Excess Incidence Of Lung Cancer Research Articles

The influence of postscreening follow-up time and participant characteristics on estimates of overdiagnosis from lung cancer screening trials.

We aimed to explore the underlying reasons that estimates of overdiagnosis vary across and within low-dose computed tomography (LDCT) lung cancer screening trials. We conducted a systematic review to identify estimates of overdiagnosis from randomised controlled trials of LDCT screening. We then analysed the association of Ps (the excess incidence of lung cancer as a proportion of screen-detected cases) with postscreening follow-up time using a linear random effects meta-regression model. Separately, we analysed annual Ps estimates from the US National Lung Screening Trial (NLST) and German Lung Cancer Screening Intervention Trial (LUSI) using exponential decay models with asymptotes. We conducted stratified analyses to investigate participant characteristics associated with Ps using the extended follow-up data from NLST. Among 12 overdiagnosis estimates from 8 trials, the postscreening follow-up ranged from 3.8 to 9.3 years, and Ps ranged from -27.0% (ITALUNG, 8.3 years follow-up) to 67.2% (DLCST, 5.0 years follow-up). Across trials, 39.1% of the variation in Ps was explained by postscreening follow-up time. The annual changes in Ps were -3.5% and -3.9% in the NLST and LUSI trials, respectively. Ps was predicted to plateau at 2.2% for NLST and 9.2% for LUSI with hypothetical infinite follow-up. In NLST, Ps increased with age from -14.9% (55-59 years) to 21.7% (70-74 years), and time trends in Ps varied by histological type. The findings suggest that differences in postscreening follow-up time partially explain variation in overdiagnosis estimates across lung cancer screening trials. Estimates of overdiagnosis should be interpreted in the context of postscreening follow-up and population characteristics.

Living alone as a risk factor for cancer incidence, case-fatality and all-cause mortality: A nationwide registry study

Lack of social contacts has been associated with an increased risk of cancer mortality, but it is not known whether living alone increases the risk of cancer incidence or case fatality. We examined the association between living alone with cancer incidence, case-fatality and all-cause mortality in eight most common cancers. All patients with their first cancer diagnosis in 2000–2017 were identified from the nationwide Finnish Cancer Registry. Information on living arrangements was derived from Statistics Finland. The incidence analyses were conducted using Poisson regression. The total Finnish population served as the population at risk. Fine-Gray model was used to estimate case-fatality and Cox proportional regression model all-cause mortality. In men, we found an association between history of living alone and excess lung cancer incidence but living alone seemed to be associated with lower incidence of prostate cancer and skin melanoma. In women, living alone was more consistently associated with higher incidence of all studied cancers. Cancer patients living alone had an 11%–80% statistically significantly increased case-fatality and all-cause mortality in all studied cancers in men and in breast, colorectal and lung cancer in women. Living alone is consistently associated with increased cancer incidence risk in women but only in some cancers in men. Both men and women living alone had an increased risk of all-cause mortality after cancer diagnosis.

ASSESSMENT OF OCCUPATIONAL RISK OF DEATH FROM LUNG CANCER IN WORKERS OF URANIUM PRODUCTION

The analysis of morbidity among workers of uranium production in Northern Kazakhstan in the period from 1971 to 2009, revealed a high proportion of lung cancer, which from the overall structure of oncological met in 68,7% of the case. This is especially evident in the age group of 50–59 years, where the experience of work more than 30 years. The differences in the number of expected and actual observed cases of death of the workers of uranium mines from lung cancer are comparable, and the ratio of observed and expected values indicate a rise in the nosology of about 1.4 times. The excess incidence of lung cancer in workers per unit of radiation exposure was 4.6 cases per one equivalent equilibrium emana for a month and was in direct dependence on the level of cumulative radiation exposure of daughter products of radon decay. The comparison of the frequency of occurrence and polymorphisms of alleles and genotypes of introns 3 and 6 of the p53 gene among the workers of a uranium mine and those of a control group. People who professionally exposed to radiation and toxic components of uranium are relatively high risk of development of oncological on the background of a decline in the immune reactivity of the organism.

