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Aerosol Toxins From Red Tides May Cause Long-term Health Threat

Date:
July 9, 2008
Source:
National Oceanic And Atmospheric Administration
Summary:
An algal toxin commonly inhaled in sea spray, attacks and damages DNA in the lungs of laboratory rats. The findings document how the body's way of disposing the toxin inadvertently converts it to a molecule that damages DNA. Human inhalation of brevetoxins produced by the red tide organism, Karenia brevis, is an increasing public health concern.
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NOAA scientists reported in the current issue of the journal Environmental Health Perspectives that an algal toxin commonly inhaled in sea spray, attacks and damages DNA in the lungs of laboratory rats. The findings document how the body's way of disposing the toxin inadvertently converts it to a molecule that damages DNA. Human inhalation of brevetoxins produced by the red tide organism, Karenia brevis, is an increasing public health concern.

The scientists, led by John Ramsdell of NOAA's Center for Environmental Health and Biomolecular Research in Charleston, S.C., determined that brevetoxins react with DNA of lung tissue and attach to the DNA-bases that code genetic information. The linkage of chemicals in the environment to DNA is a first step for many cancer causing agents and can lead to mutations in genes that normally prevent the formation of cancers.

The red tide toxin, brevetoxin, has long been recognized as a cause of both neurotoxic poisoning after both consumption of toxic shellfish as well as a respiratory irritation after inhalation of toxic sea spray. Groundbreaking research, leading to this third potential form of poisoning, identified that metabolism produces chemically reactive forms of the toxin. Recognizing the potential of these metabolites to attack DNA, NOAA scientists analyzed the DNA after the toxin was metabolized in the lung.

Scientists have not yet determined if brevetoxin damaged DNA accurately repairs itself or if gene mutations result. Brevetoxin has been measured in air during red tide events and human exposure levels have been reported; however, the long-term health risk associated with inhalation of brevetoxins remains to be defined. Individuals are continually exposed to environmental chemicals capable of damaging DNA like carcinogens found in tobacco smoke and air pollution. It is possible that exposure to brevetoxins can add to the cumulative amount of chemically altered DNA in the lungs; an indicator of cancer risk.

"This represents a significant breakthrough in defining the metabolic transformation of brevetoxins and the potential long-term health effects of red tides. It should change perceptions of risk and management of inhalation exposure to harmful algal blooms," notes Ramsdell.

Red tides in the Gulf of Mexico are common, and often persistent, naturally occurring events that release toxins into sea spray aerosols. These aerosols are a particular problem at beaches, as they can cause respiratory distress to lifeguards and beachgoers. Although these shorter-term effects of the airborne toxin are well characterized, potential longer-term effects remain a concern to health officials and coastal communities.

Scientists, in NOAA's Oceans and Human Health Initiative, are studying long term health consequences of harmful algal blooms, to predict how the condition of the coastal waters affect human health and how to reduce or eliminate health risks.


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Cite This Page:

National Oceanic And Atmospheric Administration. "Aerosol Toxins From Red Tides May Cause Long-term Health Threat." ScienceDaily. ScienceDaily, 9 July 2008. <www.sciencedaily.com/releases/2008/07/080709110049.htm>.
National Oceanic And Atmospheric Administration. (2008, July 9). Aerosol Toxins From Red Tides May Cause Long-term Health Threat. ScienceDaily. Retrieved April 19, 2024 from www.sciencedaily.com/releases/2008/07/080709110049.htm
National Oceanic And Atmospheric Administration. "Aerosol Toxins From Red Tides May Cause Long-term Health Threat." ScienceDaily. www.sciencedaily.com/releases/2008/07/080709110049.htm (accessed April 19, 2024).

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