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Coastal acidification in southeastern U.S. estuaries and coastal waters is influenced by biological activity, runoff from the land, and increasing carbon dioxide in the atmosphere. Acidification can negatively impact coastal resources such as shellfish, finfish, and coral reefs, and the communities that rely on them. Organismal responses for species located in the U.S. Southeast document large negative impacts of acidification, especially in larval stages. For example, the toxicity of pesticides increases under acidified conditions and the combination of acidification and low oxygen has profoundly negative influences on genes regulating oxygen consumption. In corals, the rate of calcification decreases with acidification and processes such as wound recovery, reproduction, and recruitment are negatively impacted. Minimizing the changes in global ocean chemistry will ultimately depend on the reduction of carbon dioxide emissions, but adaptation to these changes and mitigation of the local stressors that exacerbate global acidification can be addressed locally. The evolution of our knowledge of acidification, from basic understanding of the problem to the emergence of applied research and monitoring, has been facilitated by the development of regional Coastal Acidification Networks (CANs) across the United States. This synthesis is a product of the Southeast Coastal and Ocean Acidification Network (SOCAN). SOCAN was established to better understand acidification in the coastal waters of the U.S. Southeast and to foster communication among scientists, resource managers, businesses, and governments

Even as global and national efforts struggle to mitigate CO 2 emissions, local and state governments have policy tools to address “hot spots” of ocean acidification.

Solar ultraviolet (UV) radiation can have deleterious effects on coral assemblages in tropical and subtropical marine environments, but little information is available on UV penetration into ocean waters surrounding corals. Here we provide an extensive data set of optical properties in the UV domain (280[en]400 nm) that were obtained during 1998‐2005 at sites located in the Lower and Middle Keys and the Dry Tortugas. Absorption coefficients of the colored component of the dissolved organic carbon (DOC; colored dissolved organic matter [CDOM]) were 6× to 25× larger than particulate absorption coefficients in the UV region, indicating that CDOM controls UV penetration in the inshore coastal waters and reef tract. CDOM absorption coefficients (αCDOM) and DOC were highly correlated to diffuse attenuation coefficients (Kd) in the UV spectral region. Measurements using moored sensors showed that UV penetration at the reef tract in the Lower Keys varies significantly from day to day and diurnally. The diurnal variations were linked to tidal currents that transport CDOM over the reef tract. Summertime stratification of Case 1 bluewaters near the reef tract during periods of low wind resulted in higher temperatures and UV penetration than that observed during well‐mixed conditions. This result suggests that higher UV exposure accompanying ocean warming during low‐wind doldrums conditions significantly contributes to coral bleaching. Modeling results indicate that changes in underwater sunlight attenuation over the coral reefs can affect UV‐induced deoxyribonucleic acid (DNA) damage and inhibition of coral photosynthesis much more strongly than changes in the stratospheric ozone layer.

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American oysters, Crassostrea virginica, from a high-salinity (HS) and a low-salinity (LS) location in the Chesapeake Bay were acclimated to six salinities (6-36 ppt) in the laboratory for 3-4 weeks. After acclimation, hemolymph was drawn from oysters and granular hemocytes were tested in vitro. Measurements of time to hemocyte spreading (TTS) and rate of hemocyte locomotion (ROL) were made in six media ranging in salinity from 6-36 ppt. TTS measurements were fastest at the acclimation salinities and slowed with acute rises in salinity. The time to spreading may be a measure of the osmotic adjustment process. Locomotion was dependent on ameboid shape. ROL decreased with acute rises in salinity for both populations, and increased with acute reductions in salinity for all test conditions except HS hemocytes acclimated at 30 and 36 ppt salinity. ROL tested at the acclimation salinities showed no differences between HS oysters (complete acclimation to lower salinities) but LS oyster hemocytes at 30 and 36 ppt were still slower even after 27 days of acclimation. There were a greater number of agranular hemocytes for HS oysters at all salinities. These findings are discussed in relation to osmotic adjustment, ameboid locomotion, acclimation, and disease susceptibility.