Odds Ratio For Lung Cancer Research Articles

Lung cancer after Hodgkin's disease: a nested case-control study of the relation to treatment.

To investigate the causes of the raised risk of lung cancer in patients who have had Hodgkin's disease, and in particular the relationship to treatment. A nested case-control study was conducted within a cohort of 5,519 patients with Hodgkin's disease treated in Britain during 1963 through 1993. For 88 cases of lung cancer and 176 matched control subjects, information on treatment and other risk factors was extracted from hospital case-notes, and odds ratios for lung cancer in relation to these factors were calculated. Risk of lung cancer was borderline significantly greater in patients treated with mechlorethamine, vincristine, procarbazine, and prednisone (MOPP) chemotherapy than those who did not receive this treatment (relative risk [RR] = 1.66; 95% confidence interval [CI], 0.99 to 2.82), and increased with number of cycles of MOPP (P =.07). Exclusion of lung cancers for which histologic confirmation was not available strengthened these associations (RR = 2.41; 95% CI, 1.33 to 4.51; P =.004 for any MOPP and P =.007 for trend with number of cycles of MOPP). Risks were not raised, however, after chlorambucil, vinblastine, procarbazine, and prednisone treatment. There was evidence that the raised risk of lung cancer occurring in relation to radiotherapy was restricted to histologies other than adenocarcinoma. The results suggest that MOPP chemotherapy may lead to elevated risk of lung cancer, at least in certain subgroups of patients. The role of chemotherapy in the etiology of lung cancer after Hodgkin's disease deserves further investigation.

Lung cancer and arsenic concentrations in drinking water in Chile.

Cities in northern Chile had arsenic concentrations of 860 microg/liter in drinking water in the period 1958-1970. Concentrations have since been reduced to 40 microg/liter. We investigated the relation between lung cancer and arsenic in drinking water in northern Chile in a case-control study involving patients diagnosed with lung cancer between 1994 and 1996 and frequency-matched hospital controls. The study identified 152 lung cancer cases and 419 controls. Participants were interviewed regarding drinking water sources, cigarette smoking, and other variables. Logistic regression analysis revealed a clear trend in lung cancer odds ratios and 95% confidence intervals (CIs) with increasing concentration of arsenic in drinking water, as follows: 1, 1.6 (95% CI = 0.5-5.3), 3.9 (95% CI = 1.2-12.3), 5.2 (95% CI = 2.3-11.7), and 8.9 (95% CI = 4.0-19.6), for arsenic concentrations ranging from less than 10 microg/liter to a 65-year average concentration of 200-400 microg/liter. There was evidence of synergy between cigarette smoking and ingestion of arsenic in drinking water; the odds ratio for lung cancer was 32.0 (95% CI = 7.2-198.0) among smokers exposed to more than 200 microg/liter of arsenic in drinking water (lifetime average) compared with nonsmokers exposed to less than 50 microg/liter. This study provides strong evidence that ingestion of inorganic arsenic is associated with human lung cancer.

Relation between inducibility of CYP1A1, GSTM1 and lung cancer in a French population.

Smoking is the principal cause of lung cancer. However, not all smokers will develop this disease. Individual susceptibility to chemically induced cancer may be explained in part by genetic differences in the activation and detoxification of procarcinogens. The activation phase of polycyclic aromatic hydrocarbon (PAH) metabolism is governed by the enzyme CYP1A1, induced by PAH when it enters the body. The extent to which PAH induces CYP1A1 activity varies greatly from one subject to another. CYP1A1 inducibility has long been associated, although inconsistently, with an increased risk of lung cancer. In 1982, Kouri corroborated Kellerman's results with a new method for measuring inducibility, but few studies have reported using this method. The glutathione S-transferases (GSTs) are involved in the detoxification phase of PAH, and the allelic deletion of GSTM1 has been also associated with an increased risk of lung cancer. We conducted a case-control study to examine the risk of lung cancer related, separately and together, to CYP1A1 inducibility, GSTM1 polymorphism and cigarette smoking in a French population. The 611 subjects were 310 incident lung cancer cases and 301 hospital control subjects. We were able to constitute a DNA bank for 552 subjects (89.5%) and gather detailed information on smoking history for all of them. Inducibility could be measured for 195 cases and 183 control subjects. Results for GSTM1 polymorphism concern 247 cases and 254 control subjects. GSTM1 polymorphism and inducibility could both be assessed for 179 cases and 166 control subjects. The odds ratio related to inducibility was 1.7 [1.0-3.0] for medium and 3.1 (1.3-7.4) for hyper inducers. The association with GSTM1 was 1.6 (1.0-2.6). With a reference category of subjects who were both low inducers and GSTM1(+), we found an odds ratio for lung cancer of 8.1 (2-31) for the subjects with both risk factors [i.e. GSTM1(-) and hyper inducers]. Our data did not reveal evidence of interaction between smoking and inducibility. On the other hand, we found an interaction of 3.6 (0.6-21) between inducibility and GSTM1.