Cancer mortality among electrolysis workers: where have all the cancers gone? A challenge to occupational epidemiologists and regulatory boards

ObjectivesThe alleged absence of increased cancer mortality among electrolysis workers at the Port Colborne refinery (Canada) contrasts the excess incidence of lung cancer and nasal cancer seen among workers engaged...

Dietary Isothiocyanates, Glutathione S-Transferase M1 (GSTM1), and Lung Cancer Risk in African Americans and Caucasians from Los Angeles County, California

Isothiocyanates, found in cruciferous vegetables, are anticarcinogenic. Racial differences in smoking do not fully account for the African-American excess lung cancer incidence. African Americans consume more cruciferous vegetables than U.S. Whites. Impact on lung cancer risk is unknown. The glutathione S transferase M1 (GSTM1) gene promotes urinary isothiocyanate excretion. We evaluated dietary isothiocyanates and lung cancer using a population-based case-control study of 933 African Americans and Caucasians (non-Hispanic U.S. White) from Los Angeles County, California (311 cases; 622 controls). Broccoli, cauliflower, greens, and cabbage food-frequency variables represented isothiocyanates. Isothiocyanates were protective for lung cancer risk. Adjusted odds ratio (OR) for the uppermost quartile > 80 μ mol isothiocyanates/wk, compared to lowest, was 0.65 [95% confidence interval (CI) = 0.41–1.00, trend P = 0.02]. Association was stronger among subjects with homozygous deletion of GSTM1 (OR = 0.52, 95% CI = 0.31–0.86) than subjects with at least one GSTM1 copy (OR = 0.77, 95% CI = 0.49–1.21). The difference was not statistically significant (P = 0.16). Despite African Americans consuming more cruciferous vegetables, the isothiocyanate association did not vary by race (P = 0.52). Reduced lung cancer risk with higher isothiocyanate intake may be slightly stronger among subjects with deletion of GSTM1.

Radon dosimetry and its implication for risk

The major source of human exposure to radiation is from natural background, and the largest component of this arises from the inhalation of the short-lived daughters of radon gas ( 222Rn). It is therefore important to be able to quantify the risk from this exposure. The risk from exposure to radon daughters can be determined in two different ways. Firstly, by using statistics on the excess lung cancer incidence in miners exposed to high levels of radon gas: the so-called epidemiological approach. Secondly, by calculating the effective dose (Sv) received per unit exposure, and multiplying this by the risk per Sv: the so-called dosimetric approach. When, in 1994, the ICRP Publication 66 Human Respiratory Tract Model (HRTM) was first used in the latter approach, the estimates of risk (8.4×10 −4/WLM) exceeded those of the epidemiological approach (2.8×10 −4/WLM) by a factor of 3. Since then, there have been many attempts to reconcile these two approaches, bearing in mind that if any of the ICRP weighting factors (e.g. tissue or radiation weighting factors) were changed by a factor of 3, to make these two approaches agree, this would have a significant effect on the dosimetry of other radionuclides, and may not be justified by other experimental evidence. This paper re-examines these two approaches, and the likely uncertainties associated with each, in the light of recent scientific knowledge. Recent risk estimates using the epidemiological approach (∼5×10 −4/WLM) are nearly twice those made in 1994, while a recent detailed analysis using the dosimetric approach gives a risk about 15% lower than the 1994 study (∼7×10 −4/WLM). Based on these current estimates, the two approaches are broadly consistent. It is observed that a small change in the weighting factor for the lung, from 0.12 (rounded by ICRP from 0.11) to 0.10 is all that is needed to make these two approaches agree almost exactly.

DNA adducts as markers of exposure to carcinogens and risk of cancer

DNA adducts as markers of exposure to carcinogens and risk of cancer

Cancer incidence among male pulp and paper workers in Norway.

