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Thunderstorm Asthma, Relative Anemia, and Football Carnage

Eichner, E. Randy MD, FACSM

Current Sports Medicine Reports: May/June 2017 - Volume 16 - Issue 3 - p 116–117
doi: 10.1249/JSR.0000000000000349
Pearls and Pitfalls

Address for correspondence: E. Randy Eichner, MD, FACSM, 321 Baudin Way, Sonoma, CA 95476; E-mail:

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In this column, I cover a unique cause of “mass-casualty asthma,” revisit the perennial issue of gauging and managing iron status and anemia in female athletes, and ponder the continuing carnage from college football conditioning. I begin with thunderstorm asthma. Here is a hint as to cause: “The answer, my friend, is blowin’ in the wind.”

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Thunderstorm Asthma

Last November, thunderstorm asthma killed at least eight people in Australia. Hundreds were rushed to hospitals in Victoria with breathing problems during and soon after the storm. In one 4-h period, Ambulance Victoria got more than 1900 calls and deployed an extra 60 ambulances. In a survey by the University of Melbourne, of 2588 respondents, 74% said they experienced an asthma attack tied to the storm, and 32% said it was their first bout of asthma. Among the dead were an 18-yr-old man described as “the fittest” among his gym class and a 35-yr-old woman who died in the arms of family after waiting more than 40 min for an ambulance (7).

Thunderstorm asthma is a “freak illness” from a rare combination of weather and pollen. The pollen can be from grass, trees, or fungal spores. The Victoria “epidemic” of asthma was from rye grass pollen. Normally, rye pollen is trapped by nasal hairs and does not enter the lungs. But with the rare convergence of high pollen count, high heat and humidity, and a thunderstorm, rye grains absorb water and explode into many tiny pieces that are swept up and held close to the ground by downdraft and outflow winds. This “perfect storm” triggers asthma as allergic subjects inhale tiny rye allergens deep into their lungs (8).

Risk factors for severe thunderstorm asthma include: 1) allergy to grass pollen, 2) history of hay fever, 3) poor control of baseline asthma, and 4) being outdoors (or indoors with open windows) during the storm (6). In August 2001, Rashidi Wheeler, aged 22 yr, who had asthma, and was a senior safety football player at Northwestern University, collapsed and soon died from asthma, trying to complete a grueling “voluntary” drill of 28 conditioning sprints (4). A torrential rainstorm occurred the night before. I have seen football players and runners struggle more than usual with their asthma when training hard soon after thunderstorms.

Team physicians and athletic trainers should be alert to the possibility of thunderstorm asthma. In some cases, it may be the athlete's first-ever attack of asthma. For athletes with known asthma or hay fever, an intense conditioning drill outdoors soon after a thunderstorm is a bad idea. Depending in part on baseline control of their asthma, some athletes should shelter indoors during the thunderstorm and maybe avoid any workout soon thereafter (2).

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Relative Anemia

An informative new study keys on iron deficiency anemia in female athletes. In a retrospective chart review of hemoglobin (Hb) and serum ferritin (Fer) values of varsity athletes between 2002 and 2014 at a large public university, anemia in female athletes was defined as Hb < 11.6 g·dL−1, and iron deficiency was defined as Fer < 20 ng·mL−1. By this definition, only 5.7% of incoming female athletes were anemic, with no statistically significant variation by sport. Of all female athletes tested at any time, 4.3% were anemic, whereas 33% were iron deficient. The median annual cost for all this iron and anemia testing (including some male athletes) exceeded US $20,000.

The authors discuss the long-debated vagaries of iron status and performance in female athletes. Because only about 1 in 20 incoming female athletes was anemic, and they found no difference by sport, they suggest that targeted screening for certain teams may not be the way to go, and that nutritional education (not iron supplements for all athletes) could be a low-cost, low-risk way to optimize iron status. Their well-taken conclusion is that each institution should thoughtfully select and routinely reassess their screening practices (10).

One limitation of this study is that anemia in female athletes was defined as Hb < 11.6 g·dL−1, based on a hospital-laboratory cutoff value, from population-based norms for healthy adults in the region. With a cutoff value this low, odds are many cases of mild anemia were missed. A clue is that whereas only 1 in 20 female athletes was “anemic,” one in three was “iron deficient,” as defined by Fer < 20 ng·mL−1. In my experience, most female athletes with Fer < 20 ng·mL−1 are anemic, for them.

