Excess Of Lung Cancer Deaths Research Articles

0374 Exposure-Response Estimates for Diesel Engine Exhaust and Lung Cancer Mortality Based on Data from Three Occupational Cohorts

ObjectivesTo derive a meta-exposure-response curve (ERC) for DEE and lung cancer mortality and estimate lifetime excess risks (ELRs) of lung cancer mortality based on assumed occupational and environmental exposure scenarios.MethodWe...

Exposure-Response Estimates for Diesel Engine Exhaust and Lung Cancer Mortality Based on Data from Three Occupational Cohorts

Background: Diesel engine exhaust (DEE) has recently been classified as a known human carcinogen.Objective: We derived a meta-exposure–response curve (ERC) for DEE and lung cancer mortality and estimated lifetime excess risks (ELRs) of lung cancer mortality based on assumed occupational and environmental exposure scenarios.Methods: We conducted a meta-regression of lung cancer mortality and cumulative exposure to elemental carbon (EC), a proxy measure of DEE, based on relative risk (RR) estimates reported by three large occupational cohort studies (including two studies of workers in the trucking industry and one study of miners). Based on the derived risk function, we calculated ELRs for several lifetime occupational and environmental exposure scenarios and also calculated the fractions of annual lung cancer deaths attributable to DEE.Results: We estimated a lnRR of 0.00098 (95% CI: 0.00055, 0.0014) for lung cancer mortality with each 1-μg/m3-year increase in cumulative EC based on a linear meta-regression model. Corresponding lnRRs for the individual studies ranged from 0.00061 to 0.0012. Estimated numbers of excess lung cancer deaths through 80 years of age for lifetime occupational exposures of 1, 10, and 25 μg/m3 EC were 17, 200, and 689 per 10,000, respectively. For lifetime environmental exposure to 0.8 μg/m3 EC, we estimated 21 excess lung cancer deaths per 10,000. Based on broad assumptions regarding past occupational and environmental exposures, we estimated that approximately 6% of annual lung cancer deaths may be due to DEE exposure.Conclusions: Combined data from three U.S. occupational cohort studies suggest that DEE at levels common in the workplace and in outdoor air appear to pose substantial excess lifetime risks of lung cancer, above the usually acceptable limits in the United States and Europe, which are generally set at 1/1,000 and 1/100,000 based on lifetime exposure for the occupational and general population, respectively.Citation: Vermeulen R, Silverman DT, Garshick E, Vlaanderen J, Portengen L, Steenland K. 2014. Exposure-response estimates for diesel engine exhaust and lung cancer mortality based on data from three occupational cohorts. Environ Health Perspect 122:172–177; http://dx.doi.org/10.1289/ehp.1306880

S91 Improved Lung Cancer Survival and Reduced Emergency Diagnoses Resulting from an Early Diagnosis Campaign in Leeds 2011

BackgroundLung cancer survival in the UK lags behind other developed nations, and excess early deaths following diagnosis suggest advanced disease at presentation. Patients diagnosed with lung cancer following emergency presentation...

Occupational Risk Factors for Lung Cancer among U. S. Women

Lung cancer accounts for 29% of cancer deaths among U.S. women, i.e., 162,460 estimated deaths in 2006. Between 2–20% of lung cancer deaths in women are estimated to be due to classic industrial lung carcinogens, or workplace exposure to side-stream smoke or radon. There are a limited number of studies of occupational lung cancer in women. Our aim was to identify occupations and industries with elevated proportionate lung cancer mortality among working women, and to focus attention on preventable occupational risk factors for lung cancer. We reviewed the scientific literature on risk factors for occupational lung cancer in women, and undertook a race-specific proportionate mortality (PMR) analysis of nearly 4 million deaths among women who died from 1984–1998 in the 28 U.S. states that code industry sector and occupation on death certificates. Industries with significantly elevated proportionate mortality ratios (PMRs) accounting for the largest number of lung cancer deaths among white working women during the 15-year period were eating and drinking places (PMR=136; n=7783 deaths), hotels and motels (PMR=135; n=1422), several wholesale and retail trades (PMRs range 126–145; n=1405 deaths), several manufacturing sub-sectors (PMRs range 126–142; n=2108), real estate (PMR=137; n=1863), and construction (PMR=125; n=940). Industries accounting for excess lung cancer deaths among white and black women were entertainment and recreation services (PMR=136 white women, PMR=143 black women; n=1209), beauty and barber shops (PMR=124 white women, PMR=122 black women; n=2274), and among black women, public administration (PMR=147; n=718). Focusing on occupation, our analysis revealed significant excess proportionate lung cancer mortality among white women working as waitresses (PMR=152), in sales (PMR=139), as legislative and public administrators (PMR=130), and as managers or administrators (PMR=130). Among black women, financial officers (PMR=175) and receptionists (PMR=183) also experienced excess lung cancer deaths. Women experience significant excess lung cancer mortality associated with occupation. Review of potential exposures in the occupations and industry sectors with elevated lung cancer PMRs suggested several potential lung carcinogens. Workplace exposure to cigarette smoke is a risk factor in some of these industries and occupations, e.g., occupations in the hospitality industry. Other possible explanatory factors in some work environments include a number of known occupational carcinogens. Our findings suggest a need for additional research on occupational risk factors for lung cancer among women working in a wide range of industrial and white collar settings.

