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K Steenland

Publications and source records attributed to K Steenland.

At least 19 recordsLinked to original sources
PubMed1992

Use of multiple-cause mortality data in epidemiologic analyses: US rate and proportion files developed by the National Institute for Occupational Safety and Health and the National Cancer Institute.

The authors have created US mortality rates (age, sex, race, and calendar-time specific) and proportions, using multiple cause-of-death data, for the years 1960-1989. Multiple cause-of-death data include the usual underlying cause of death from the death certificate as well as contributory causes and other significant conditions. US multiple-cause rates and proportions enable the user to calculate the expected occurrences of disease on the death certificates of a cohort under study. There is an average of 2.66 causes and/or contributory conditions listed on US death certificates, increasing over time from 2.54 in the 1960s to 2.76 in the 1980s. The ratio of multiple-cause listings to underlying cause listings varies by disease, from low ratios for cancers to high ratios for diseases such as diabetes, arthritis, prostate disease, hypertension, pneumoconiosis, and renal disease. Use of these data is illustrated with two cohorts. Multiple-cause analysis (but not underlying cause analysis) revealed twofold significant excesses of renal disease and arthritis among granite cutters. For workers exposed to dioxin, neither multiple-cause nor underlying cause analysis indicated any excess of diabetes, an outcome of a priori interest. Good candidates for multiple-cause analysis are diseases that are of long duration, not necessarily fatal, yet serious enough to be listed on the death certificate.

Cause of Death↗
PubMed1992

Passive smoking and the risk of heart disease.

OBJECTIVE: This paper reviews the evidence that exposure to environmental tobacco smoke (ETS) increases the risk of heart disease death among persons who have never smoked (never-smokers). The annual number of heart disease deaths in the United States attributable to ETS is estimated, as is the individual risk of heart disease death for exposed never-smokers. DATA SOURCES: Nine epidemiologic studies and numerous experimental studies are available to evaluate the association of ETS and heart disease. DATA SYNTHESIS: The relative risk for never-smokers living with current or former smokers, compared with never-smokers living with nonsmokers, has ranged from 0.9 to 3.0 in nine studies. Seven studies were positive, one was positive for women but not men, and one was negative. Several studies have shown a dose-response relationship and have controlled for other risk factors. Evidence from experimental studies suggests that ETS can damage the cardiovascular system, via both short-term and long-term mechanisms. Assuming that the observed heart disease risk for those exposed to ETS is not an artifact of misclassification or confounding, approximately 35,000 to 40,000 deaths from ischemic heart disease among never-smokers and long-term former smokers are estimated to have occurred annually in the United States as a result of ETS exposure in the early 1980s. An individual male never-smoker living with a current or former smoker is estimated to have an approximately 9.6% chance of dying of ischemic heart disease by the age of 74 years, compared with a 7.4% chance for a male never-smoker living with a nonsmoker. The corresponding lifetime risks for women are 6.1% and 4.9%. CONCLUSIONS: The public health burden due to ETS exposure is likely to be much greater for heart disease than for lung cancer, which has been the focus of most debate to date. Individual lifetime excess risks of heart disease death due to ETS of one to three per 100 can be compared with much lower excess risks of one death per 100,000, which are often used in determining environmental limits for other toxins. Exposure to ETS is not currently regulated at the federal level, except for domestic air traffic.

Adult↗
PubMed1992

A mortality study of workers at seven beryllium processing plants.

