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

A job-exposure matrix has been applied in a case-control study of lung and bladder cancer on the basis of occupational information abstracted from British death certificates. The expected association between lung cancer and jobs entailing exposure to asbestos was clearly demonstrated (relative risk, 1.5; 95% confidence interval, 1.2-1.9). The effects of three other known industrial carcinogens were not apparent, and reasons for this were discussed. Also included in the matrix were five substances whose carcinogenicity in humans has not been established. Formaldehyde, diesel fumes, and cutting oils were all associated with carcinoma of the bronchus, but the absence of a risk in "high-exposure" occupations was against a causal relationship. Bladder cancer was more common in jobs involving high exposure to printing inks (relative risk, 5.0; 95% confidence interval, 1.0-25.8) and cutting oils (relative risk, 1.5; 95% confidence interval, 0.8-2.8). Use of the job-exposure matrix added considerably to the conventional analysis of cancer risk in individual occupational categories.
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PMID:Use of job-exposure matrix in an occupational analysis of lung and bladder cancers on the basis of death certificates. 636 90

Membership lists of the Royal College of Pathologists from 1974 to 1980 were used to establish a population of 2307 men and 413 women. During the period of study 126 of these pathologists died and death certificates were obtained for 121. The standardised mortality ratios (SMR) for all causes in men were 56 and in women 99. Deaths from accidents, poisoning, violence, and especially suicide, were noted to be in excess of that expected from the general population but similar to that for medical practitioners. Drug overdose was the cause of each suicide. Excess deaths from lymphatic and haemopoietic neoplasms noted in a previous study were not present but an excess of brain tumours was found. Including 1981 data thus far collected, deaths from brain tumour were apparently in excess (observed 6, expected less than 2.0, p less than 0.02). Possible aetiological hypotheses include previous exposure to organic solvents or tuberculosis infection. In view of the pathologists' exposure to formaldehyde it is interesting to note that no nasal or nasal sinus tumours were reported and the SMR for lung cancer was 41.
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PMID:Mortality study of British pathologists 1974-80. 672 45

Formaldehyde, a genotoxic and potent animal carcinogen, is widespread in the working environment as well as in private homes. The risk for cancer morbidity in Denmark during 1970-84 was estimated from standardized proportionate incidence ratios (SPIR) among men whose longest employment had been held since 1964, at least 10 years before diagnosis, in 265 companies in which exposure to formaldehyde was identified. The results do not support the hypothesis that formaldehyde is associated with lung cancer (SPIR = 1.0, 410 cases). Significantly elevated risks were found for cancers of the colon (SPIR = 1.2, 166 cases), kidney (SPIR = 1.3, 60 cases), and sino-nasal cavities (SPIR = 2.3, 13 cases). For sino-nasal cancer, a relative risk of 3.0 (95 percent confidence interval = 1.4-5.7) was found among blue-collar workers with no probable exposure to wood dust, the major confounder. This study provides further evidence that occupational exposure to formaldehyde increases the risk for sino-nasal cancer.
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PMID:Formaldehyde and cancer morbidity among male employees in Denmark. 754 23

In the final phase of the mortality study of workers at an automotive iron foundry, a subset (N = 3929) of the original cohort of 8147 men, consisting of those exposed to formaldehyde during the period from January 1960 through May 1987, was analyzed. In addition to the external US population, an internal population (N = 2032), consisting of men who had worked in the same foundry during the same time period but not in formaldehyde-exposed jobs, was also used as a referent. Follow-up continued through December 31, 1989. Smoking status was ascertained for 65.4% of the exposed and for 55.1% of the unexposed cohorts. Detailed work histories and evaluation of occupational exposures by an industrial hygienist enabled us to categorize cumulative formaldehyde and silica exposures. Standardized mortality ratios were used to compare the mortality experience of the exposed cohort with the US population and, because of concerns about the healthy worker effect, with an occupational referent population. Relative risks for race, formaldehyde exposure status, smoking status, and silica exposure level were estimated by fitting a Poisson regression model to four causes of death: cancers of the buccal cavity and pharynx, lung cancer, diseases of the respiratory system, and emphysema. No association between formaldehyde exposure and deaths from malignant or nonmalignant diseases of the respiratory system was found. Cigarette smoking and silica exposure were found to be significantly associated with deaths attributed to lung cancer and disease of the respiratory system.
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PMID:Mortality of iron foundry workers: IV. Analysis of a subcohort exposed to formaldehyde. 755 67

