Misty J. Hein

Neurodegenerative causes of death among retired National Football League players

Objective: To analyze neurodegenerative causes of death, specifically Alzheimer disease (AD), Parkinson disease, and amyotrophic lateral sclerosis (ALS), among a cohort of professional football players. Methods: This was a cohort mortality study of 3,439 National Football League players with at least 5 pension-credited playing seasons from 1959 to 1988. Vital status was ascertained through 2007. For analysis purposes, players were placed into 2 strata based on characteristics of position played: nonspeed players (linemen) and speed players (all other positions except punter/kicker). External comparisons with the US population used standardized mortality ratios (SMRs); internal comparisons between speed and nonspeed player positions used standardized rate ratios (SRRs). Results: Overall player mortality compared with that of the US population was reduced (SMR 0.53, 95% confidence interval [CI] 0.48−0.59). Neurodegenerative mortality was increased using both underlying cause of death rate files (SMR 2.83, 95% CI 1.36−5.21) and multiple cause of death (MCOD) rate files (SMR 3.26, 95% CI 1.90−5.22). Of the neurodegenerative causes, results were elevated (using MCOD rates) for both ALS (SMR 4.31, 95% CI 1.73−8.87) and AD (SMR 3.86, 95% CI 1.55−7.95). In internal analysis (using MCOD rates), higher neurodegenerative mortality was observed among players in speed positions compared with players in nonspeed positions (SRR 3.29, 95% CI 0.92−11.7). Conclusions: The neurodegenerative mortality of this cohort is 3 times higher than that of the general US population; that for 2 of the major neurodegenerative subcategories, AD and ALS, is 4 times higher. These results are consistent with recent studies that suggest an increased risk of neurodegenerative disease among football players.

Mortality among a cohort of garment workers exposed to formaldehyde: an update

Aims: To evaluate the mortality experience of 11 039 workers exposed to formaldehyde for three months or more in three garment plants. The mean time weighted average formaldehyde exposure at the plants in the early 1980s was 0.15 ppm but past exposures may have been substantially higher. Methods: Vital status was updated through 1998, and life table analyses were conducted. Results: Mortality from all causes (2206 deaths, standardised mortality ratio (SMR) 0.92, 95% CI 0.88 to 0.96) and all cancers (SMR 0.89, 95% CI 0.82 to 0.97) was less than expected based on US mortality rates. A non-significant increase in mortality from myeloid leukaemia (15 deaths, SMR 1.44, 95% CI 0.80 to 2.37) was observed. Mortality from myeloid leukaemia was greatest among workers first exposed in the earliest years when exposures were presumably higher, among workers with 10 or more years of exposure, and among workers with 20 or more years since first exposure. No nasal or nasopharyngeal cancers were observed. Mortality from trachea, bronchus, and lung cancer (147 deaths, SMR 0.98, 95% CI 0.82 to 1.15) was not increased. Multiple cause mortality from leukaemia was increased almost twofold among workers with both 10 or more years of exposure and 20 years or more since first exposure (15 deaths, SMR 1.92, 95% CI 1.08 to 3.17). Multiple cause mortality from myeloid leukaemia among this group of workers was also significantly increased (8 deaths, SMR 2.55, 95% CI 1.10 to 5.03). Conclusions: Results support a possible relation between formaldehyde exposure and myeloid leukaemia mortality. Previous epidemiological studies supporting a relation between formaldehyde exposure and leukaemia mortality have been primarily of formaldehyde exposed professional groups, not formaldehyde exposed industrial workers. Limitations include limited power to detect an excess for rare cancers such as nasal and nasopharyngeal cancers and lack of individual exposure estimates.

