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

Since 1940, 760 cases of silicosis have been diagnosed as part of the State of North Carolina's (NC) pneumoconiosis surveillance program for dusty trades workers. Vital status was ascertained through 1983 for 714 cases that had been diagnosed since 1940 and death certificates were obtained for 546 of the 550 deceased. Mortality from tuberculosis, cancer of the intestine and lung, pneumonia, bronchitis, emphysema, asthma, pneumoconiosis, and kidney disease was significantly increased in whites. Mortality from tuberculosis, ischemic heart disease, and pneumoconiosis was significantly increased in non-whites. The standardized mortality ratio (95% CI) for lung cancer based on U.S. rates was 2.6 (1.8-3.6) in whites, 2.3 (1.5-3.4) in those who had no exposure to other known occupational carcinogens, and 2.4 (1.5-3.6) in those who had no other exposure and who had been diagnosed for silicosis while employed in the NC dusty trades. Age-adjusted lung cancer rates in silicotics who had no exposure to other known occupational carcinogens were 1.5 (.8-2.9) times higher than that in a referent group of coal miners with coalworkers' pneumoconiosis (CWP) and 2.4 (1.5-3.9) times higher than that in a referent group of non-silicotic metal miners. Age- and smoking-adjusted rates in silicotics were 3.9 (2.4-6.4) times higher than that in metal miners. This analysis effectively controls for confounding by age, cigarette smoking, and exposure to other known occupational carcinogens, and it is unlikely that other correlates of silica exposure could explain the excess lung cancer mortality in the silicotics.
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PMID:Silicosis and lung cancer in North Carolina dusty trades workers. 186 18

In an earlier case-referent study from a soft-paper mill with levels of paper dust exceeding 5 mg/m3, an increased mortality was found (OR = 3.8, p less than 0.05) from asthma and chronic obstructive pulmonary disease (COPD) among the employed. Furthermore, other studies on paper mill workers have also indicated an increased mortality from lung cancer. The main objectives of the present case-referent study were to investigate the mortality from asthma. COPD, and lung cancer in two other Swedish paper mills. In these mills, the levels of paper dust have been below 3 mg/m3. The subjects for the study were all men who died between 1961 and 1985 from asthma and COPD (n = 31), respiratory cancer (n = 27), and stomach cancer (n = 33) selected in three parishes surrounding two paper mills. As referents we randomly selected about six times as many men who had died from nonmalignant nonrespiratory diseases in these parishes (n = 550). On the basis of information found in the personnel records in the mills, the men were classified into different occupational categories or as unexposed. No increased risk of asthma or COPD was found among the workers exposed to paper dust. However, it was found that there was significantly increased mortality (OR = 5.7, p less than 0.05) for asthma and COPD among workers in a previous log sorting department. The study also showed a significantly increased risk of lung cancer (OR = 2.1, p less than 0.05) among maintenance workers. There was no increased risk of stomach cancer in the study.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mortality from asthma, chronic obstructive pulmonary disease, respiratory system cancer, and stomach cancer among paper mill workers: a case-referent study. 188 51

In a previous study conducted by mail questionnaire and with a large proportion of surrogate responders, we found differences in smoking habits, age at diagnosis, tumour cell type distribution and occupational exposures between men and women who developed primary lung cancer. This study was designed to confirm those findings by conducting personal case interviews and extend them by examining the impact of certain biological factors. We have investigated demographic, smoking, occupational and medical history sex differences in cases with primary lung cancer by interviewing 273 male and 103 female cases diagnosed between November 1983 and July 1986. The females were significantly younger at diagnosis, a pattern consistent for all cell types. Squamous cell (40%), small cell anaplastic (20%) and adenocarcinomas (16%) were the most prevalent cell types in men. In women, similar frequencies of adenocarcinomas (32%) and squamous cell carcinomas (29%) occurred. Despite a higher prevalence of physician diagnosed allergy and asthma among women, minimal sex differences in the prevalence of atopy as measured by prick skin test were found. Female cases were more likely to be lifetime non-smokers (15% vs 3%), to have started smoking on average 3 years older and to smoke 6 fewer cigarettes per day. The mean pack years of female cases was significantly lower than males' for squamous, adenocarcinoma and small cell anaplastic tumours. The majority of these women had not been occupationally exposed to any substance known to be carcinogenic or to damage the lung. However, in a small subset of cases pulmonary function variables were as depressed in women as in men with significantly higher mean pack years.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Men, women and primary lung cancer--a Saskatchewan personal interview study. 203 58