The study investigated cancer incidence among 23,718 male pulp and paper workers employed continuously for at least 1 year between 1920 and 1993 in Norway. The name, date of birth, personal identification number, dates of hire and termination for all employment periods, specific department, and job categories were registered for each worker. Six subcohorts were established (sulfite mill, sulfate mill, paper mill, maintenance department, administrative staff and other departments). Data on the cohort were linked with data in the Norwegian Cancer Register. The follow-up period for cancer incidence, date of death, or emigration was from 1953 through 1993. An excess incidence of lung cancer was found among both short- and long-term employees [standardized incidence ratio (SIR) 1.5, 95% confidence interval (95% CI) 1.13-2.03 and SIR 1.2, 95% CI 1.09-1.34, respectively], especially for workers with the longest latency (SIR 1.3, 95% CI 1.08-1.44) and for sulfite mill workers (SIR 1.5, 95% CI 1.09-1.99). The risk for pleural mesothelioma was also increased (SIR 2.4, 95% CI 1.45-3.75), especially among maintenance workers. The results also showed an increased risk for malignant melanoma (SIR 1.3, 95% CI 1.04-1.60), an unexpected finding. Almost all the increased risk for lung cancer can be explained by a combination of smoking habits and asbestos use. although an effect of other work-related exposures (sulfur and chloride compounds, wood dust) cannot be excluded. Most of the cases of pleural mesothelioma occurred in departments where asbestos was used. There is no clear explanation for the excess of malignant melanoma, and the finding may be a chance occurrence.

Excess lung cancer incidence and radon indoors in a Bulgarian town.

Excess lung cancer incidence and radon indoors in a Bulgarian town.

β-Carotene and lung cancer: a case study

The conflicting evidence of the relation between beta-carotene and lung cancer in humans serves as a poignant case study with respect to what types of evidence are sufficient to support or change a nutrition recommendation. This article is a review of the available evidence of the relation between beta-carotene and lung cancer, including data regarding beta-carotene intake (from diet and supplements), beta-carotene biochemical status, and vegetable and fruit consumption, and a discussion of the role of this evidence in making nutrition recommendations. More than 30 case-control and cohort studies were conducted over many years in various populations and indicated that people who eat more vegetables and fruit, foods rich in carotenoids, and carotenoids (beta-carotene in particular), as well as those with higher blood beta-carotene concentrations, have a lower risk of lung cancer than those who eat fewer such foods or have lower beta-carotene concentrations. In contrast, the intervention results from large, controlled trials of beta-carotene supplementation do not support the observed beneficial associations or a role for supplemental beta-carotene in lung cancer prevention; instead, they provide striking evidence for adverse effects (ie, excess lung cancer incidence and overall mortality) in smokers. The findings require that caution be exercised in recommending supplemental beta-carotene, particularly for smokers, and argue against changing the vegetable-fruit recommendations in the direction of greater nutrient specificity. This case study of beta-carotene and lung cancer stresses the importance of having results from at least one, and preferably more, large, randomized intervention trial before public health recommendations concerning micronutrient supplementation are considered.

Excess Incidence of Lung Cancer among Pulmonary Tuberculosis Patients

Reviewing the epidemiological studies on coexistent pulmonary tuberculosis and lung cancer since 1960, it was confirmed that patients with active pulmonary tuberculosis have a higher risk of dying from lung cancer or other malignancies, in spite of a very high mortality from tuberculosis per se. Females showed a higher risk than males. An antagonistic hypothesis between the above two diseases since 1854 seemed based on the facts that tuberculosis patients had mostly died in young age groups and had had little chance of surviving to cancer age groups before the advent of modern treatments, and that the lack of an adequate disease registration system might have caused a failure to reveal any association between the two diseases. Specific causative factors of the excess incidence of cancer among active pulmonary tuberculosis patients, however, have so far not be clarified.

Book reviews

This report of a Task Group of the International Commission on Radiological Protection is specifically concerned with indoor exposure to inhaled radon and radon daughter nuclides, and therefore with exposure of members of the public. It follows on from a previous report by the same Task Group, ICRP Publication 32 (1981), which dealt, however, with limits to inhalation exposure of radon for workers such as uranium miners and similarly exposed groups. For these workers, in the past, exposure was high enough to produce a significant excess incidence of lung cancer.