CYP1A1 polymorphisms and lung cancer risk: a meta-analysis.

To examine the risk of lung cancer associated with the MspI-restriction fragment length polymorphism and Exon7-Val polymorphisms of CYP1A1, a meta-analysis of published case-control studies was undertaken using a random effects model. The principal outcome measure was the odds ratio for the risk of lung cancer, using homozygosity of the 'wild-type allele' as the reference group. Fifteen reports detailing the relationship between the lung cancer and the MspI and Ile-Val polymorphisms of CYP1A1 were identified. The odds ratio of lung cancer associated with the MspI combined variant and homozygous genotypes were 1.09 (0.94-1.25) and 1.27 (0.91-1.77), respectively. The odds ratio of lung cancer associated with the Ile-Val combined variant and homozygous genotypes were 1.16 (0.92-1.48) and 1.62 (0.93-2.82), respectively. The hypothesis that the modulation of carcinogen metabolism is under genetic control is a plausible and attractive mechanism for explaining inter-individual susceptibility of lung cancer. However, the results from this analysis provide little support for the role of variation in the CYP1A1 gene defined by either polymorphisms represents as lung cancer risk factor. Additional well-designed studies based on sample sizes commensurate with the detection of small genotypic risks may allow a more definitive conclusion.

Relative Risk for Lung Cancer According to Smoking Habits in Korean

Background : While the incidence of lung cancer is gradually leveling off in developed countries, it is continuing to rise in Korea. With the rapid increase in the prevalence of smoking among women and the young, the incidence of lung cancer is also expected to increase within the next three and four decades. The aims of the present study are to analyze the smoking habits in patients with lung cancer and to evaluate of the relative risk of lung cancer according to patients' smoking habits. Method : This investigation was a hospital-based, case control study, which included data of 93 case subjects with lung cancer and 1132 controls with disease unrelated to smoking, obtained through a smoking history questionnaire by a direct personal interview. Result : Compared with non-smokers, those who smoked for more than 50 years had an odds ratio for lung cancer of 8.8(1.8-20.7). The odds ratios was 8.5(3.5-20.7) for those who smoke more than a total of 40 cigarettes per day and 5.5(2.3-13.3) for men who started habitual smoking under the age of 20. The risk increased for men with more than of cigarette smoking(OR : 5.5, 95% CIa : 2.6-11.9). Odds ratios associated with cigarette smoking were 2.5(1.1-5.8) and 5.1(2.6-10.4) for ex-smokers and current smokers, respectively and 2.2(0.0-4.6) for non-filter smokers of more than 16 years. Conclusion : There was a clear dose-response relationship between the risk of lung cancer and smoking. It can be concluded that dose is an important risk factor for lung cancer, as well as smoking habits.

Residential randon exposure and lung cancer risk in Misasa, Japan: a case-control study.

In order to investigate an association between residential radon exposure and risk of lung cancer, a case-control study was conducted in Misasa Town, Tottori Prefecture, Japan. The case series consisted of 28 people who had died of lung cancer in the years 1976-96 and 36 controls chosen randomly from the residents in 1976, matched by sex and year of birth. Individual residential radon concentrations were measured for 1 year with alpha track detectors. The average radon concentration was 46 Bq/m3 for cases and 51 Bq/m3 for controls. Compared to the level of 24 or less Bq/m3, the adjusted odds ratios of lung cancer associated with radon levels of 25-49, 50-99 and 100 or more Bq/m3, were 1.13 (95% confidence interval; 0.29-4.40), 1.23 (0.16-9.39) and 0.25 (0.03-2.33), respectively. None of the estimates showed statistical significance, due to small sample size. When the subjects were limited to only include residents of more than 30 years, the estimates did not change substantially. This study did not find that the risk pattern of lung cancer, possibly associated with residential radon exposure, in Misasa Town differed from patterns observed in other countries.