The International Agency for Research on Cancer (IARC) has found that the evidence for the carcinogenicity of beryllium is sufficient based on animal data but "limited" based on human data. This analysis reports on a retrospective cohort mortality study among 9,225 male workers employed at seven beryllium processing facilities for at least 2 days between January 1, 1940, and December 31, 1969. Vital status was ascertained through December 31, 1988. The standardized mortality ratio (SMR) for lung cancer in the total cohort was 1.26 (95% confidence interval [CI] = 1.12-1.42); significant SMRs for lung cancer were observed for two of the oldest plants located in Lorain, Ohio (SMR = 1.69; 95% CI = 1.28-2.19) and Reading, Pennsylvania (SMR = 1.24; 95% CI = 1.03-1.48). For the overall cohort, significantly elevated SMRs were found for "all deaths" (SMR = 1.05; 95% CI = 1.01-1.08), "ischemic heart disease" (SMR = 1.08; 95% CI = 1.01-1.14), "pneumoconiosis and other respiratory diseases" (SMR = 1.48; 95% CI = 1.21-1.80), and "chronic and unspecified nephritis, renal failure, and other renal sclerosis" (SMR = 1.49; 95% CI = 1.00-2.12). Lung cancer SMRs did not increase with longer duration of employment, but did increase with longer latency (time since first exposure). Lung cancer was particularly elevated (SMR = 3.33; 95% CI = 1.66-5.95) among workers at the Lorain plant with a history of (primarily) acute beryllium disease, which is associated with very high beryllium exposure. The lung cancer excess was not restricted to plants operating in the 1940s, when beryllium exposures were known to be extraordinarily high. Elevated lung cancer SMRs were also observed for four of the five plants operating in the 1950s for workers hired during that decade. Neither smoking nor geographic location fully explains the increased lung cancer risk. Occupational exposure to beryllium compounds is the most plausible explanation for the increased risk of lung cancer observed in this study. Continued mortality follow-up of this cohort will provide a more definitive assessment of lung cancer risk at the newer plants and among cohort members hired in the 1950s or later at the older plants. Further clarification of the potential for specific beryllium compounds to induce lung cancer in humans, and the possible contribution of other exposures in specific processes at these plants, would require a nested case-control study. We are currently assessing whether available industrial hygiene data would support such an analysis.

Berylliosis↗
PubMed1992

Colon and stomach cancer mortality among automotive wood model makers.

Automotive wood model makers have been reported to be at excess risk for colon and other cancers in recent epidemiologic studies. To further explore these risks, we conducted a retrospective cohort mortality study, with follow-up from 1940 through 1984, of 2294 white male wood model makers employed at any time until 1980 by three US auto makers. Using US mortality rates for comparison, we found elevated standardized mortality ratios of 1.2 (95% CI, 0.8-1.9) for colon cancer and 1.6 (95% CI, 0.9-2.6) for stomach cancer. We also conducted nested case-control studies for 20 colon and 17 stomach cancer cases and 543 age-matched controls. We found no trend of increased risk for colon or stomach cancer mortality with increased exposure to wood dust or to duration employed in wood model making.

Automobiles↗
PubMed1992

The mortality of lead smelter workers: an update.

OBJECTIVES: Mortality studies of lead workers have shown excesses of nonmalignant renal disease and cerebrovascular disease. Animal studies and one human study have shown excess kidney cancer. We have updated a mortality study of male lead smelter workers (n = 1990). METHODS: An analysis was conducted using standard life table techniques. The updated analysis added 11 years of follow-up and 363 new deaths. RESULTS: The original study had found elevated but nonsignificant risks for kidney cancer, stroke, and nonmalignant renal disease, probably attributable to lead exposure. Deaths from accidents and nonmalignant respiratory disease were significantly elevated, but probably not as a result of lead exposure. In the updated study, no new deaths from nonmalignant renal disease occurred (9 observed, standardized mortality ratio = 1.21). Three more deaths from kidney cancer were observed, yielding a standardized mortality ratio of 1.93 (9 observed, 95% CI = 0.88, 3.67), which increased for those who had worked in areas with the highest lead exposure (8 observed, standardized mortality ratio = 2.39, 95% CI = 1.03, 4.71). Cerebrovascular disease remained elevated for those with more than 20 years of exposure (26 observed, standardized mortality ratio = 1.41, 95% CI = 0.92, 2.07). CONCLUSIONS: This cohort with high lead exposure showed a diminishing excess of death from nonmalignant renal disease, a continued excess from kidney cancer, and an excess of cerebrovascular disease only in those with longest exposure to lead.

Accidents, Occupational↗
PubMed1991

Lung cancer incidence among patients with beryllium disease: a cohort mortality study.

