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

The patterns of mortality are described for 35,000 male employees, with a minimum of 1 year's continuous service, who worked at 8 refineries in the U. K. in the period 1 January 1950-31 December 1975. The trace rate of those involved was 99.8%. Overall the ratio of observed to expected deaths was 0.84 (O = 4406, E = 5259.9 P less than 0.00001). The numbers of deaths for many of the chronic degenerative diseases were lower than "expected." The number of observed deaths from all cancers were appreciably less than expected (O = 1147, E = 1286.4, O/E = 0.89, P = 0.00006). Lung cancer was particularly reduced (O = 416, E = 532.7, O/E = 0.78, P less than 0.00001); there was no excess of leukemia ( in workers including some exposed to benzene). Other comparable studies have suggested an excess of gastrointestinal cancer. In the present study deaths from esophageal, stomach, intestinal, and rectal cancer were slightly raised for all workers (O = 346, E = 328.6, O/E = 1.05, P less than 0.4); this was particularly true for those joining before 1950 with long service and increased latent interval. There were also excesses based on small numbers of deaths from nasal cancer (O = 7, E = 3.1, O/E = 2.24, P less than 0.05), and melanoma (O = 14, E = 6.5, O/E = 2.16, P less than 0.01). There was no evidence of an excess of brain tumors (O = 36, E =- 44.8, O/E = 0.80, P less than 0.2).
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PMID:Mortality patterns in eight U. K. oil refineries. 695 84

An overview of published information on occupational cancer and recorded ongoing occupational cancer research in developing countries is presented. The main cancers reported, of possible occupational origin, are skin carcinoma, leukemia due to exposure to benzene, asbestos-caused mesothelioma, vinyl chloride-induced hepatic angiosarcoma, carcinoma of bilharzial urinary bladder, stomach cancer reportedly associated with nitrogen fertilizers, lung cancer of nickel smelters, and nasopharyngeal and pulmonary carcinoma in workers exposed to the dust of hard wood. The difficulties of developing efficient occupational cancer prevention are discussed. Some options are analyzed regarding legislative, technological, environmental, medical, administrative, and educational cancer control applicable under conditions of developing countries.
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PMID:Problems of occupational carcinogenesis in developing countries. 734 83

As part of a program to determine the underlying factors responsible for genotoxicity and perhaps lung cancer risk in Chinese women, we qualitatively identified the volatile components emitted during the heating of cooking oils to 265 degrees C. 1,3-Butadiene, benzene, and a series of aldehydes, olefins, and saturated hydrocarbons were elucidated in vapors from Chinese rapeseed oil. On a relative basis, the intensity of 1,3-butadiene vapors from this were 15.7-, 6.3-, and 1.4-fold greater than in the vapors from peanut, soybean, and Canola oils, respectively. Thus, the Chinese rapeseed oil yielded a higher emission rate of 1,3-butadiene than the other three oils investigated. The benzene formation rate followed a similar trend, i.e., its intensity in Chinese rapeseed oil was 14-, 6.6-, and 1.7-fold greater than in vapors from peanut, soybean, and Canola oils, respectively.
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PMID:Identification of 1,3-butadiene, benzene, and other volatile organics from wok oil emissions. 766 51

Risk assessment models strive to predict risks to humans from toxic agents. Safety factors and assumptions are incorporated into these models to allow a margin of error. In the case of cancer, substantial evidence shows that the carcinogenic process is a multistage process driven by the interaction of exogenous carcinogenic exposures, genetic traits, and other endogenous factors. Current risk assessment models fail to consider genetic predispositions that make people more sensitive or resistant to exogenous exposures and endogenous processes. Several cytochrome P450 enzymes, responsible for metabolically activating carcinogens and medications, express wide interindividual variation whose genetic coding has now been identified as polymorphic and linked to cancer risk. For example, a restriction fragment-length polymorphism for cytochrome P4501A1, which metabolizes polycyclic aromatic hydrocarbons, and cytochrome P4502E1, which metabolizes N-nitrosamines and benzene, is linked to lung cancer risk. Cytochrome P4502D6, responsible for metabolizing many clinically important medications, also is linked to lung cancer risk. The frequency for each of these genetic polymorphisms vary among different ethnic and racial groups. In addition to inherited factors for the detection of sensitive populations, determining the biologically effective doses for carcinogenic exposures also should quantitatively and qualitatively enhance the risk assessment process. Levels of carcinogen-DNA adducts reflect the net effect of exposure, absorption, metabolic activation, detoxification, and DNA repair. These effects are genetically predetermined, inducibility notwithstanding. The combination of adduct and genotyping assays provide an assessment of risk that reflects recent exogenous exposure as well as one's lifetime ability to activate and detoxify carcinogens.
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PMID:Pharmacogenetics: detecting sensitive populations. 773 47