Residential radon exposure and risk of lung cancer in Missouri.

This study investigated residential radon exposure and lung cancer risk, using both standard radon dosimetry and a new radon monitoring technology that, evidence suggests, is a better measure of cumulative radon exposure. Missouri women (aged 30 to 84 years) newly diagnosed with primary lung cancer during the period January 1, 1993, to January 31, 1994, were invited to participate in this population-based case-control study. Both indoor air radon detectors and CR-39 alpha-particle detectors (surface monitors) were used. When surface monitors were used, a significant trend in lung cancer odds ratios was observed for 20-year time-weighted-average radon concentrations. When surface monitors were used, but not when standard radon dosimetry was used, a significant lung cancer risk was found for radon concentrations at and above the action level for mitigation of houses currently used in the United States (148 Bqm-3). The risk was below the action level used in Canada (750 Bqm-3) and many European countries (200-400 Bqm-3).

Radiographic silicosis and lung cancer risk among workers in Ontario.

A case-control study, nested in a cohort of workers under surveillance for silicosis in 1979 or later, was undertaken to assess lung cancer risk in relation to the ILO coding scheme for the pneumoconioses. The subjects of this study are from the 41 matched quarters, consisting of one workers with silicosis and three age-matched controls, in which a lung cancer case was diagnosed. The odds ratio for lung cancer among subjects with ILO classification 1/0 or more, in comparison to subjects with category < or = 0/1, was 3.27 (95% CI =1.32-8.2). Adjustment of the radiographic risk for the effect of cumulative radon exposure had the effect of increasing the odds ratio for the association between ILO category > or = 1/0 and lung cancer. Although small smoking differences could account for the increased lung cancer odds ratio among workers with silicosis, the empirical evidence suggests that these smoking differences do not exist. It is concluded on the basis of two North American studies of silica exposed workers that radiographic silicosis is a marker for an increased risk of lung cancer.

Risk factors for lung cancer in young adults.

Risk factors for early onset of lung cancer are relatively unknown. In a case-control study, carried out in Germany between 1990 and 1996, the effects of smoking and familial aggregation of cancer were compared in 251 young cases and 280 young controls (< or = 45 years) and in 2,009 older cases and 2,039 older controls (55-69 years). The male/female ratio was 2.6/1 in young patients and 5.6/1 in older patients. Adenocarcinomas were more frequent in young men than in older men (41 % vs. 28%). Duration of smoking and amount smoked showed significantly increased odds ratios for lung cancer in both age groups. Lung cancer in a first degree relative was associated with a 2.6-fold (95% confidence interval (CI) 1.1-6.0) increase in the risk of lung cancer in the young age group, but no elevated risk was seen in the older group (OR = 1.2, 95% CI 0.9-1.6). Smoking-related cancer in relatives with the age at diagnosis under 46 years was associated with an increased risk of lung cancer in the young group (OR = 5.6, 95% CI 0.7-46.9) but not in the older group (OR = 0.7, 95% CI 0.3-1.5). Results indicated that lung cancer risk in young and older age groups shows remarkable differences with respect to sex, histologic type, and genetic predisposition.

Historical Cohort Mortality Study of a Continuous Filament Fiberglass Manufacturing Plant

An historical cohort mortality study of a continuous filament fiberglass manufacturing plant was undertaken to determine whether an elevated lung cancer risk would be observed on a cohort basis. A nested case-control study of white male lung cancer deaths was incorporated into the study design. An interview survey to obtain information on sociodemographic factors, including smoking, and an historical environmental reconstruction to identify elements in the plant environment to which workers might be exposed were included in the study design. Respirable glass (Beta) fibers were produced only from 1963 to 1968. The lung cancer odds ratio (OR) among those workers exposed to respirable glass fibers is below unity, as are ORs for exposure to asbestos, refractory ceramic fibers, respirable silica (except for the lowest exposure level), total chrome and arsenic. There is a suggestion of an increase with exposure among smokers only for exposure to formaldehyde, although the OR for the highest level is based on only one case and is not likely to be meaningful. None of these plant exposures suggests an increase in lung cancer risk for this population. Although the lung cancer standardized mortality ratios are slightly elevated, results of the case-control investigation confirm that neither respirable glass fibers nor any of the substances investigated as part of the plant environment are associated with an increase in lung cancer risk for this population.