FOLLOW-UP STUDY OF CHRYSOTILE TEXTILE WORKERS: COHORT MORTALITY AND EXPOSURE-RESPONSE

Objectives: This report provides an update of the mortality experience of a cohort of South Carolina asbestos textile workers. Methods: A cohort of 3072 workers exposed to chrysotile in a South Carolina asbestos textile plant (1916–77) was followed up for mortality through 2001. Standardised mortality ratios (SMRs) were computed using US and South Carolina mortality rates. A job exposure matrix provided calendar time dependent estimates of chrysotile exposure concentrations. Poisson regression models were fitted for lung cancer and asbestosis. Covariates considered included sex, race, age, calendar time, birth cohort and time since first exposure. Cumulative exposure lags of 5 and 10 years were considered by disregarding exposure in the most recent 5 and 10 years, respectively. Results: A majority of the cohort was deceased (64%) and 702 of the 1961 deaths occurred since the previous update. Mortality was elevated based on US referent rates for a priori causes of interest including all causes combined (SMR 1.33, 95% CI 1.28 to 1.39); all cancers (SMR 1.27, 95% CI 1.16 to 1.39); oesophageal cancer (SMR 1.87, 95% CI 1.09 to 2.99); lung cancer (SMR 1.95, 95% CI 1.68 to 2.24); ischaemic heart disease (SMR 1.20, 95% CI 1.10 to 1.32); and pneumoconiosis and other respiratory diseases (SMR 4.81, 95% CI 3.84 to 5.94). Mortality remained elevated for these causes when South Carolina referent rates were used. Three cases of mesothelioma were observed among cohort members. Exposure-response modelling for lung cancer, using a linear relative risk model, produced a slope coefficient of 0.0198 (fibre-years/ml) (standard error 0.00496), when cumulative exposure was lagged 10 years. Poisson regression modelling confirmed significant positive relations between estimated chrysotile exposure and lung cancer and asbestosis mortality observed in previous updates of this cohort. Conclusions: This study confirms the findings from previous investigations of excess mortality from lung cancer and asbestosis and a strong exposure-response relation between estimated exposure to chrysotile and mortality from lung cancer and asbestosis.

Polychlorinated Biphenyls and Neurodegenerative Disease Mortality in an Occupational Cohort

Background: Production of polychlorinated biphenyls (PCBs) ended in the United States in the 1970s, but PCBs persist in the environment and are detectable in the blood of approximately 80% of Americans over age 50. PCBs decrease dopamine levels in rats and monkeys. Loss of dopamine is the hallmark of Parkinson disease, a neurodegenerative disease. There are no epidemiologic studies of PCBs and neurodegenerative disease. Methods: We conducted a retrospective mortality study of 17,321 PCB-exposed workers to determine whether mortality from Parkinson disease, dementia, and amyotrophic lateral sclerosis was elevated compared with the U.S. population. All workers had a least 90 days employment in 1 of 3 electrical capacitor plants using PCBs from the 1940s to the 1970s. PCB serum levels from a sample of these workers in the 1970s were approximately 10 times the level of community controls. Results: We found no overall excess of Parkinson disease, amyotrophic lateral sclerosis, or dementia in the PCB-exposed cohort (standardized mortality ratios [SMRs]-1.40, 1.11, and 1.26, respectively, and number of deaths-14, 10, and 28 respectively). However, sex-specific analyses revealed that women had an excess of amyotrophic lateral sclerosis (SMR-2.26; 95% confidence interval [CI] = 1.08–4.15; 10 deaths). Furthermore, among highly exposed women (defined by a job-exposure matrix), we found an excess of Parkinson disease (SMR-2.95; 95% CI = 1.08–6.42; 6 deaths) and dementia (SMR-2.04; 95% CI = 1.12–3.43; 14 deaths). Conclusions: Our data are limited due to small numbers and reliance on mortality rather than incidence data, but are suggestive of an effect of PCBs on neurodegenerative disease for women. The literature does not offer an explanation for why women would be more affected than men by PCB exposure for these outcomes.

Mortality and Exposure Response among 14,458 Electrical Capacitor Manufacturing Workers Exposed to Polychlorinated Biphenyls (PCBs)

