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.
BackgroundApproximately 40,000 rescue and recovery workers were exposed to caustic dust and toxic pollutants following the 11 September 2001 attacks on the World Trade Center (WTC). These workers included traditional first responders, such as firefighters and police, and a diverse population of construction, utility, and public sector workers.MethodsTo characterize WTC-related health effects, the WTC Worker and Volunteer Medical Screening Program was established. This multicenter clinical program provides free standardized examinations to responders. Examinations include medical, mental health, and exposure assessment questionnaires; physical examinations; spirometry; and chest X rays.ResultsOf 9,442 responders examined between July 2002 and April 2004, 69% reported new or worsened respiratory symptoms while performing WTC work. Symptoms persisted to the time of examination in 59% of these workers. Among those who had been asymptomatic before September 11, 61% developed respiratory symptoms while performing WTC work. Twenty-eight percent had abnormal spirometry; forced vital capacity (FVC) was low in 21%; and obstruction was present in 5%. Among nonsmokers, 27% had abnormal spirometry compared with 13% in the general U.S. population. Prevalence of low FVC among nonsmokers was 5-fold greater than in the U.S. population (20% vs. 4%). Respiratory symptoms and spirometry abnormalities were significantly associated with early arrival at the site.ConclusionWTC responders had exposure-related increases in respiratory symptoms and pulmonary function test abnormalities that persisted up to 2.5 years after the attacks. Long-term medical monitoring is required to track persistence of these abnormalities and identify late effects, including possible malignancies. Lessons learned should guide future responses to civil disasters.
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.
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