Long term passive exposure to tobacco smoke can be a cause of disease in sensitive non smokers, particularly in children of smoking mothers, who may suffer more frequently from respiratory tract infection, otitis media and chronic cough as well as exacerbation of pre-existent asthma. In adults, the relationship is less obvious. A slight but significant alteration of lung function has been observed. The increase in the incidence of lung cancer in non-smoking spouses (men and women) of smokers can be regarded as proven.
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PMID:[Passive smoking]. 204 28

This study was conducted to investigate the adverse health effects of exposure to bitumen fumes. A cohort of 679 mastic asphalt workers was followed from 1959 to 10 June 1986, during this period 169 deaths occurred. The overall standardized mortality ratio (SMR) was 163 (95% confidence interval (95% CI) 141-190), the SMR was 225 (95% CI 172-288) for cancer and 223 (95% CI 130-358) for external causes. Among persons aged 40 to 89 years, significant increases were seen for lung cancer (SMR 290, 95% CI 188-429), nonpulmonary cancer (SMR 200, 95% CI 141-276), and liver cirrhosis (SMR 467, 95% CI 188-962). Bronchitis, emphysema, and asthma also occurred in excess (SMR 207, 95% CI 95-393). In conclusion, the inhalation of bitumen fumes may have contributed to the elevated mortality from cancer and respiratory diseases among mastic asphalt workers.
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PMID:Mortality of mastic asphalt workers. 160 75

The authors report the results of a non-randomised study comparing the efficacy (in terms of confirmation of the diagnosis, the extent of disease, and measurements of airflow obstruction, and of the therapeutic index), and the efficiency in 58 patients suffering from lung cancer as well as 62 patients suffering from chronic airflow obstruction, and 42 asthmatics. These patients were seen in one of three possible services of a respiratory medicine department of a university hospital. The possibilities were inpatient stay in hospital, day hospital, or outpatient consultation. All the patients except one were totally independent, and could be taken into anyone of the three hospital services. The diagnostic efficacy for lung cancer was independent of the type of service used. The day hospital was four times more efficient than inpatient care for lung cancer, and consultation was 3.5 and 4.6 times more efficient than the day hospital for asthma and chronic airflow obstruction respectively. The balance of efficiency and the index of satisfaction experienced by the patients on the service used accentuated these differences.
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PMID:[Cost effectiveness of inpatient hospital care, day hospital care and outpatient consultation in pneumology. Apropos of 162 patients]. 211 45

Fifty nine scientific papers had been published in english or french literature, by 1988, on the matter of respiratory health effects of environmental tobacco smoke exposure (ETS). Fifteen dealt with lung cancer. An original meta-analytical approach was used in order to assess the consistency of these results, where the quality of the papers contributes to the weighing scheme, along with the traditional precision parameters. Lung cancer studies converge towards a point estimate of the relative risk (RR) near 1.5, contrasting non smokers exposed during a long time to ETS (mostly at home) and non exposed non smokers (95% confidence interval = 1.3-1.6). Important methodological difficulties did not allow, to date, to show consistent dose-effect relationship with duration or intensity of exposure. Chronic infections of lower respiratory tract related to ETS have been frequently observed (RR = 1.3; 1.2-1.4) as well among adults as among children. Wheezing and asthma are likewise more frequent among children exposed to ETS at home (RR = 1.2; 1.1-1.4). A modest, although statistically significant decrease of Forced Expiratory Volume at One Second is associated with passive smoking among children (mean effect = -0.5%). Health risk related to passive smoking are much lower than those caused by active smoking. However, this hazard should not be underlooked, since ETS is universally present in everyday life and since anyone may be exposed, including children, the elderly and those who suffer from chronic respiratory diseases. Many research needs are underscored by this meta-analysis. It remains that the current state of knowledge on health risks associated with passive smoking warrants that strong preventive action, educative or statutory, be promoted.
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PMID:[Passive smoking respiratory risk. A quantitative synthesis of the literature]. 214 55