Background We expanded an existing cohort of workers (n = 2,588) considered highly exposed to polychlorinated biphenyls (PCBs) at two capacitor manufacturing plants to include all workers with at least 90 days of potential PCB exposure during 1939–1977 (n = 14,458). Causes of death of a priori interest included liver and rectal cancers, previously reported for the original cohort, and non-Hodgkin lymphoma (NHL), melanoma, and breast, brain, intestine, stomach, and prostate cancers, based on other studies. Methods We ascertained vital status of the workers through 1998, and cumulative PCB exposure was estimated using a new job exposure matrix. Analyses employed standardized mortality ratios (SMRs; U.S., state, and county referents) and Poisson regression modeling. Results Mortality from NHL, melanoma, and rectal, breast, and brain cancers were neither in excess nor associated with cumulative exposure. Mortality was not elevated for liver cancer [21 deaths; SMR 0.89; 95% confidence interval (CI), 0.55–1.36], but increased with cumulative exposure (trend p-value = 0.071). Among men, stomach cancer mortality was elevated (24 deaths; SMR 1.53; 95% CI, 0.98–2.28) and increased with cumulative exposure (trend p-value = 0.039). Among women, intestinal cancer mortality was elevated (67 deaths; SMR 1.31; 95% CI, 1.02–1.66), especially in higher cumulative exposure categories, but without a clear trend. Prostate cancer mortality, which was not elevated (34 deaths; SMR 1.04; 95% CI, 0.72–1.45), increased with cumulative exposure (trend p-value = 0.0001). Conclusions This study corroborates previous studies showing increased liver cancer mortality, but we cannot clearly associate rectal, stomach, and intestinal cancers with PCB exposure. This is the first PCB cohort showing a strong exposure–response relationship for prostate cancer mortality.

Pesticide Contamination Inside Farm and Nonfarm Homes

Twenty-five farm (F) households and 25 nonfarm (NF) households in Iowa were enrolled in a study investigating agricultural pesticide contamination inside homes. Air, surface wipe, and dust samples were collected. Samples from 39 homes (20 F and 19 NF) were analyzed for atrazine, metolachlor, acetochlor, alachlor, and chlorpyrifos. Samples from 11 homes (5 F and 6 NF) were analyzed for glyphosate and 2,4-Dichlorophenoxyac etic acid (2,4-D). Greater than 88% of the air and greater than 74% of the wipe samples were below the limit of detection (LOD). Among the air and wipe samples, chlorpyrifos was detected most frequently in homes. In the dust samples, all the pesticides were detected in greater than 50% of the samples except acetochlor and alachlor, which were detected in less than 30% of the samples. Pesticides in dust samples were detected more often in farm homes except 2,4-D, which was detected in 100% of the farm and nonfarm home samples. The average concentration in dust was higher in farm homes versus nonfarm homes for each pesticide. Further analysis of the data was limited to those pesticides with at least 50% of the dust samples above the LOD. All farms that sprayed a pesticide had higher levels of that pesticide in dust than both farms that did not spray that pesticide and nonfarms; however, only atrazine and metolachlor were significantly higher. The adjusted geometric mean pesticide concentration in dust for farms that sprayed a particular pesticide ranged from 94 to 1300 ng/g compared with 12 to 1000 ng/g for farms that did not spray a particular pesticide, and 2.4 to 320 ng/g for nonfarms. The distributions of the pesticides throughout the various rooms sampled suggest that the strictly agricultural herbicides atrazine and metolachlor are potentially being brought into the home on the farmers shoes and clothing. These herbicides are not applied in or around the home but they appear to be getting into the home para-occupationally. For agricultural pesticides, take-home exposure may be an important source of home contamination.

Surface Sampling Methods for Bacillus anthracis Spore Contamination

During an investigation conducted December 17–20, 2001, we collected environmental samples from a U.S. postal facility in Washington, D.C., known to be extensively contaminated with Bacillus anthracis spores. Because methods for collecting and analyzing B. anthracis spores have not yet been validated, our objective was to compare the relative effectiveness of sampling methods used for collecting spores from contaminated surfaces. Comparison of wipe, wet and dry swab, and HEPA vacuum sock samples on nonporous surfaces indicated good agreement between results with HEPA vacuum and wipe samples. However, results from HEPA vacuum sock and wipe samples agreed poorly with the swab samples. Dry swabs failed to detect spores >75% of the time they were detected by wipe and HEPA vacuum samples. Wipe samples collected after HEPA vacuum samples and HEPA vacuum samples after wipe samples indicated that neither method completely removed spores from the sampled surfaces.

