throughout the bronchial tree may contribute to the risk of lung cancer and not just the dose received by certain cells in the large central airways. It is probably also appropriate to evaluate the dose absorbed by cells throughout the depth of bronchial epithelium, i.e. the mean dose,... [Pg.402]

One of the major toxicity issues in cannabis consumption relates to the fact that it is most often smoked. Cannabis and tobacco smoke, apart from having different psychoactive constituents, are actually very similar in their composition (Hoffman et ai. 1975). Cannabis smoke is mutagenic, which gives it carcinogenic potential (Nahas and Latour 1992). Although no specific reports of lung cancer or emphysema from cannabis smoke exist, it is at least as harmful as tobacco smoke, containing three times as much tar and five times as much carbon monoxide (Wu et al. 1988). Cannabis smoke inflames the airways and reduces respiratory capacity. Airway obstruction and squamous metaplasias may also occur. [Pg.437]

One hint of possible trouble to come is provided by the information we described in Chapter 4, related to airborne particulate matter (PM). The available evidence ascribes significant increases in the risks of asthma and other respiratory diseases, certain cardiovascular conditions, and lung cancer to PM exposure, particularly those that average less than 2.5 pm (2500 nm) in size. As we noted, the chemical composition of these particles varies widely, depending upon source, but may not be as important as particle size as a risk determinant. Moreover, there is some experimental evidence pointing to the so-called ultra-fines, PM with dimensions below 100 nm, as significant contributors to PM risk. In addition some experimental studies have demonstrated that ultrafines not only distribute themselves throughout the airways, but seem to be able to translocate to other parts of the body - liver, heart, perhaps the CNS. [Pg.268]

Smoking leads to respiratory problems other than lung cancer. It causes chronic bronchitis, emphysema, and lower resistance to flu and pneumonia. It worsens asthma symptoms in adults and children. As these problems persist, chronic obstructive pulmonary disease (COPD, airway obstruction) develops. Eighty to 85% of deaths due to COPD are from smoking. The role of nicotine in chronic lung diseases such as COPD, emphysema, and asthma is uncertain. However it is known that nicotine can cause an enzyme to be released which is able to destroy parts of the lungs as is seen in emphysema. [Pg.372]

The effects of these aerosols on human health have been widely studied. Inevitably, humans inhale aerosols during a normal day. Depending on the size and type of aerosol, this inhalation can have harmful effects on health. Asthma, lung cancer, and other diseases of the lungs and airways have been linked to the harmful inhalation of aerosols. [Pg.78]

Asbestosis, alveolar damage, diffuse pleural fibrosis, lung cancer Acute upper airway injury, tracheobronchitis, chemical pneumonitis, beryllosis Upper airway injury, pneumonitis Byssinosis... [Pg.249]

Comparative Toxicokinetics. Available data Ifom ehronic rat inhalation bioassays show similar asbestos-induced respiratory effects to those in humans assoeiated with oeeupational exposure to asbestos (pulmonary fibrosis, lung cancer, and pleural mesothelioma), but the use of the rat data to predict human health risks from exposure to airborne asbestos has a number of areas of uneertainty, including those associated with interspecies differences in lifespan, airway morphometry, and breathing patterns. The development of rat and human lung retention models that incorporate species differences in anatomical and physiological parameters influencing deposition and clearance of asbestos fibers may decrease the... [Pg.149]

Tissue-mediated induction of CYPl may be, at least partly, a factor in determining the target site of chemical carcinogenesis. Extensive studies in humans have established a good relationship between lung cancer and CYPlAl levels in the lungs of smokers [36,37], Interestingly, activation of polycyclic hydrocarbons by CYPIA appears to occur in the same part of the airways, and in the same cell types, as those in which carcinomas are encountered [37] ... [Pg.192]

G.J. Herder, R.H. Breuer, E.F. Comans, et al. (2001). Positron emission tomography scans can detect radiographically occult lung cancer in the central airways. J. Clin. Oncol, 19, 4271-4272. [Pg.175]

Lung diseases characterized by remodeling of the lung parenchyma or airway wall involve alterations in PGs. Changes in PGs have been best characterized in pulmonary fibrosis and, to a lesser extent, in asthma. Their roles in such diseases as emphysema, lung cancer, and ventilation-induced lung injury have not been as well defined. [Pg.119]


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See also in sourсe #XX -- [ Pg.385 , Pg.386 ]




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