Chromosome 13 poly(ADP-ribose) polymerase polymorphisms and lung cancer risk

A 193 base pair repeat polymorphism in the human poly(ADP-ribose) polymerase (PADPRP) pseudogene found on chromosome 13 has been associated with lung cancer, endemic Burkitt lymphoma, B-cell lymphoma, breast cancer and colorectal carcinoma. We investigated the frequency of the PADPRP genetic polymorphism in a hospital-based case-control study of lung cancer for 54 cases and 47 controls. There was a statistically significant difference in allelic frequency between Caucasians and African Americans (p<0.001). For African Americans, the odds ratio for lung cancer and the 'B' allele was 2.38 (95% C.I.=0.73, 7.69) and for Caucasians 0.44 (95% C.I.=0.11, 1.77). The results for the African Americans, however, were not in Hardy-Weinberg equilibrium, although the Caucasians were. Thus, this study, albeit small, does not find that the PADPRP pseudogene duplicated region located on chromosome 13 is a risk factor for lung cancer.

The healthy worker survivor effect and mortality at two automotive engine manufacturing plants.

Attributes such as time since hire or length of followup may be important in occupational mortality due to the "healthy worker survivor effect." In a regression analysis of mortality odds ratios at two automotive engine plants, strong effects of overall employment duration (latency weighted) were observed in addition to effects for (similarly weighted) cumulative exposures. The duration effects were negative for several cancer and noncancer outcomes, and confounded exposure effects. The lung cancer odds ratio declined to 0.68 (95% CI = 0.51, 0.90) at the mean duration of employment. With control for employment duration, adjusted lung cancer odds ratios for work as millwrights increased from 3.0 to 3.8, and for work in cylinder head production, from 3.3 to 3.9. Several causes of death with strong duration effects were smoking-related, suggesting diminished smoking risk factors with increasing employment duration. Similarly, trends for cirrhosis of the liver mortality suggested the alcohol risk factor is smaller in long-duration workers. If personal risk factors are an important component of the healthy worker survivor effect, they could be powerful negative confounders of exposure-response for related outcomes. Including a term for employment duration in regression models appears to partially correct for healthy worker survivor bias.

Pet birds and risk of lung cancer in Sweden: a case-control study.

To investigate the association between keeping birds and the risk of lung cancer in Sweden. Case control study based on cases of lung cancer and community controls. Interviews were performed by two nurses specially trained for this project. Three major referral hospitals located in southwest Sweden. All patients aged 75 and under with newly diagnosed lung cancer and of Scandinavian birth who lived in one of 26 municipalities in Gothenburg and Bohus county or Alvsborg county. Potential control subjects matched on county of residence, sex, and closest date of birth were selected from population registries. In the context of a larger case-control study, information on pet birds was obtained from 380 patients with lung cancer (252 men) and 696 controls (433 men). Odds ratios for lung cancer in relation to whether or not pet birds were kept and the duration of keeping pet birds. The adjusted odds ratio for ever versus never exposed to pet birds at home was 0.94 (95% confidence interval 0.64 to 1.39) for men and 1.10 (0.64 to 1.90) for women. There was no evidence of a trend for increased risk of lung cancer with duration of bird ownership. Bird keeping does not seem to confer any excess risk of lung cancer to Swedish men or women.