Mortality of workers employed in shoe manufacturing: An update

In the late 1970s, the National Institute for Occupational Safety and Health identified two shoe manufacturing facilities where workers experienced relatively "pure" exposures to toluene. A mortality study was conducted through December 31, 1982. An original study did not detect elevated leukemia mortality but did detect increased lung cancer mortality. The present study is an update of the mortality of the original cohort. The study cohort consisted of workers employed 1 month or more between 1940 and 1979 at two Ohio shoe manufacturing plants. Vital status was ascertained through December 31, 1999. Seven thousand eight hundred twenty eight workers, contributing 300,777 person years, were available for analysis. An excess of lung cancer deaths persisted with additional years of follow-up (SMR = 1.36, 95% confidence interval (CI) = 1.19-1.54). Trend tests did not indicate a positive trend between lung cancer risk and duration of employment. Mortality from leukemia was not significantly elevated in the updated analysis. Results indicate a possible association between lung cancer mortality and exposure to chronic, low-levels of organic solvents. Although the strength of this conclusion was weakened by the lack of increasing lung cancer risk in relation to duration of employment, other studies have supported this association.

Mortality of workers at a nickel carbonyl refinery, 1958–2000

Background: Excess risks of respiratory cancer have been shown in some groups of nickel exposed workers. It is clear, however, that not all forms of nickel exposure are implicated in...

Lung cancer mortality among a cohort of men in a silicotic register.

To examine any association between silicosis and lung cancer, the clinic records of a cohort of 1502 silicotic workers diagnosed after 1981 were reviewed. All of the essential data, including occupational exposure, smoking habits, radiographic extent of silicosis, and vital status of each subject, were noted. The standardized mortality ratio for various causes of death was calculated. Thirty-three patients died from lung cancer, giving a standardized mortality ratio of 1.94 (95% confidence interval, 1.35 to 2.70). However, smoking accounted for most of the excess of lung cancer deaths among the silicotic workers in the cohort, and no consistent relationship between lung cancer mortality risk and either duration of exposure to silica dust or severity of silicosis was observed. There is no conclusive evidence in our data to support the hypothesis that lung cancer may be associated with silicosis.

Linear extrapolation models of lung cancer risk associated with exposure to environmental tobacco smoke.

This paper presents a model to estimate the number of lung cancer deaths due to ETS exposure among the 1992 U.S. never-smoking population, based on downward linear extrapolation from the estimated risks of active smokers. The model uses several recently available data sources including an extensive review of the published literature on indoor concentration of ETS constituents measured under real-world conditions and data from the National Mortality Followback Survey and the National Health Interview Survey which furnish nationally representative estimates of the distribution of the U.S. population and the persons who died from lung cancer by sex, age, and smoking status. The linear extrapolation model estimates that five male and six female excess lung cancer deaths due to ETS exposure would be expected in the 1992 U.S. population of over 52 million never smokers age 35 and over. Explanations for differences between the results of our downward extrapolation model and those of others are presented.

A Meta‐Analysis on the Relationship between Pneumoconiosis and Lung Cancer

A Meta‐Analysis on the Relationship between Pneumoconiosis and Lung Cancer: Toshihide Tsuda, et al. Department of Hygiene and Preventive Medicine, Okayama University Medical School—An excess of lung cancer deaths among pneumoconiosis patients has been noted for many years but there has not been agreement on the excess of lung cancer deaths among pneumoconiosis patients in Japan. A meta‐analysis on the relationship between silicosis/pneumoconiosis and lung cancer mortality was conducted, by using 36 mortality studies published from 1980 to 1994. MEDLINE and other information sources were used for the information retrieval. After the critical appraisal, 32 eligible studies were identified. Study estimates were then pooled by using both the fixed effect model and the random effect model. An excess of lung cancer mortality among people with silicosis/pneumoconiosis was shown in all 32 studies. Although homogeneity among the studies was rejected (p<0.05) because the shape of the funnel plots assumed a symmetrical pyramidal shape, the summary rate ratio was estimated. The estimated rate ratio was 2.74 (95 percent confidence interval 2.60‐2.90) in all 32 studies, and 2.77 (2.61‐2.94) in 25 cohort studies. The random effect model results were almost the same as the fixed model results. The estimates in the Japanese studies were a little higher than the overall estimates, which indicated that lung cancer mortality was about three times higher among silicotic patients than among people in the control. This indicated a causal‐relationship between silicosis and lung cancer. This means that lung cancer should be regarded as one of the important complications of silicosis/pneumoconiosis. We recommend further research on the relationship between silica exposure and lung cancer.