An epidemiological study of the role of chrysotile asbestos fibre dimensions in determining respiratory disease risk in exposed workers

Background: Evidence from toxicological studies indicates that the risk of respiratory diseases varies with asbestos fibre length and width. However, there is a total lack of epidemiological evidence concerning this question. Methods: Data were obtained from a cohort mortality study of 3072 workers from an asbestos textile plant which was recently updated for vital status through 2001. A previously developed job exposure matrix based on phase contrast microscopy (PCM) was modified to provide fibre size-specific exposure estimates using data from a re-analysis of samples by transmission electron microscopy (TEM). Cox proportional hazards models were fit using alternative exposure metrics for single and multiple combinations of fibre length and diameter. Results: TEM-based cumulative exposure estimates were found to provide stronger predictions of asbestosis and lung cancer mortality than PCM-based estimates. Cumulative exposures based on individual fibre size-specific categories were all found to be highly statistically significant predictors of lung cancer and asbestosis. Both lung cancer and asbestosis were most strongly associated with exposure to thin fibres (<0.25 μm). Longer (>10 μm) fibres were found to be the strongest predictors of lung cancer, but an inconsistent pattern with fibre length was observed for asbestosis. Cumulative exposures were highly correlated across all fibre size categories in this cohort (0.28–0.99, p values <0.001), which complicates the interpretation of the study findings. Conclusions: Asbestos fibre dimension appears to be an important determinant of respiratory disease risk. Current PCM-based methods may underestimate asbestos exposures to the thinnest fibres, which were the strongest predictor of lung cancer or asbestosis mortality in this study. Additional studies are needed of other asbestos cohorts to further elucidate the role of fibre dimension and type.

Body mass index, playing position, race, and the cardiovascular mortality of retired professional football players.

Concern exists about cardiovascular disease (CVD) in professional football players. We examined whether playing position and size influence CVD mortality in 3,439 National Football League players with ≥ 5 pension-credited playing seasons from 1959 to 1988. Standardized mortality ratios (SMRs) compared player mortality through 2007 to the United States population of men stratified by age, race, and calendar year. Cox proportional hazards models evaluated associations of playing-time body mass index (BMI), race, and position with CVD mortality. Overall player mortality was significantly decreased (SMR 0.53, 95% confidence interval [CI] 0.48 to 0.59) as was mortality from cancer (SMR 0.58, 95% CI 0.46 to 0.72), and CVD (SMR 0.68, 95% CI 0.56 to 0.81). CVD mortality was increased for defensive linemen (SMR 1.42, 95% CI 1.02 to 1.92) but not for offensive linemen (SMR 0.70, 95% CI 0.45 to 1.05). Defensive linemens cardiomyopathy mortality was also increased (SMR 5.34, 95% CI 2.30 to 10.5). Internal analyses found that CVD mortality was increased for players of nonwhite race (hazard ratio 1.69, 95% CI 1.13 to 2.51). After adjusting for age, race, and calendar year, CVD mortality was increased for those with a playing-time BMI ≥ 30 kg/m2 (hazard ratio 2.02, 95% CI 1.06 to 3.85) and for defensive linemen compared to offensive linemen (hazard ratio 2.07, 95% CI 1.24 to 3.46). In conclusion, National Football League players from the 1959 through 1988 seasons had decreased overall mortality but those with a playing-time BMI ≥ 30 kg/m2 had 2 times the risk of CVD mortality compared to other players and African-American players and defensive linemen had higher CVD mortality compared to other players even after adjusting for playing-time BMI.

Update of the NIOSH life table analysis system: A person-years analysis program for the windows computing environment†

BACKGROUND Person-years analysis is a fundamental tool of occupational epidemiology. A life table analysis system (LTAS), previously developed by the National Institute for Occupational Safety and Health, was limited by its platform and analysis and reporting capabilities. We describe the updating of LTAS for the Windows operating system (LTAS.NET) with improved properties. SOFTWARE DEVELOPMENT PROCESS A group of epidemiologists, programmers, and statisticians developed software, platform, and computing requirements. Statistical methods include the use of (indirectly) standardized mortality ratios, (directly) standardized rate ratios, confidence intervals, and P values based on the normal approximation and exact Poisson methods, and a trend estimator for linear exposure-response associations. SOFTWARE FEATURES We show examples using LTAS.NET to stratify and analyze multiple fixed and time-dependent variables. Data import, stratification, and reporting options are highly flexible. Users may export stratified data for Poisson regression modeling. CONCLUSIONS LTAS.NET incorporates improvements that will facilitate more complex person-years analysis of occupational cohort data.