Asbestos‐associated cancers in the Ontario refinery and petrochemical sector

Asbestos has been widely used in the refinery and petrochemical sector. Mesothelioma has occurred among maintenance employees, and it was hypothesized that mesothelioma is a marker for exposures which might increase lung cancer risk. A death certificate-based case-control study of mesothelioma and lung cancer from 1980 to 1992 was conducted in an Ontario county with a substantial presence of these industries. Each of the 17 men who died of mesothelioma and 424 with lung cancer were matched with controls who died of other causes. The Job and Industry fields on the death certificates were abstracted. Employment as a maintenance worker in the refinery and petrochemical sector was associated with an increased risk of mesothelioma (odds ratio: 24.5; 90% confidence interval 3.1–102). The risk of lung cancer among petrochemical workers, in comparison with all other workers in the county, was 0.88. In an internal comparison of maintenance employees with other blue-collar workers in the refinery and petrochemical sector, the odds ratio for lung cancer was 1.73 (90% confidence interval 0.83–3.6). This finding is consistent with no difference in risk between maintenance and other employees, but it is also compatible with study power being too low to achieve statistical significance. The hypothesis of increased lung cancer risk could be examined more fully with nested case-control studies in existing cohorts. Meanwhile, it would be prudent to reinforce adherence to asbestos control measures in the refinery and petrochemical sector. © 1996 Wiley-Liss, Inc.

Asbestos-associated cancers in the Ontario refinery and petrochemical sector.

Asbestos has been widely used in the refinery and petrochemical sector. Mesothelioma has occurred among maintenance employees, and it was hypothesized that mesothelioma is a marker for exposures which might increase lung cancer risk. A death certificate-based case-control study of mesothelioma and lung cancer from 1980 to 1992 was conducted in an Ontario county with a substantial presence of these industries. Each of the 17 men who died of mesothelioma and 424 with lung cancer were matched with controls who died of other causes. The Job and Industry fields on the death certificates were abstracted. Employment as a maintenance worker in the refinery and petrochemical sector was associated with an increased risk of mesothelioma (odds ratio: 24.5; 90% confidence interval 3.1-102). The risk of lung cancer among petrochemical workers, in comparison with all other workers in the county, was 0.88. In an internal comparison of maintenance employees with other blue-collar workers in the refinery and petrochemical sector, the odds ratio for lung cancer was 1.73 (90% confidence interval 0.83-3.6). This finding is consistent with no difference in risk between maintenance and other employees, but it is also compatible with study power being too low to achieve statistical significance. The hypothesis of increased lung cancer risk could be examined more fully with nested case-control studies in existing cohorts. Meanwhile, it would be prudent to reinforce adherence to asbestos control measures in the refinery and petrochemical sector.

Carcinogenic effects of diesel emissions and lung cancer: The epidemiologic evidence is not causal

The effects of diesel engine exhaust in lung carcinogenesis have been evaluated by several scientific organizations and government agencies. This complex issue has required a multidisciplinary approach including atmospheric measurements, toxicology, chemical carcinogenesis, epidemiology, and risk assessment. One important aspect of the epidemiological studies that deserves further attention is the confounding effects of cigarette smoking. Only some epidemiological studies have statistically adjusted for cigarette smoking, usually by years of smoking, cigarettes per day, or pack-years. Some studies obtained smoking information from proxy interviews. However, differences in “tar” intake, interpuff interval, depth of inhalation, and other smoking behavior patterns were not evaluated. These smoking parameters are rarely collected for occupational data analysis, yet the inability to adjust statistically for such parameters may result in a small degree of residual confounding. Because the highest odds ratios for lung cancer associated with diesel engine exhaust are usually less than 2 or 1.5, possible residual confounding effects of smoking may have resulted in spurious associations.

Occupational risk factors for lung cancer in Tianjin, China.

Information about occupation and industry of cancer patients is routinely recorded in the Cancer Registry of Tianjin, People's Republic of China. Occupational risk factors of lung cancer for the period of 1981-1987 were assessed using other cancers as controls. For each occupation and industry, workers employed in it were considered exposed and were compared with all other workers. Elevated risks were found for a number of industries for both sexes, including, in particular, the textile, wood, metal, and construction industries. Results by occupation were similar to those by industry. Smoking scores were calculated for various occupations on the basis of a separate population survey in Tianjin. Smoking cannot explain the elevated odds ratios in males, while among females a strong correlation was observed between smoking scores and lung cancer odds ratios, suggesting a confounding effect.

Is lung cancer associated with asbestos exposure when there are no small opacities on the chest radiograph?

