Everett J. Lehman

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.

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.

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.

Suicide mortality among retired National Football League players who played 5 or more seasons

Background: There is current disagreement in the scientific literature about the relationship between playing football and suicide risk, particularly among professional players in the National Football League (NFL). While some research indicates players are at high risk of football-related concussions, which may lead to chronic traumatic encephalopathy and suicide, other research finds such a connection to be speculative and unsupported by methodologically sound research. Purpose: To compare the suicide mortality of a cohort of NFL players to what would be expected in the general population of the United States. Study Design: Cohort study; Level of evidence, 3. Methods: A cohort of 3439 NFL players with at least 5 credited playing seasons between 1959 and 1988 was assembled for statistical analysis. The vital status for this cohort was updated through 2013. Standardized mortality ratios (SMRs), the ratio of observed deaths to expected deaths, and 95% CIs were computed for the cohort; 95% CIs that excluded unity were considered statistically significant. For internal comparison purposes, standardized rate ratios were calculated to compare mortality results between players stratified into speed and nonspeed position types. Results: Suicide among this cohort of professional football players was significantly less than would be expected in comparison with the United States population (SMR = 0.47; 95% CI, 0.24-0.82). There were no significant differences in suicide mortality between speed and nonspeed position players. Conclusion: There is no indication of elevated suicide risk in this cohort of professional football players with 5 or more credited seasons of play. Because of the unique nature of this cohort, these study results may not be applicable to professional football players who played fewer than 5 years or to college or high school players.

Epidemiology of neurodegeneration in American-style professional football players

The purpose of this article is to review the history of head injuries in relation to American-style football play, summarize recent research that has linked football head injuries to neurodegeneration, and provide a discussion of the next steps for refining the examination of neurodegeneration in football players. For most of the history of football, the focus of media reports and scientific studies on football-related head injuries was on the acute or short-term effects of serious, traumatic head injuries. Beginning about 10 years ago, a growing concern developed among neurologists and researchers about the long-term effects that playing professional football has on the neurologic health of the players. Autopsy-based studies identified a pathologically distinct neurodegenerative disorder, chronic traumatic encephalopathy, among athletes who were known to have experienced concussive and subconcussive blows to the head during their playing careers. Football players have been well represented in these autopsy findings. A mortality study of a large cohort of retired professional football players found a significantly increased risk of death from neurodegeneration. Further analysis found that non-line players were at higher risk than line players, possibly because of an increased risk of concussion. Although the results of the studies reviewed do not establish a cause effect relationship between football-related head injury and neurodegenerative disorders, a growing body of research supports the hypothesis that professional football players are at an increased risk of neurodegeneration. Significant progress has been made in the last few years on detecting and defining the pathology of neurodegenerative diseases. However, less progress has been made on other factors related to the progression of those diseases in football players. This review identifies three areas for further research: (a) quantification of exposure - a consensus is needed on the use of clinically practical measurements of blows to the head among football players; (b) genetic susceptibility factors - a more rigorous set of unbiased epidemiological and clinical studies is needed before any causal relationships can be drawn between suspected genetic factors, head injury, and neurodegeneration; and (c) earlier detection and prevention of neurodegenerative diseases.

Bloodborne pathogen risk reduction activities in the body piercing and tattooing industry

BACKGROUND This study examines how well regulations for bloodborne pathogens (BBPs), established primarily to reduce exposure risk for health care workers, are being followed by workers and employers in the tattooing and body piercing industry. METHOD Twelve shops performing tattooing and/or body piercing (body art) in Pennsylvania and Texas were assessed for compliance with 5 administrative and 10 infection control standards for reducing exposure to BBPs. RESULTS All shops demonstrated compliance with infection control standards, but not with administrative standards, such as maintaining an exposure control plan, offering hepatitis B vaccine, and training staff. Shops staffed with members of professional body art organizations demonstrated higher compliance with the administrative standards. Shops in locations where the body art industry was regulated and shops in nonregulated locations demonstrated similar compliance, as did contractor- and employee-staffed shops. CONCLUSIONS Regulations to control occupational exposure to BBPs have been in place since 1991. This study corroborates noncompliance with some standards within the body art industry reported by previous studies. Without notable enforcement, regulation at national, state, or local levels does not affect compliance. In this study, the factor most closely associated with compliance with administrative regulations was the artists membership in a professional body art association.

Proportionate mortality study of the united association of Journeymen and Apprentices of the plumbing and pipe fitting industry

BACKGROUND This study examined causes of deaths among unionized plumbers, pipefitters and allied trades. METHODS Deaths of union members from the years 1971, 1979, 1987, and 1995 were selected as a representative sample from a computer file provided by the union. These years provided 15,411 deaths for proportionate mortality ratio (PMR) analysis. RESULTS PMRs for lung cancer and asbestosis were significantly elevated compared to U.S. white males. PMRs for chronic disease of the endocardium and cardiomyopathy were also elevated. Elevations were not observed in other a priori causes: laryngeal cancer, lymphatic cancer, and neurological disorders. PMRs for transportation accidents for pipe/steam-fitters were elevated in 1971 and 1979, but not in 1987 or 1995. CONCLUSION Despite the limitations of a PMR analysis, study results indicate mortality related to asbestos exposure is, and will continue to be, an area of concern for members of the union.

Mortality of lead smelter workers: A follow-up study with exposure assessment

BACKGROUND Lead exposure has been linked to impaired renal function and kidney failure. High lead exposures have been associated with increased mortality from certain cancers, hypertension, cardiovascular disease, and amyotrophic lateral sclerosis (ALS). METHODS We extended vital status follow-up on a cohort of 1,990 lead smelter workers by 25 years and computed standardized mortality ratios and rate ratios (RR) stratified by cumulative lead exposure. RESULTS The update added 13,823 person-years at risk and 721 deaths. Increased risk of mortality was observed for the a priori outcomes of lung cancer, cardiovascular disease (including cerebrovascular disease), chronic kidney disease, and ALS. However, of these outcomes, only cardiovascular, cerebrovascular, and chronic kidney diseases were associated with a positive exposure-response in RR analyses. CONCLUSIONS This study reaffirms the association of lead exposure with cardiovascular and kidney diseases; however, increased mortality observed for certain cancers is not likely to be due to lead exposure. Am. J. Ind. Med. 59:979-986, 2016. Published 2016. This article is a U.S. Government work and is in the public domain in the USA.

Neurodegenerative causes of death among retired National Football League playersAuthor Response

Lehman et al.1 reported an increased risk of death from amyotrophic lateral sclerosis (ALS) and AD among retired National Football League players, especially among players in speed positions. A 40-fold higher prevalence rate for ALS was reported in football players who played after 1960.2 There was no risk of ALS in high school students who played football from 1946 to 1956, when headgear was less protective than today.3 I am surprised that Lehman et al. discussed only the causal hypothesis of recurrent traumatic brain injuries or concussions whereas other possible etiologic factors were not mentioned (i.e., intense physical activity, use of drugs, exposure to neurotoxins).1 In Italy, a 12-fold higher risk of death from ALS in professional soccer players was observed but not from AD or Parkinson disease.4 In 6 of 8 subjects, age at death was younger than 59 years.4 The risk of ALS was also significantly increased for midfielders but not for other positions.5 Lehman et al. found a different pattern of risk of death for ALS and AD vs Parkinson disease1 so this may indicate a different origin for these diseases. It might be important to know the mean age at death of players deceased from ALS and AD in this study.1 Further cohort studies in professional players of different sports should be conducted with particular attention to the position of players because this could supply important etiologic cues.