A nested case-control study was undertaken to identify the determinants of lung cancer mortality in a cohort of 8147 foundry men among whom an excess of lung cancer deaths was previously observed. The present study consisted of all lung cancer deaths (N = 220) that occurred within this cohort between 1950 and 1989. both living and dead controls, matched on race and attained age, were selected in the ratio of 10:1 (N = 2200) by means of the incidence density sampling procedure. All cases and two controls per case, randomly selected from each case's 10 controls, were included in a smoking history survey. Basic smoking history information was obtained for about 71% of these study subjects. For the purpose of this study, formaldehyde exposure levels were categorized as high, medium, low, and none. Airborne silica exposure was categorized only as high, medium, and low levels, because all foundry workers were known to be exposed to silica. Conditional logistic regression analyses indicated that cigarette smoking was a strong predictor of lung cancer mortality in this cohort. Neither exposure to formaldehyde nor silica exposure level, nor employment in any of the six major work areas within the foundry, showed an association with lung cancer.
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PMID:Mortality of iron foundry workers. III. Lung cancer case-control study. 788 71

A joint study on effects of formaldehyde exposure in industrial populations by the National Cancer Institute and the Formaldehyde Institute, Inc. (Blair et al. [1986]: J Natl Cancer Inst 76: 1071-1084; Blair and Stewart [1989]: J Occup Med 31: 881, Blair et al. [1990]: Am J Ind Med 17:683-700) reported no significant elevation in risk ratios standardized to the general population. Using the same data as Blair et al., we compared more exposed to less exposed workers to compute relative risk for respiratory and lung cancers using a multivariate, log-linear model incorporating factors for job type (hourly vs. salaried), cumulative exposure (0.1-0.5, 0.5-2, 2+ vs. < 0.1 ppm/years), length of exposure (1-5, 5-10, 10+ vs. < 1 years), and age. Models were fit for all workers, all males, all workers less than 65 years of age, and for all males less than 65 years of age. Hourly workers have a significantly elevated relative risk when compared to salaried workers. While only high levels of cumulative exposure show a significant elevation in relative lung cancer risk, trend analyses of the coefficients of a log-linear model show a significant trend of increasing risk with increasing formaldehyde exposure. The significantly elevated respiratory and lung cancer risk for workers younger than 65 may indicate a shift of respiratory cancer mortality towards younger ages among those occupationally exposed to formaldehyde.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mortality from respiratory cancers (including lung cancer) among workers employed in formaldehyde industries. 775 19

K-ras gene point mutation is a highly frequent event in human malignancy. About one third of non-small cell lung cancer (NSCLC) patients harbor K-ras gene point mutational activations. This study investigates the prevalence of K-ras mutation in autopsy tumors with NSCLC, and the correlation of K-ras gene point mutations between primary tumors and metastases in NSCLC. Formalin-fixed, paraffin-embedded tissue sections of 15 primary lung tumors and their metastases, (obtained from autopsy), were examined for the presence of point mutations in K-ras gene codon 12, 13 and 61 by oligodeoxynucleotide hybridization analysis of DNA fragments, amplified by polymerase chain reaction (PCR). K-ras gene point mutations were detected in five cases of lung carcinoma, of which four were adenocarcinomas and one was squamous cell carcinoma. In each of these cases, identical K-ras gene mutations were found in the DNA of both the primary tumor and its corresponding distant metastases. Activating K-ras base-substitutions correlate well between the primary tumor and its corresponding metastases in NSCLC. In the negative cases where no K-ras mutation was found in the primary tumors, no newly acquired K-ras mutation appeared in the metastases. Our study indicates that K-ras point mutation serves as a stable tumor marker in NSCLC.
Lung Cancer 1994 Jul
PMID:K-ras gene point mutation: a stable tumor marker in non-small cell lung carcinoma. 808 2

