Lung cancer fibrosis

Chronic Pulmonary Toxicity Chronic damage to the lungs may be due to several subsequent exposures or due to one large dose that markedly exceeds the capacity of pulmonary defense, clearance, and repair mechanisms. Chronic pulmonary toxicity includes emphysema, chronic bronchitis, asthma, lung fibrosis, and lung cancer. The single most important reason for chronic pulmonary toxicity is tobacco smoke, which induces all types of chronic pulmonary toxicity, with the exception of fibrosis. 

Inflammation and pulmonary fibrosis have been associated with an increased risk for lung cancer, thus justifying assessments ofgenotoxic events possibly accompanying CNT exposure. However, the results obtained to date are not consistent. 

Lomustine (CCNU) -nitrosourea alkylating agent cell cycle independent -bone marrow suppression (delayed, prolonged, and cumulative) -nausea and vomiting -pulmonary fibrosis Lung Cancer... 

Cigarette smoking is responsible for about 80% of lung cancer cases. Other risk factors include exposure to respiratory carcinogens (e.g., asbestos, benzene), genetic risk factors, and history of other lung diseases (e.g., tuberculosis, pulmonary fibrosis). 

Cohort and case control analyses of 1576 workers found no statistically significant associations between titanium dioxide exposure and risk of lung cancer, chronic respiratory disease, and chest roentgenogram abnormalities. No cases of pulmonary fibrosis were observed among titanium dioxide-exposed employees. 

Beryllium Ore extraction, ceramics, alloys Fibrosis, lung cancer... 

Pulmonary gene therapy is attractive for the treatmment of chronic bronchitis, cystic fibrosis, a-1 antitrypsin deficiency, familial emphysema, asthma, pulmonary infections, surfactant deficiency, pulmonary hypertension, lung cancer, and malignant mesothelioma. The pulmonary endothelium may act as a bioreactor for the production and secretion of therapeutic proteins, such as clotting factors and erythropoietin into the blood circulation. There is a potential benefit for acquired lung diseases, as well as cancers, to be controlled and possibly treated by expression of cytokines, surfactant, antioxidant enzymes, or mucoproteins within lung cells. 

While the respiratory system is well-equipped to defend against exposure to a vast array of toxic substances, the intricate cellular and molecular mechanisms designed to repair injured lung tissues often fail, resulting in a number of chronic lung diseases, including cancer, fibrosis, asthma, hypersensitivity pnuemonitis, and chronic obstructive pulmonary disease (COPD), which is a combination of bronchitis and emphysema. 

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

SAFETY PROFILE Iron dust can cause conjunctivitis, choroiditis, retinitis, and siderosis of tissues if iron contacts and remains in these tissues. Iron ore dust can cause palpebral conjunctivitis, massive pulmonary fibrosis, and an increased incidence of lung cancer. Questionable carcinogen with experimental neoplastigenic data. 

There is some evidence from animal studies that asbestos-induced lung cancer stems from regions in the lung with advanced fibrosis (asbestosis) however, lung cancer with chrysotile was also produced at fiber concentrations that did not lead to detectable fibrosis. 

The vast majority of experimental studies of asbestos have been performed in rodent model systems. Results from inhalation studies indicate that rats are suitable qualitative models for asbestos-induced pulmonary diseases, demonstrating chronic inflammation, pulmonary fibrosis (see Section 3.2.1.2), lung cancer (see Section 3.2.1.8), and mesothelioma (see Section 3.2.1.8) following chronic asbestos exposure. Hamsters seem to be more sensitive than rats to mesothelioma development, but less sensitive to the development of pulmonary tumors (Warheit and Hartsky 1994). 

As discussed in Section 3.2 and Chapter 2, numerous studies of occupationally-exposed adult workers identify respiratory effects including interstitial fibrosis, lung cancer, and pleural and/or peritoneal mesotheliomas, as critical health effects, of concern from exposure to airborne asbestos. T ically, these health effects follow chronic exposures and exhibit latencies of 10-40 years, although some cases of asbestosis and pleural plaques have been reported following subchronic exposure. 

In contrast to the interactive effect of smoking on lung cancer and fibrosis, smoking does not appear to increase the risk of mesothelioma (Berry et al. 1985 Hammond et al. 1979 Selikoff et al. 1980). 

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... 

Katjalainen A, Anttila S, Heikkila L. 1993b. Ix)be of origin of lung cancer among asbestos-exposed patients with or without diffuse interstitial fibrosis. Scand J Work Environ Health 19(4) 102-107. 

Can lung cancer be attributed to asbestos exposure (regardless of fiber type) in the absence ofpulmonary fibrosis ... 

Identification of the molecular and cellular responses leading to the progressive development of asbestos-induced lung cancer, mesothelioma, pulmonary fibrosis, and pleural thickening and effusion has been the subject of extensive research within the past two decades. Published reviews of this work include those by Begin et al. (1992), Kamp and Weitzman (1997, 1999), Kamp et al. (1992), Luster and Simeonova (1998), Mossman and Churg (1998), Mossman et al. (1983, 1996), Rom et al. (1991), and Tanaka et al. (1998). 

Exposure to tremolite asbestos or other forms of asbestos can increase risks for developing pleural plaques, pleural thickening (i.e. pleural fibrosis), pleural effusions, interstitial lung fibrosis, lung cancer, and mesothelioma. 

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