We have conducted a cohort mortality study on 689 patients with beryllium disease who were included in a case registry. An earlier mortality study on 421 of these patients was limited to males and resulted in a determination of a nonsignificant twofold lung cancer excess based on only seven lung cancer deaths. We have extended this earlier study by including females and by adding 13 years of follow-up. Comparison of the 689 beryllium disease patients with the U.S. population resulted in a lung cancer standardized mortality ratio (SMR) of 2.00 (95% confidence interval = 1.33-2.89) based on 28 observed lung cancer deaths. Adjustment for smoking did not change these results. All causes of mortality were also significantly elevated (SMR = 2.19), largely because of the very high rate of deaths due to pneumoconioses (primarily beryllium disease) (SMR = 34.23; 158 deaths). No other causes of death were significantly elevated. The excess of lung cancer was consistent for both sexes and did not appear to increase with duration of exposure to beryllium or with time elapsed since first exposure to this element. The case registry included those with acute beryllium disease, which resembles a chemical pneumonitis, and those with chronic beryllium disease, which resembles other pneumoconioses. The lung cancer excess was more pronounced among those with acute disease (SMR = 2.32) than among those with chronic disease (SMR = 1.57).

Adult↗
PubMed1991

Mortality among workers exposed to ethylene oxide.

BACKGROUND: Ethylene oxide is a sterilant gas that causes leukemia and other cancers in animals. Studies in Sweden have shown an excess of leukemia and stomach cancer in humans exposed to ethylene oxide, but other studies have generally failed to confirm these findings. METHODS: We conducted a study of mortality in 18,254 U.S. workers exposed to ethylene oxide at 14 plants producing sterilized medical supplies and spices. The subjects averaged 4.9 years of exposure to the gas and 16 years of follow-up. The exposure levels in recent years averaged 4.3 ppm (eight-hour time-weighted adjusted exposure) for sterilizer operators and 2.0 ppm for other workers. The levels in earlier years are likely to have been several times higher. Mortality in this cohort was compared with that in the general U.S. population. RESULTS: Overall there was no significant increase in mortality from any cause in the study cohort. The standardized mortality ratios (SMRs) were 0.97 for leukemia (95 percent confidence interval, 0.52 to 1.67; 13 deaths observed), 1.06 for all hematopoietic cancers (95 percent confidence interval, 0.75 to 1.47; 36 deaths), and 0.94 for stomach cancer (95 percent confidence interval, 0.45 to 1.70; 11 deaths). Analyses according to job category and according to the duration of exposure showed no excess in cancers, as compared with the rate in the general population, but there was a significant trend toward increased mortality with increasing lengths of time since the first exposure for all hematopoietic cancers. The rate of death from hematopoietic cancer (especially non-Hodgkin's lymphoma) was significantly increased among men (SMR, 1.55; 27 deaths). Mortality from leukemia in recent years (1985 through 1987) was significantly increased among men (SMR, 3.45; 5 deaths). CONCLUSIONS: For the entire cohort, there was no increase in mortality from hematopoietic cancer. There was a slight but significant increase among men, however. Among men and women combined, there was a trend toward an increased risk of death from hematopoietic cancer with increasing lengths of time since the first exposure to ethylene oxide.

Cohort Studies↗
PubMed1991

Lung cancer in mild steel welders.

To investigate lung cancer risk, the authors conducted a historical cohort mortality study of 4,459 mild steel welders who had been employed at three midwestern plants which manufactured heavy equipment. Follow-up began in the mid-1950s and extended through 1988. All welders had at least 2 years welding experience (average duration, 8.5 years). This cohort had no occupational exposure to asbestos or stainless steel fumes (containing nickel and chromium), two potential confounders in previous welders studies. A comparison population of 4,286 nonwelders, all with at least 2 years employment at the same plants, was also studied. Nonwelders had never been welders and were allowed to have no more than 90 days employment as a painter, foundryman, or machinist. Sampling data collected from 1974-1987 indicated that welders were exposed to 6-7 mg/m3 of total particulate and 3-4 mg/m3 of iron oxide, while nonwelders had negligible exposures to welding fumes. When compared with the United States population, both welders and nonwelders had elevated rates for lung cancer (standardized mortality ratios (SMRs): welders, SMR = 1.07; nonwelders, SMR = 1.17), but neither SMR was significantly elevated. Limited smoking data based on a 1985 survey indicated that both welders and nonwelders smoked more than the United States population, possibly accounting for part of their elevated lung cancer rates. There was no trend of increased risk for welders with increased duration of exposure. The only other cause of death significantly elevated was emphysema among welders. Nonmalignant respiratory disease was not elevated for welders (SMR = 0.96). When welders were compared with nonwelders directly for lung cancer, the rate ratio was 0.90.