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

A case-control study of malignant and non-malignant respiratory disease among employees of the Owens-Corning Fiberglas Corporation's Newark, Ohio plant was undertaken. The aim was to determine the extent to which exposures to substances in the Newark plant environment, to non-workplace factors, or to a combination may play a part in the risk of mortality from respiratory disease among workers in this plant. A historical environmental reconstruction of the plant was undertaken to characterise the exposure profile for workers in this plant from its beginnings in 1934 to the end of 1987. The exposure profile provided estimates of cumulative exposure to respirable fibres, fine fibres, asbestos, talc, formaldehyde, silica, and asphalt fumes. Employment histories from Owens-Corning Fiberglas provided information on employment characteristics (duration of employment, year of hire, age at first hire) and an interview survey obtained information on demographic characteristics (birthdate, race, education, marital state, parent's ethnic background, and place of birth), lifetime residence, occupational and smoking histories, hobbies, and personal and family medical history. Matched, unadjusted odds ratios (ORs) were used to assess the association between lung cancer or non-malignant respiratory disease and the cumulative exposure history, demographic characteristics, and employment variables. Only the smoking variables and employment characteristics (year of hire and age at first hire) were statistically significant for lung cancer. For non-malignant respiratory disease, only the smoking variables were statistically significant in the univariate analysis. Of the variables entered into a conditional logistic regression model for lung cancer, only smoking (smoked for six months or more v never smoked: OR = 26.17, 95% confidence interval (95% CI) 3.316-206.5) and age at first hire (35 and over v less than 35: OR = 0.244, 95% CI 0.083-0.717) were statistically significant. There were, however, increased ORs for year of employment (first hired before 1945 v first hire after 1945: OR = 1.944, 95% CI 0.850-4.445), talc (cumulative exposure >1000 fibres/ml days v never exposed: OR = 1.355, 95% CI 0.407-5.515), and asphalt fumes (cumulative exposure >0.01 mg/m(3) days v never exposed: OR 1.131, 95% CI 0.468-2.730). For non-malignant respiratory disease, only the smoking variable was significant in the conditional logistic regression analysis (OR = 2.637, 95% CI 1.146-6.069). There were raised ORs for the higher cumulative exposure categories for respirable fibres, asbestos, silica, and asphalt fumes. For both silica and asphalt fumes, ORs were more than double the reference groups for all exposure categories. A limited number of subjects were exposed to fine fibres. The scarcity of cases and controls limits the extent to which analyses for fine fibre may be carried out. Within those limitations, among those who had worked with fine fibre, the unadjusted, unmatched OR for lung cancer was (1.0 (95% CI 0.229-4.373) and for non-malignant respiratory disease, the OR was 1.5 (95% CI 0.336-6.702). The unadjusted OR for lung cancer for exposure to fine fibre was consistent with that for all respirable fibre and does not suggest an association. For non-malignant respiratory disease, the unadjusted OR for fine fibre was opposite in direction from that for all respirable fibres. Within the limitations of the available data on fibre, there is o suggestion that exposure to fine fibre has resulted in an increase in risk of lung cancer. The increased OR for non-malignant respiratory disease is inconclusive. The results of this population, in this place and time, neither respirable fibres nor any of the substances investigated as part of the plant environment are statistically significant factors for lung cancer risk although there are increased ORs for exposure to talc and asphalt fumes. Smoking is the most important factors in risk for lung cancer in this population. The situation is less clear for non-malignant respiratory disease. Unlike lung cancer, non-malignant respiratory represents a constellation of outcomes and not a single well defined end point. Although smoking was the only statistically significant factor for non-malignant respiratory disease in this analysis, the ORs for respirable fibres, asbestos, silica, and asphalt fumes were greater than unity for the highest exposure categories. Although the raised ORs for these substances may represent the results of a random process, they may be suggestive of an increased risk and require further investigation.
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PMID:A case-control study of malignant and non-malignant respiratory disease among employees of a fiberglass manufacturing facility. II. Exposure assessment. 839 58

A cohort study of workers exposed to formaldehyde in the British chemical industry in any one of six factories has been extended after the earlier published report in 1984. A further eight years of follow up to the end of 1989 have been included for the originally reported 7660 workers first employed before 1965, and a first follow up to the same date has been carried out for 6357 workers first employed since 1964. Extensive checking of the database has taken place including records at the factories, the MRC Environmental Epidemiology Unit, and the National Health Service Central Register. The updated findings include one death from nasal cancer compared with 1.7 expected in this number of men during the follow up period--which gives no support to the original hypothesis based on animal experimental data that formaldehyde may be a nasal carcinogen in humans. There have been no cases of nasopharyngeal cancer in the cohort compared with an estimated 1.3 expected--which gives no support to the findings in a similarly designed study in the United States of an excess of cancers of the nasopharynx associated with exposure to formaldehyde. There has been a slight excess of about 12% for lung cancer with 402 deaths compared with about 359 expected. This is similar to that found in the United States study, but higher than we reported earlier before the checking procedures and extended follow up. Further analysis gives no definitive indication of this excess of lung cancer being clearly related to formaldehyde exposure, and the increase is within that generally thought consistent with possible confounding effects of cigarette smoking (although no data are available on this point).
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PMID:A cohort study of workers exposed to formaldehyde in the British chemical industry: an update. 839 77


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