Diesel Emissions and Lung Cancer1

This paper uses two different methods to assess the potential risk of human lung cancer from exposure to diesel engine emissions. One method analyzes the best available epidemiological evidence on the lung cancer risks of persons exposed in their occupations to diesel engine emissions. The second conducts a comparative analysis of laboratory and epidemiological data on diesel engine emissions and two chemically related environmental exposures–coke oven emissions and roofing tar emissions. The estimates of potential risk derived from these two distinct methods are compared. The sources of uncertainty in each method are explicitly characterized. The value of these estimates for comparing the potential lung cancer risks from exposure to diesel engine emissions with other personal and societal risks are discussed. Also considered are the limitations of these results in predicting the possible excess incidence of lung cancer from ambient exposure to diesel emissions.

Lung cancer in ferrous foundry workers: a review.

Epidemiologic studies indicate that an increased incidence of lung cancer may be associated with specific work areas in ferrous foundries. With the exception of crane operators, who were found to have an elevated lung cancer rate in one foundry, the excess lung cancer incidence is generally confined to molders, casters, and cleaning room operators whose lung cancer risk is two- to threefold higher than that of standard populations. These studies reflect conditions that existed in the foundries several decades ago. The lung cancer risk today may differ as a result of the introduction of new foundry practices and the use of new molding materials. Benzo(a)pyrene and certain other polycyclic aromatic hydrocarbons have been found in many locations in the foundries. It is not known if tumor promoters, co-carcinogens, or other classes of chemical carcinogens are present. The contribution of tobacco smoke to the lung cancer risk of ferrous foundry workers is also unknown. Current studies are examining the composition and long-term health effects of emissions from molds composed of modern synthetic chemical molding materials as well as those from the more traditional green sand molds.

Asbestos and lung cancer: an analysis of the epidemiological evidence on the asbestos-smoking interaction.

Three simple models for the asbestos-smoking interaction on human lung cancer production are considered. In the first model the excess incidence of lung cancer independently due to asbestos and to smoking adds together when both agents are present (additive model). In the second the addition of each one of the two agents produces an effect (increase in lung cancer incidence) which is proportional to the effect of the other (multiplicative model). In the third, asbestos can only increase lung cancer incidence in the presence of smoking. As previously found by other investigators, the additive model appears the least plausible in the light of the data from two published epidemiological studies. A discrimination between the other two models is attempted through a detailed analysis of the five published epidemiological studies today available which provide information on occupational asbestos exposure, smoking habits and lung cancer risk. Although the data do not allow a definitive discrimination, the multiplicative model appears to be more plausible, being also consistent with a multi-stage carcinogenic mechanism and with evidence from animal (rat) experiments. It is relevant both for biology and for public health that in this model asbestos and smoking are regarded as independently capable of producing lung cancer in humans and that they act synergistically when exposure to both occurs.

The exposure of United Kingdom miners to radon.

<b>Duggan, M.J., Soilleux, P.J., Strong, J.C., and Howell, D.M. (1970).</b><i>Brit. J. industr. Med.,</i><b>27,</b> 106-109. <b>The exposure of United Kingdom miners to radon.</b> Airborne radon has been recognized as a probable cause of lung cancer since the epidemiological studies made in the mining communities of Schneeberg and Jachymov during the 1920s and 1930s. Uranium miners are generally exposed to high concentrations of radon, and the growth of the uranium mining industry in the past 20 years has therefore stimulated a great amount of work on the risk from inhalation of radon and its daughters. However, there is still no general agreement on either the physical measurements in which the maximum permissible concentration in air should be expressed or the numerical value of this concentration. There are no uranium mines being worked in the United Kingdom but there are considerable numbers of coal and other mines. It was therefore decided to make some radon measurements in a selection of mines in the UK to see if there was any prospect of obtaining useful dose-risk data. Measurements were made in 22 mines in all - 12 coal mines and 10 other mines - and the highest concentrations were found in three haematite mines in West Cumberland and in the two tin mines which were visited. The concentrations in these five mines were, in general, greater than 0·3 of a working level (WL) and in many locations were greater than 1 WL. Because of these findings and also because an excess incidence of lung cancer among West Cumberland haematite miners has been previously reported, a further study of the mortality experience of West Cumberland miners has been carried out by Boyd, Doll, Faulds, and Leiper (1970). Their findings are reported in this Journal (p. 97).