Mild anemia is relative. Not only does the lower limit of normal for Hb level vary by sex, by age, by altitude, and even by heritage (lower in African-Americans than in whites), but what is anemic for me may not be anemic for you. It is better to define mild anemia not relative to a laboratory cutoff based on a “population norm,” but relative to your normal baseline. Thus, a female athlete with a Hb level of 12 g·dL−1—or even 13 g·dL−1—is anemic—and it will sap her athletic stamina—if her normal Hb level is 14 g·dL−1. Female athletes with mild or relative anemia were missed in this new study. No magic cutoff defines anemia (3).

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Football Carnage

A vital new sports medicine article begins by quoting Sir Roger Bannister and then details the continuing carnage in American football conditioning (1). Bannister, the acclaimed English neurologist who, while a medical student in 1954, ran the first sub 4-min mile, said: “The notion that courage and esprit de corps can somehow defeat the principles of physiology is not only wrong but dangerously wrong.” It seems, alas, that few football coaches read or heed Bannister.

The new article covers the carnage: From 2000 through 2016 in National Collegiate Athletic Association (NCAA) football, 33 players have died in their sport: 27 nontraumatic deaths versus only six traumatic deaths. In other words, it is now 4.5 times more likely that a player will die from training for football in the offseason than from trauma while playing football. Almost all the nontraumatic deaths were from rigorous or extreme conditioning drills, usually in offseason. The causes of death reflect the reckless carnage by coaches: 12 were from exertional sickling, five from exertional heat stroke, and one from exertional asthma. All these causes of death are preventable, as we have recently proved in the case of exertional sickling in NCAA Division I football conditioning (5).

The final nine nontraumatic deaths were sudden cardiac deaths, all but one in offseason workouts. The author argues that sudden cardiac deaths are excused as foreordained, but because such deaths do not occur during the play of the game, it seems likely that players with mild or covert cardiac anomalies are surviving, if not thriving, in football and for decades thereafter, but some are not able to survive the irrational intensity of an offseason workout (1).

The problem is that some football coaches ignore best practices, consensus guidelines, and even commonsense precautions, thereby increasing the risk of nontraumatic death. The offseason has been called “college football's killing season” by journalists (11). As the author of this new article concludes, adherence to established principles of exercise physiology and best-practice training standards, which is long overdue, will help prevent these tragic deaths in football conditioning (1).

A similar case was made in Current Sports Medicine Reports in 2010 by team physician Christopher McGrew, MD, who said that the burden of preventing deaths falls on the shoulders of the football coaches who design and conduct the conditioning program, and that coaches should be held accountable for adverse outcomes that are clearly preventable (9).

I end with a poignant quote from a college head football coach. Terry Bowden said this in 2008, nearly a decade ago: “There is no reasonable expectation of death while playing football. So why are lives being lost preparing for the game? Maybe these tragic deaths are not inevitable. Maybe it’s time to start asking ourselves different questions. Are we demanding much more from these athletes than is required to safely play?”

The author declares no conflict of interest and does not have any financial disclosures.

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1. Anderson S. NCAA football off-season training: unanswered prayers… A prayer answered. J. Athl. Train. 2017; 52:145–8.
2. Dabrera G, Murray V, Emberlin J, et al. Thunderstorm asthma: an overview of the evidence base and implications for public health advice. QJM. 2013; 106:207–17.
3. Eichner ER. Sports medicine pearls and pitfalls: anemia in athletes. Curr. Sports Med. Rep. 2007; 6:2–3.
4. Eichner ER. Asthma in athletes: scope, risks, mimics, trends. Curr. Sports Med. Rep. 2008; 7:118–9.
5. Eichner ER. Observations on iron, anemia, and sickle cell trait. Curr. Sports Med. Rep. 2017; 16:2–3.
6. Girgis ST, Marks GB, Downs SH, et al. Thunderstorm-associated asthma in an inland town in south-eastern Australia. Who is at risk? Eur. Respir. J. 2000; 16:3–8.
7. Griffiths J, Alexander R. Thunderstorm asthma: 8 dead in Australia from freak illness. Available from: Accessed 3/19/17.
8. Marks GB, Colquhoun JR, Girgis ST, et al. Thunderstorm outflows preceding epidemics of asthma during spring and summer. Thorax. 2001; 56:468–71.
9. McGrew CA. NCAA football and conditioning drills. Curr. Sports Med. Rep. 2010; 9:185–6.
10. Parks RB, Hetzel SJ, Brooks MA. Iron deficiency and anemia among collegiate athletes: a retrospective chart review. Med. Sci. Sports Exerc. 2017; Epub ahead of print, accepted for publication: 5 March 2017.
11. Solomon J, Dodd D. The unregulated world of strength coaches and college football’s killing season. Available from: Accessed 3/19/17.
Copyright © 2017 by the American College of Sports Medicine.