Cause of Death↗
PubMed1991

Cancer mortality in workers exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin.

BACKGROUND: In both animal and epidemiologic studies, exposure to dioxin (2,3,7,8-tetrachlorodibenzo-p-dioxin, or TCDD) has been associated with an increased risk of cancer. METHODS: We conducted a retrospective cohort study of mortality among the 5172 workers at 12 plants in the United States that produced chemicals contaminated with TCDD. Occupational exposure was documented by reviewing job descriptions and by measuring TCDD in serum from a sample of 253 workers. Causes of death were taken from death certificates. RESULTS: Mortality from several cancers previously associated with TCDD (stomach, liver, and nasal cancers, Hodgkin's disease, and non-Hodgkin's lymphoma) was not significantly elevated in this cohort. Mortality from soft-tissue sarcoma was increased, but not significantly (4 deaths; standardized mortality ratio [SMR], 338; 95 percent confidence interval, 92 to 865). In the subcohort of 1520 workers with greater than or equal to 1 year of exposure and greater than or equal to 20 years of latency, however, mortality was significantly increased for soft-tissue sarcoma (3 deaths; SMR, 922; 95 percent confidence interval, 190 to 2695) and for cancers of the respiratory system (SMR, 142; 95 percent confidence interval, 103 to 192). Mortality from all cancers combined was slightly but significantly elevated in the overall cohort (SMR, 115; 95 percent confidence interval, 102 to 130) and was higher in the subcohort with greater than or equal to 1 year of exposure and greater than or equal to 20 years of latency (SMR, 146; 95 percent confidence interval, 121 to 176). CONCLUSIONS: This study of mortality among workers with occupational exposure to TCDD does not confirm the high relative risks reported for many cancers in previous studies. Conclusions about an increase in the risk of soft-tissue sarcoma are limited by small numbers and misclassification on death certificates. Excess mortality from all cancers combined, cancers of the respiratory tract, and soft-tissue sarcoma may result from exposure to TCDD, although we cannot exclude the possible contribution of factors such as smoking and occupational exposure to other chemicals.

Bronchial Neoplasms↗
PubMed1991

Quantitative determination of trucking industry workers' exposures to diesel exhaust particles.

As part of a case-control mortality study of trucking industry workers, exposures to diesel aerosol were measured among the four major presumably exposed job groups (road drivers, local drivers, dock workers, and mechanics) in the industry. Eight industrial hygiene surveys were conducted during both warm and cold weather at eight U.S. terminals and truck repair shops. A single-stage personal impactor was used to sample submicrometer-sized diesel particles on quartz fiber filters. Laboratory and field studies demonstrated that the elemental carbon content of the particles is a useful and practical marker of exposure to vehicular diesel exhaust. A thermal-optical analysis technique was used to determine the concentration of elemental carbon in the filter samples. Overall geometric mean exposures to submicrometer-sized elemental carbon ranged from 3.8 micrograms/m3 in road (long distance) drivers (N = 72) to 13.8 micrograms/m3 in dock workers (N = 75). Geometric mean background area concentrations, measured in the same cities where workers were sampled, were 2.5 micrograms/m3 on major highways (N = 21) and 1.1 micrograms/m3 in residential areas (N = 23). A factorial analysis of variance indicated that exposures in two job groups, dock workers (particularly those exposed primarily via diesel forklift trucks, introduced relatively recently) and mechanics (working in poorly ventilated shops during cold weather), were significantly higher than background concentrations and were significantly higher than the exposures in the local and road drivers. The exposures of the truck drivers could not be distinguished from background highway concentrations but were significantly higher than background concentrations in residential areas.

Air Pollutants, Occupational↗
PubMed1991

The importance of employment status in occupational cohort mortality studies.