Mortality of Iron Foundry Workers

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.

Mortality among taxi drivers in Rome: a cohort study.

The mortality pattern of taxi drivers in Rome as possibly exposed mainly to gasoline engine exhausts was evaluated by means of a historical cohort study. A total of 2,311 male subjects registered as taxi drivers between 1950 and 1975 was followed from 1965 through 1988. The overall mortality was lower than expected on the basis of regional (Latium) reference rates (692 deaths, standardized mortality ratio [SMR] = 0.89, 95% confidence interval [CI] 0.82-0.96), whereas the number of recorded deaths for malignant neoplasms was about the expected (205 deaths, SMR = 0.99, 95% CI 0.86-1.13). Mortality from circulatory and respiratory diseases was lower than expected. Diabetes was significantly increased (42 deaths, SMR = 1.73, 95% CI = 1.25-2.34). An increased SMR appeared for respiratory cancer (SMR = 1.23, 95% CI = 0.98-1.50), mainly due to lung cancer (observed [O] = 76, SMR = 1.23, 95% CI = 0.97-1.54); two pleural cancers were also recorded. The excess of lung cancer deaths was present only among those enrolled in the most recent period (1965-1975) (45 deaths, SMR = 1.40, 95% CI = 1.02-1.87), especially among those of younger age (< 65 years) (SMR = 1.86); there was no relation between lung cancer mortality and latency since first enrollment in the cooperatives or duration of membership. There are difficulties in interpreting the excess of lung cancer on the basis of occupational exposures; however, the increased risk observed among workers employed in more recent calendar periods may be due to heavier exposure in the last decades; further follow-up of the cohort may elucidate whether there is an increasing lung cancer risk among taxi drivers.

Retrospective follow-up study of foundry and engine plant workers.

A retrospective follow-up study of 21,013 workers employed at a foundry and two engine manufacturing plants was conducted to determine if these workers had an unusual mortality experience. A total of 2,235 deaths occurred during the follow-up period of 1970-1987. Mortality from all causes was lower than expected. Men experienced a 6-13% excess of lung cancer deaths, depending on the choice of the comparison group. The data displayed evidence of a positive trend between lung cancer mortality and increasing duration of employment (p = 0.008). White men experienced a statistically significant excess of deaths from stomach cancer (standardized mortality ratio [SMR] = 158; 95% confidence interval [CI] = 101-234). Black men had increased mortality from pancreatic cancer, especially among engine plant workers (SMR = 303; CI = 121-624), and an excess of prostate cancer, concentrated among foundry workers (SMR = 234; CI = 112-430).

Mortality among professional drivers.

The mortality of truck drivers and taxi drivers was studied in Reykjavík. The national mortality rate was used for comparison, and the follow-up lasted until 1 December 1988. The 868 truck drivers (28,788.0 person-years) had an excess of lung cancer deaths [24 observed, 11.2 expected, standardized mortality ratio (SMR) 2.14], but fewer deaths than expected from respiratory diseases (15 observed versus 30.1 expected). The SMR from lung cancer did not steadily increase as the duration of employment increased, nor did it change with the length of follow-up. The SMR values did not deviate substantially from unity for the taxi drivers. Since the high mortality from lung cancer among the truck drivers did not seem to be due to their smoking habits, it might have been caused by one or more occupational factors, especially in light of this group's exposure to engine exhaust gases.

Lung cancer and alpha radiation

The considerable radiosensitivity of the human lung together with the highly localized alpha-doses in the bronchial and pulmonary regions from naturally occurring and man-enhanced radon decay products make the respiratory tract the most critical organ for cancer from exposure to ionizing radiation in our environment. From indoor radon, the tracheobronchial region of the lung generally receives radiation doses which are at least an order of magnitude above the total dose to any other organ. Excess lung cancer deaths found in epidemiological studies on heavily exposed populations of miners can be fitted reasonably well to a relative risk model, when declines in relative risk with both age at risk evaluation, and time since exposure, are incorporated. Smoking seems to act synergistically. A comparison of the major radon risk projections shows considerable discrepancies in the best estimates of risk, indicating that the uncertainties remain large.

