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Aerosolized red-tide toxins (brevetoxins) and asthma
Fleming, L.E; Kirkpatrick, B.; Backer, L.C.; Bean, J.A.; Wanner, A.; Reich, A.; Zaias, J.; Cheng, Y.S.; Pierce, R.; Naar, J.; Abraham, W.M.; Baden, D.G. (2007). Aerosolized red-tide toxins (brevetoxins) and asthma. Chest 131(1): 187-194.
In: Chest: the cardiopulmonary and critical care journal. American College of Chest Physicians: Chicago, Ill.. ISSN 0012-3692, more
Peer reviewed article  

Available in  Authors 

    Algal blooms; Marine

Authors  Top 
  • Fleming, L.E
  • Kirkpatrick, B.
  • Backer, L.C.
  • Bean, J.A.
  • Wanner, A.
  • Reich, A.
  • Zaias, J.
  • Cheng, Y.S.
  • Pierce, R.
  • Naar, J.
  • Abraham, W.M.
  • Baden, D.G.

    Background: With the increasing incidence of asthma, there is increasing concern over environmental exposures that may trigger asthma exacerbations. Blooms of the marine microalgae, Karenia brevis, cause red tides (or harmful algal blooms) annually throughout the Gulf of Mexico. K. brevis produces highly potent natural polyether toxins, called brevetoxins, which are sodium channel blockers, and possibly histamine activators. In experimental animals, brevetoxins cause significant bronchoconstriction. In humans, a significant increase in self-reported respiratory symptoms has been described after recreational and occupational exposures to Florida red-tide aerosols, particularly among individuals with asthma. Methods: Before and after 1 h spent on beaches with and without an active K. brevis red-tide exposure, 97 persons >12 years of age with physician-diagnosed asthma were evaluated by questionnaire and spirometry. Concomitant environmental monitoring, water and air sampling, and personal monitoring for brevetoxins were performed. Results: Participants were significantly more likely to report respiratory symptoms after K. brevis red-tide aerosol exposure than before exposure. Participants demonstrated small, but statistically significant, decreases in FEV1, midexpiratory phase of forced expiratory flow, and peak expiratory flow after exposure, particularly among those participants regularly using asthma medications. No significant differences were detected when there was no Florida red tide (ie, during nonexposure periods). Conclusions: This study demonstrated objectively measurable adverse changes in lung function from exposure to aerosolized Florida red-tide toxins in asthmatic subjects, particularly among those requiring regular therapy with asthma medications. Future studies will assess these susceptible subpopulations in more depth, as well as the possible long-term effects of these toxins.

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