The type of lung disease caused by metal compounds depends on the nature of the offending agent, its physicochemical form, the dose, exposure conditions and host factors. The fumes or gaseous forms of several metals, e.g. cadmium (Cd), manganese (Mn), mercury (Hg), nickel carbonyl (Nl(CO)4, zinc chloride (ZnCl2), vanadium pentoxide (V2O5), may lead to acute chemical pneumonitis and pulmonary oedema or to acute tracheobronchitis. Metal fume fever, which may follow the inhalation of metal fumes e.g. zinc (Zn), copper (Cu) and many others, is a poorly understood influenza-like reaction, accompanied by an acute self-limiting neutrophil alveolitis. Chronic obstructive lung disease may result from occupational exposure to mineral dusts, including probably some metallic dusts, or from jobs involving the working of metal compounds, such as welding. Exposure to cadmium may lead to emphysema. Bronchial asthma may be caused by complex platinum salts, nickel, chromium or cobalt, presumably on the basis of allergic sensitization. The cause of asthma in aluminium workers is unknown. It is remarkable that asthma induced by nickel (Ni) or chromium (Cr) is apparently infrequent, considering their potency and frequent involvement as dermal sensitizers. Metallic dusts deposited in the lung may give rise to pulmonary fibrosis and functional impairment, depending on the fibrogenic potential of the agent and on poorly understood host factors. Inhalation of iron compounds causes siderosis, a pneumoconiosis with little or no fibrosis. Hard metal lung disease is a fibrosis characterized by desquamative and giant cell interstitial pneumonitis and is probably caused by cobalt, since a similar disease has been observed in workers exposed to cobalt in the absence of tungsten carbide. Chronic beryllium disease is a fibrosis with sarcoid-like epitheloid granulomas and is presumably due to a cell-mediated immune response to beryllium. Such a mechanism may be responsible for the pulmonary fibrosis occasionally found in subjects exposed to other metals e.g. aluminium (Al), titanium (Ti), rare earths. The proportion of lung cancer attributable to occupation is around 15%, with exposure to metals being frequently incriminated. Underground mining of e.g. uranium or iron is associated with a high incidence of lung cancer, as a result of exposure to radon. At least some forms of arsenic, chromium and nickel are well established lung carcinogens in humans. There is also evidence for increased lung cancer mortality in cadmium workers and in iron or steel workers.
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PMID:Metal toxicity and the respiratory tract. 217 66

Although much of the evidence in environmental lung disease remains equivocal, some environmental exposures are known to be clinically relevant. Ambient air pollution remains of concern as a source of morbidity, particularly for susceptible populations such as persons with asthma, chronic obstructive pulmonary disease, or cardiac disease and the elderly. The adverse effects of several components of indoor air pollution have been established. Environmental tobacco smoke contributes to lower-respiratory illness in infants; office workers exposed to thermophilic actinomycetes contaminating ventilation systems have developed hypersensitivity pneumonitis; and in the home, components of house dust and fungus spores may provoke asthma via immediate hypersensitivity. The evidence is less compelling for a link between other exposures and disorders of the respiratory tract. For example, formaldehyde may be responsible for provoking vague respiratory symptoms and even nasal cancers; however, the associations are unproved. Likewise, the relation between low-level exposure to asbestos and the development of lung cancer, although a concern, is not conclusively established. The clinician should be aware of practical measures for patients who inquire about air cleaning. Often, relatively simple solutions are effective. A knowledge of sources and exposures as well as an understanding of the principles of inhalation lung injury should prove useful in directing patient care.
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PMID:Environmentally mediated disorders of the respiratory tract. 218 Dec 9

Cobalt metal and cobalt compounds are extensively used for the production of high-temperature alloys, diamond tools, cemented carbides and hard metals, for the production of various salts used in electroplating and as catalysts, drying agents in paints, additives in animal feeds and pigments. Cobalt oxides are used not only in the enameling industry and for pigments, but also in catalytic applications. There is no indication that cobalt metal and cobalt compounds constitute a health risk for the general population. Allergic reactions (asthma, contact dermatitis) can be induced by certain cobalt compounds. Interstitial fibrosis has also been observed in workers exposed to high concentrations of dust containing cobalt, tungsten, iron, etc., mainly in the cemented carbides and the diamond-polishing industries. Several experiments have demonstrated that single or repeated injections of cobalt metal powder or some forms of cobalt salt and cobalt oxide may give rise to injection site sarcoma in rats and in rabbits but the human health significance of such data is questionable. Intratracheal administration of a high dose of one type of cobalt oxide induces lung tumors in rats but not in hamsters. In the latter long-term inhalation of cobalt oxide (10 mg/m3) did not increase the incidence of lung cancer. The human data are too limited to assess the potential carcinogenic risk for workers. Co2+ interacts with protein and nucleic acid synthesis and displays only weak mutagenic activity in microorganisms. Some cobalt salts have been reported to enhance morphological transformation of Syrian hamster embryo cells. Cobalt chloride displays some limited mutagenic activity in yeast and some cobalt compounds are able to produce numerical and structural chromosome aberrations in plant cells. Cobalt and its salts appear to be devoid of mutagenic and clastogenic activity in mammalian cells. Cobaltous acetate and cobaltous chloride have not been found to be teratogenic in hamsters and rats respectively.
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PMID:Mutagenicity, carcinogenicity and teratogenicity of cobalt metal and cobalt compounds. 219 31


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