Mortality from respiratory cancer and other causes in United Kingdom chromate production workers.

This report updates a 1981 study of mortality at three United Kingdom chromate producing factories, and pays special attention to workers engaged after major plant and process changes were completed during 1958-60. The study covers 2298 payroll workers in post on 1 January 1950 or entering employment up to 30 June 1976 and remaining at least one year, with mortality observed up to 31 December 1988. Expected numbers of deaths were calculated from national death rates adjusted for social class and area differences. At the two largest factories 1422 men starting work before the process changes showed a highly significant excess of deaths from lung cancer (observed deaths/adjusted expected deaths (obs/expA) 175/88.97, adjusted standardised mortality ratio (SMRA) 197). They also had a significant excess of deaths from nasal cancer (obs/expA 4/0.26, SMRA 1538); the four affected men all had over 20 years of employment. Six hundred and seventy seven men starting work after the completion of process changes showed no excess of lung cancer deaths (obs/expA 14/13.7, SMRA 102, 95% confidence interval (95% CI) 56-171), but the possibility of the risk persisting at a reduced level cannot be excluded. The risk among earlier entrants affected men with two or more years of employment and was highest among those working for 10 years or longer (SMRA 225). The relative risk was already raised 5-14 years after first employment; it was highest in the 25-40 year period, but was still raised 50 years after first exposure. The risk showed most clearly at young ages, with a SMRA of 355 for ages under 50 (obs/expA 21/5.91). The excess was greater among men in jobs with high exposure to chromates (obs/expA 151/61.73, SMRA 245) than among men in less exposed jobs (obs/expA 21/19.57, SMRA 107). Less evidence of a lung cancer excess was found among 199 men employed at a third small factory (obs/expA 12/9.91, SMRA 121). No risk was apparent in further groups of 214 salaried works staff (obs/expA 1/2.53), or 95 workers at an adjacent fertiliser plant (obs/expA 3/3.95). No significant excesses of deaths from cancers of other sites were found.

Mortality of Iron Foundry Workers: I. Overall Findings

A retrospective cohort mortality study was conducted among 8147 men and 627 women employed in a gray iron foundry for at least 6 months between 1950 and 1979. More than 1700 deaths occurred during a 35-year period of observation. Standardized mortality ratios (SMRs) for all causes were close to expected values based on the US general population as the standard. The mortality of nonwhite men was significantly increased for lung cancer (SMR 132) and ischemic heart disease (SMR 126). Other moderate, but nonsignificant excesses were noted among nonwhite men for cancers of the stomach, pancreas, and prostate, for diabetes mellitus and pulmonary emphysema, and among white men for cancers of the lung and stomach, gastric and duodenal ulcers, pulmonary emphysema, and suicide. Small mortality increases were observed in both racial groups for cerebrovascular disease. The lack of a trend with time since hire and duration of foundry employment suggests that lung cancer mortality may not be associated with exposure to the foundry environment. Utilizing indirect measures of smoking, it appears that virtually all excess lung cancer deaths among whites and at least some of the excess among nonwhites could be explained by smoking habits. Similarly, smoking may have been responsible for the mortality excesses from emphysema, cerebrovascular diseases, and ischemic heart disease.

Estimates of radiation dose and health risks to the United States population following the Chernobyl nuclear plant accident.

Estimates of both individual and collective doses received by the United States population following the Chernobyl accident have been made by using the data obtained from the U.S. Environmental Protection Agency's Environmental Radiation Ambient Monitoring System. Radionuclides associated with the debris first were measured in precipitation and surface air particulates at Portland, OR and Olympia, WA on 5 May 1986. Iodine-131 was the most consistently measured nuclide in all media, although several Cs and Ru isotopes also were observed. Strontium and any actinides notably were absent from the samples at the lower level of detection. The highest calculated individual-organ dose due to intake during May and June 1986 was 0.52 mSv to the infant thyroid in the state of Washington. This was predominantly (98%) from the ingestion of milk. The maximum U.S. collective dose equivalent to any organ was calculated to be 3,300 person-Sv to the thyroid. Risk estimates project three excess lung cancer deaths and an additional four deaths due to cancers of thyroid, breast and leukemia in the U.S. population over the next 45 y from exposure during the May-June 1986 interval. The only long-lived radionuclide measured in milk samples following the accident was 137Cs. We estimate 20 excess fatalities from the ingestion of 137Cs in milk during all subsequent years, with six of these due to lung cancer and the majority of the remainder distributed approximately equally among cancers of the thyroid, breast, liver and leukemia. A total of 100 excess fatalities from all dietary components was estimated. Because of the uncertainty of risk estimates from data such as those available for this study, all calculated values carry a range of uncertainty from a minimum of one-half the calculated value to a maximum of two times the calculated value. The estimated excess fatalities given above may be compared with corresponding projected cancer mortality from all other causes: 41,000 fatalities from thyroid cancer and 3,800,000 fatalities from lung cancer are estimated to occur within the U.S. population during the next 45 y.

