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] 0.48Ϫ0.59). Neurodegenerative mortality was increased using both underlying cause of death rate files (SMR 2.83, 95% CI 1.36Ϫ5.21) and multiple cause of death (MCOD) rate files (SMR 3.26, 95% CI 1.90Ϫ5.22). Of the neurodegenerative causes, results were elevated (using MCOD rates) for both ALS (SMR 4.31, 95% CI 1.73Ϫ8.87) and AD (SMR 3.86, 95% CI 1.55Ϫ7.95). 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 0.92Ϫ11.7). 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.

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.

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 linemen's 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.