To address earlier reports of excess cancer mortality associated with employment at a large transformer manufacturing plant, each plant operation was rated for seven exposures: Pyranol (a mixture of polychlorinated biphenyls and trichlorobenzene), trichloroethylene, benzene, mixed solvents, asbestos, synthetic resins, and machining fluids. Site-specific cancer deaths among active or retired employees were cases; controls were selected from deaths (primarily cardiovascular deaths) presumed to be unassociated with any of the study exposures. Using job records, we then computed person-years of exposure for each subject. All subjects were white males. The only unequivocal association was that of resin systems with lung cancer (odds ratio = 2.2 at 16.6 years of exposure, P = 0.001, in a multiple logistic regression including asbestos, age, year of death, and year of hire). Certain other odds ratios appeared larger, but no other association was so robust and remained as distinct after considering the multiplicity of comparisons. Study power was very limited for most associations, and several biases may have affected our results. Nevertheless, further investigation of synthetic resin systems of the type used in the study plant appears warranted.
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PMID:A case-control study of cancer mortality at a transformer-assembly facility. 792 43

Human cytochrome P4502E1 (CYP2E1) is inducible by ethanol and is involved in metabolism of many known carcinogens including N-nitrosodimethylamine, butadiene, benzene, and carbon tetrachloride. A 50-fold variability in CYP2E1 enzyme activity in humans has been observed but it is unknown whether the basis for this variation is genetic or environmental. Recently, two restriction fragment length polymorphisms (RFLPs) within the CYP2E1 gene have been suggested as genetic markers of risk for cancer. The first was a Rsa I polymorphism in the 5' regulatory region that appeared to alter transcriptional activation of the gene and the second was a Dra I polymorphism located approximately 7000 bp downstream in an intron. Rare alleles at each of these loci have been associated with a reduced risk for lung cancer in Japanese and Swedish populations. We have used a polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method to determine the genotype frequency for each of these CYP2E1 RFLPs in 695 individuals of Taiwanese, African-American or European-American background. Genotype and allele frequencies for Taiwanese were significantly different from those of African-Americans and European-Americans at either Rsa I or Dra I sites (p < 0.0001). Allele frequencies for African-Americans and European-Americans were significantly different at the Rsa I site (p = 0.03). The rare alleles (c2 and C) occurred at frequencies of 0.28 and 0.24 in Taiwanese, 0.01 and 0.08 in African-Americans, and 0.04 and 0.11 in European-Americans. In addition, we describe three haplotypes common to all three population samples and a fourth haplotype that was only detected in the Taiwanese population sample. This fourth haplotype may have been caused by a recombination event between these markers.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ethnic variation in the CYP2E1 gene: polymorphism analysis of 695 African-Americans, European-Americans and Taiwanese. 798 2

The authors report the results of a case-cohort study of 338 lung cancer deaths in 1950-1988 and a random sample (sub-cohort) of 1,138 from among 16,297 men who had worked at least one year between 1950 and 1979 in manual jobs at a large aluminum production plant. In the past, certain workers were exposed to substantial quantities of coal tar pitch volatiles, a mixture known to include polynuclear (polycyclic) aromatic hydrocarbons, and thus suspected to be capable of causing lung cancer. After they controlled for the effects of smoking, the authors found that rate ratios rose with cumulative exposure to coal tar pitch volatiles measured as benzene-soluble material to 2.25 (95% confidence interval (CI) 1.50-3.38) at 10-19 mg/m3-years benzene-soluble matter, but did not rise further at higher exposures. The data are compatible with a linear relation with benzene-soluble matter (rate ratio (RR) = 1 + 0.031 mg/m3-years benzene-soluble matter). This model predicts a rate ratio of 1.25, and lifelong excess risk of 2.2%, after 40 years exposure at the current hygiene standard (0.2 mg/m3). A curved relation (RR = 1 + 0.098 mg/m3-years benzene-soluble matter 0.7) fitted somewhat better. Under this model, the predicted risks after this exposure are higher: 1.42 and 3.8%. The data are compatible with both additive and multiplicative models for the combined effect of smoking and coal tar pitch volatiles.
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PMID:Lung cancer mortality and polynuclear aromatic hydrocarbons: a case-cohort study of aluminum production workers in Arvida, Quebec, Canada. 811