Estimates of lifetime lung cancer risks resulting from Rn progeny exposure.

Data on five mining populations exposed to Rn progeny have been used to estimate the lifetime risk of lung cancer resulting from occupational and environmental exposure under current standards. Slopes of dose-response relations for lung cancer show a tendency to decrease with increasing dose. Our best estimate of curvilinearity is given by raising dose to the power 0.92 +/- 0.07, but the improvement in fit beyond simple linearity is not significant. On the other hand, the addition of a cell-killing term significantly improves the fit of the linear model. In any event, linear extrapolation is unlikely to underestimate the excess risk at low doses by more than a factor of 1.5. However, these inferences about curvilinearity are highly subject to error from the choice of reference populations, dosimetry, and latency. Under the linear-cell-killing model, our best estimate of excess relative risk is 2.28 +/- 0.35 per 100 working level month (WLM) (a doubling dose of 44 WLM). Attributable risks in these five studies range from 3.4-17.8 per 10(6) person-yr WLM-1. Risks from Rn progeny appear to interact with age and smoking in a form intermediate between additive and multiplicative. The "relative risk" model is therefore preferable for projecting lifetime risks, but life-table projections are described for a wide variety of assumptions. Our best estimate of the effect of a 50-yr occupational exposure to 4 WLM yr-1 is 130 excess lung cancer deaths per 1000 persons (0.65 per 1000 person-WLM), with a range from 60-250 per 1000. Similar calculations for lifetime exposure to an additional 0.02 working level (WL) beyond normal background produces an estimate of 20 excess lung cancers per 1000 persons.

Serum cholesterol and cancer mortality in the Seven Countries Study.

In the Seven Countries Study, carried out in Finland, Greece, Italy, Japan, The Netherlands, the United States, and Yugoslavia, among 11,325 "healthy" men aged 40-59 years in 15 years, there were 594 cancer deaths. Among 477 cancer deaths five years after cholesterol measurement, there was a significant excess of lung cancer deaths in the bottom 20% of the cholesterol distributions in the populations. Age, blood pressure, smoking habits, occupation, and relative body weight did not help explain this. A U-shaped relationship between cancer and cholesterol was not seen in any population. Trend analysis with various cutting points indicated increasing risk of lung cancer death at cholesterol levels under 170 mg/dl. The 45 men dead from cancer in the first two years had lower cholesterol levels than their compatriots who died from cancer later but they did not differ in relative weight or fatness. In contrast to relationships for individuals within populations, the highest cancer death rates were in northern Europe, where the general level of cholesterol was also highest. Other characteristics of the populations--age, relative weight, smoking habits, blood pressure, physical activity, and vitamin A and ascorbic acid in the diet--did not help in the attempt to understand the regional differences in cancer mortality. There is no evidence that any of the observed cancer-serum cholesterol relationships among or within the populations involve an effect of serum cholesterol concentration on oncogenesis or cancer mortality but the possibility of such an effect cannot be denied.

Mortality among rubber workers: X. Reclaim workers

This study evaluated the mortality experience of 1,352 white and 438 nonwhite men who worked in the rubber-reclaiming division of a large rubber manufacturing company. In comparisons of mortality of white reclaim workers with that of nonreclaim workers rate ratios were 2.7 for esophageal cancer (six observed deaths among reclaim workers), 2.1 for bladder cancer (seven observed deaths), and 4.5 for multiple myeloma (six observed deaths). The excess of bladder cancer among white reclaim workers may be associated with their employment in other high-risk areas of the plant, whereas no such explanation was found for the excesses of esophageal cancer and multiple myeloma. Overall, the lung cancer mortality rate of white reclaim workers was similar to the rate of US white males and other white rubber workers. There was a 50% excess of lung cancer deaths among nonwhite reclaim workers compared with other nonwhite rubber workers. However, this observation is based on small numbers, and no firm conclusions can be reached about the risk of lung cancer associated with reclaim operations in this group of rubber workers.