Person-years at risk in occupational cohort mortality studies may be defined as "active" (when a person is working) or "inactive" (after a person has left employment at the plant under study). To investigate the effects of employment status (active/inactive) both across studies and within them, we have analyzed ten large cohort studies conducted by the National Institute for Occupational Safety and Health in which no occupational risk had been observed. These ten data sets included 89,376 workers, 1,984,505 person-years, and 18,840 deaths. In these ten studies, the SMR for all causes was positively correlated with the percentage of inactive person-years in the study (r = 0.57, p = 0.08). Considering only inactive person-years, the all-causes SMR was 1.12 (approximately 1.25 before age 65, dropping to 1.00 after age 65). Stratification of inactive person-years by time-since-last-employment showed markedly increased mortality during the first year following employment. The all-causes SMR during active person-years was 0.40 and was fairly constant across age categories. With active and inactive person-years combined, a strong negative trend in SMRs with duration of employment was observed for all causes and for heart disease. These trends were not apparent when person-years were stratified by employment status. These results indicate that investigators should evaluate the effects of employment status when comparing SMRs between multiple cohorts or when interpreting trends in rate ratios within cohorts.

Cohort Studies↗
PubMed1990

New developments in the Life Table Analysis System of the National Institute for Occupational Safety and Health.

In the 1970s, the National Institute for Occupational Safety and Health developed a Life Table Analysis System to analyze occupational cohort studies. We have updated the original system by adding two new features: direct standardization with a test for linear trend, and analyses by lagged exposure (either duration of exposure or cumulative exposure). We have also updated US reference rates through 1989. The updated systems and documentation (version F) are available upon request. In collaboration with the National Cancer Institute, we have also developed multiple cause-of-death rate files, which consider contributory as well as underlying cause. These files (also available upon request) will enable investigators to derive the expected prevalence of diseases at death, which can then be compared with the observed prevalence in an exposed cohort. Work is currently underway to produce a personal computer version of the Life Table Analysis System.

Cause of Death↗
PubMed1989

Lung cancer mortality among nonsmoking uranium miners exposed to radon daughters.

Radon daughters, both in the workplace and in the household, are a continuing cause for concern because of the well-documented association between exposure to radon daughters and lung cancer. To estimate the risk of lung cancer mortality among nonsmokers exposed to varying levels of radon daughters, 516 white men who never smoked cigarettes, pipes, or cigars were selected from the US Public Health Service cohort of Colorado Plateau uranium miners and followed up from 1950 through 1984. Age-specific mortality rates for nonsmokers from a study of US veterans were used for comparison. Fourteen deaths from lung cancer were observed among the nonsmoking miners, while 1.1 deaths were expected, yielding a standardized mortality ratio of 12.7 with 95% confidence limits of 8.0 and 20.1. These results confirm that exposure to radon daughters in the absence of cigarette smoking is a potent carcinogen that should be strictly controlled.

Adult↗
PubMed1989

Further follow-up and adjustment for smoking in a study of lung cancer and acid mists.

Follow-up of a cohort of 1,165 steelworkers exposed to acid mists has been extended from 1981 to early 1986 for most cohort members, and information on smoking has also been collected. We obtained an SMR for lung cancer (unadjusted for smoking) of 1.56 (95% CI 1.12-2.11, 41 observed). For those with 20 years or more since first exposure, the SMR was 1.72 (1.21-2.39). However, no trend was found with duration of exposure. To adjust for smoking, we used an indirect adjustment as suggested by Axelson to account for the fact that the exposed cohort smoked slightly more than the U.S. referent population. The SMR for the whole cohort dropped to 1.36 (0.97-1.84), while for those with more than 20 years since first exposure, the SMR was 1.50 (1.05-2.07). These results indicate that an excess risk for lung cancer persists after control for confounding by smoking.

Aerosols↗
PubMed1989

A computer program for incidence density sampling of controls in case-control studies nested within occupational cohort studies.

A nested case-control study is a case-control study performed with a cohort study. The nested case-control design is useful because the number of study subjects for whom risk factor information is needed is smaller than in the original cohort study. The approach is especially helpful when collection of data is expensive or time consuming, as when it is necessary to contact subjects or next of kin. Selection of controls in nested case-control studies is best performed with a method called "incidence density" sampling. An approach to incidence density sampling that yields a valid estimate of the rate ratio is sampling without replacement from noncases at the time of case occurrence. To implement this approach, a system of computer programs was written that randomly selects a user defined number of controls for each case. The case-control data produced by this program can be analyzed by conditional logistic regression.

Cohort Studies↗