This study was designed to test the hypothesis that the risk of lung cancer from asbestos exposure is confined to persons with radiographic evidence of pulmonary fibrosis. Occupational and smoking histories were obtained from 271 patients with a confirmed diagnosis of primary lung cancer and 678 referents (279 with other respiratory disease and 399 with cardiac disease). Histories were reviewed blind to assess the timing, duration, and probability of exposure to asbestos. To allow for a lag between asbestos exposure and the development of lung cancer, subjects were classified by the time they had spent in an occupation entailing definite or probable exposure more than 15 years before diagnosis. The presence and extent of fibrosis was assessed blindly from chest radiographs by three readers and scored for small opacities with the ILO 1989 International Classification of Radiographs of the Pneumoconioses. 93 (34·3%) cases had worked in an occupation with definite or probable asbestos exposure compared with 176 (25·8%) referents (crude odds ratio for lung cancer 1·49, 95% Cl 1·09-2·04). After adjustment for age, sex, smoking history, and area of referral, the odds ratio (95% Cl) was 2·03 (1·00-4·13) in the subgroup of 211 with a median ILO score for small parenchymal opacities of 1/0 or more, and 1·56 (1·02-2·39) in the 738 with a score of 0/1 or less (ie, those without radiological evidence of pulmonary fibrosis). These results suggest that asbestos is associated with lung cancer even in the absence of radiologically apparent pulmonary fibrosis.

Asbestos exposure and the risk of lung cancer in a general urban population.

The aim of the study was to investigate the asbestos-associated risk of lung cancer according to histological type of cancer, lobe of origin, pulmonary concentration, and type of amphibole fibers and also to estimate the etiologic fraction of asbestos for lung cancer. The pulmonary concentration of asbestos fibers in 113 surgically treated male lung cancer patients and 297 autopsy cases among men serving as referents was determined by scanning electron microscopy. The age- and smoking-adjusted odds ratios of lung cancer were calculated according to pulmonary fiber concentration for all lung cancer types, squamous-cell carcinoma, and adenocarcinoma and for the lower-lobe and the upper- and middle-lobe cancers. The risk of lung cancer was increased according to the pulmonary concentration of asbestos fibers (f) of 1.0 to 4.99 x 10(6) f.g-1 [odds ratio (OR) 1.7] and > or = 5.0 x 10(6) f.g-1 (OR 5.3). The odds ratios associated with fiber concentrations of > or = 1.0 x 10(6) f.g-1 were higher for adenocarcinoma (OR 4.0) than for squamous-cell carcinoma (OR 1.6). The asbestos-associated risk was higher for lower lobe tumors than for upper lobe tumors. The risk estimates for anthophyllite and crocidolite-amosite fibers were similar, except for the risk of squamous-cell carcinoma. An etiologic fraction of 19% was calculated for asbestos among male surgical lung cancer patients in the greater Helsinki area. Past exposure to asbestos is a significant factor in the etiology of lung cancer in southern Finland. The asbestos-associated risk seems to be higher for pulmonary adenocarcinoma and lower-lobe tumors than for squamous-cell carcinoma and upper-lobe tumors.

Increased risk for small cell lung cancer following residential exposure to low-dose radon: a pilot study.

Alpha track radon detectors were placed in the homes of 35 lung cancer patients and 35 matched controls for a period of 8 to 10 mo. Twenty lung cancer patients had small cell lung carcinoma; 11 had adenocarcinoma, 2 had squamous cell carcinoma, and 2 had unclassified carcinoma among 15 nonsmokers. Mean overall living on ground level was significantly higher in the group with small cell lung carcinoma (50 y +/- 15) than among controls (33 y +/- 19); the adjusted odds ratio for lung cancer was 5.2 (90% confidence interval [90% CI] = 1.1-24.9) per decade of living on the ground floor for the group with small cell lung carcinoma. Radon exposure of more than 1.0 pci/l in the group with small cell lung carcinoma was associated with increased risk of lung cancer, although it did not reach statistical significance [odds ratio = 1.5 (90% CI = 0.4-5.4)], adjusting for differences in smoking habits. Our study supports the presence of a differentially increased risk for small cell lung carcinoma following long-term radon exposure.