The background of regulatory limit values for carcinogenic agents in Sweden is discussed and exemplified with the ambient and occupational air pollutants benzene and PAH (especially benzo[a]pyrene, BaP), ionizing radiation, and radon. The estimated cancer risks at different limit values are compared, as is the estimated number of cancer cases annually due to existing pollutant levels. Although the individual lifetime cancer risks are much higher at the occupational limit values for benzene and BaP than what is recommended for the general public, the estimated number of cancer cases annually is lower at existing pollutant levels. The individual cancer risk at the occupational dose limit for ionizing radiation is comparable to the occupational cancer risk with BaP, but higher than the one for benzene. At the dose limit for the general public, the radiation risk would be higher than what is recommended for individual air pollutants. However, doses from man-made radiation are usually much lower than the dose limit due to optimization. Thus, the estimated number of cancer cases annually due to radiation is low and comparable to the estimated number due to the chemical air pollutants discussed. In contrast, the lung cancer risk with radon in dwellings both at limit values and existing levels is high and comparable to occupational limits for the chemical carcinogens and for radiation. The estimated number of cancer cases annually at existing radon concentrations (1100 cases) is much higher than for the other discussed pollutants (0.03-7 cases each) and also higher than the estimated number of lung cancer cases due to total air pollution (approximately 100 cases).
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PMID:Risk comparisons between limit values for ionizing radiation, PAH, and benzene in Sweden. 812

A retrospective cohort mortality study was conducted among 7814 white shoe manufacturing workers followed from 1940 through 1982. The workers were potentially exposed to solvents (including toluene) and solvent-based adhesives. Benzene may have been present as an impurity of toluene. Mortality due to leukemia and aleukemia was not statistically significantly elevated. Statistically significant excess mortality due to cancer of the trachea, bronchus and lung was observed in the total cohort [standardized mortality ratio (SMR) 147, 95% confidence interval (95% CI) 120-180] and showed a statistically significant trend in standardized relative risk with increasing potential latency, but not with increasing duration of employment. Chronic nonmalignant respiratory disease was significantly elevated among the men (SMR 158, 95% CI 114-217) but was less than expected among the women (SMR 79), a finding suggesting a possible contribution of smoking to the mortality from respiratory cancer. However, adjustment for the potential effects of smoking did not completely eliminate the increased risk for lung cancer.
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PMID:Mortality of workers employed in shoe manufacturing. 831 84

This paper summarizes what is known about preventable causes of occupational cancer, including single agents, complex mixtures, and broad occupational associations. Epidemiologic methods have been very successful in documenting cancer risks associated with single agents. Epidemiologic data are most conclusive when an exposure-response relationship can be demonstrated. Examples of agents for which epidemiologic studies provide evidence of an exposure-response relationship include benzene and (concurrent exposure to) ortho-toluidine and aniline. Vinyl chloride and bischloromethyl ether are examples of associations between single agents and rare histologic types of cancer. It is more difficult to conduct epidemiologic studies to identify cancer risks associated with complex mixtures. Studies of diesel exhaust and lung cancer and metal machining oils are cited as having employed advanced industrial hygiene and epidemiologic methods for studies of complex mixtures. Elevated cancer risks have also been identified in broad occupational groups, including painters and dry cleaners. Epidemiologic case-control studies are often used to detect such associations but are limited in their abilities to detect the causal agents. Major gaps exist in knowledge of occupational cancer risks among women workers and workers of color. Because epidemiologic research measures illness and mortality that have already occurred, a positive study can be interpreted to represent a failure in prevention. The challenge we face in the next decade is to identify interventions earlier in the causal pathway (toxicologic testing, biomarkers of exposure or precancerous changes, institution of engineering and good industrial hygiene practices to reduce occupational exposure levels) so that occupational cancer can be prevented.
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PMID:Overview of preventable industrial causes of occupational cancer. 874 83


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