Coastal Eutrophication and Hypoxia: Implications for Mercury Methylation, Mercury Biomagnification, and Human Health.

Hypoxic zones in the worlds oceans are increasing in both number and scale throughout the world. Caused by elevated nutrient loadings to coastal ecosystems, these eutrophic “dead zones” have sufficiently low dissolved oxygen levels in bottom waters to drive away fish and kill benthic organisms. Hypoxic zones have obvious implications for coastal ecosystem health, on coastal economies dependent on productive commercial fisheries, and subsistence fishers. The nutrients loadings that lead to hypoxia have also been linked to noxious algal blooms, such as red tide and Pfiesteria, that can directly impact human health through consumption of phytotoxin-contaminated seafood, and by ingestion or inhalation of toxics directly from the water and air.

Little is known, however, about the potential role that coastal eutrophication and hypoxia play in controlling methyl mercury (MHg) production, biomagnification of MHg in coastal food webs, and human exposure to MHg. MHg is a potent human developmental neurotoxin, and presents itself as a growing global problem. In recognition of this problem, fish consumption advisories have been issued for 15% and 30% of US lake area and river miles, respectively, and 80% of these advisories are due to elevated levels of mercury measured in fish tissue [USEPA, 2003]. In addition, 11 US states (including all the Gulf states) have statewide consumption advisories for fish caught in their coastal waters [USEPA, 2003]. Research conducted across a variety of systems would suggest that eutrophication can contribute to the increase of mercury methylation rates in coastal sediments. To some degree, the increased organic carbon flux to coastal bottom waters that occurs due to eutrophicatoin should create conditions that favor mercury methylation in the sediments. However, excess organic carbon and high levels of sulfide in anoxic sediments have been shown to decrease mercury methylation rates.

Through this proposed research, we plan to address the following question: Do coastal eutrophication and hypoxia play a role in controlling Hg methylation and biomagnification, and thereby impact human exposure to MHg via seafood consumption? We propose to conduct this research in the Gulf of Mexico, where nutrients exported from the Mississippi and Atchafalaya Rivers regularly lead to seasonal hypoxia that extends over 1000s of km2. Through biogeochemical field investigations, studies of Hg levels in fish tissue, and biomarker studies and fish consumption surveysof recreational anglers, we plan to address the following specific aims:

Specific Aim #1 – Test the hypothesis that rates of methyl mercury production in coastal sediments are in part controlled by temporal and spatial hypoxia patterns that result from coastal eutrophication, and that maximum MHg production occurs in regions adjacent to hypoxic zones.
Specific Aim #2 – Test the hypothesis that coastal eutrophication and hypoxia can result in elevated methyl Hg accumulation and biomagnification in red snapper and gray snapper, both commercially and recreationally important fish species in this region
Specific Aim #3 – Test the hypothesis that anglers who disproportionately consume fish from areas of higher MHg mercury production related to hypoxia will have higher rates of mercury exposure (as measured by the concentration of mercury in hair) than anglers consuming similar amounts of fish from other coastal Louisiana locations where hypoxia does not occur.