Tuesday, April 18, 2006
Lessons From the Mussel Kill
Below is the abstract from an article published in Ecology by Brown University scientists Andrew Altieri and Jon Witman showing that large numbers of blue mussels in Narragansett Bay died in 2001 due to low dissolved oxygen.
Over the past five years, I have fielded a number of pollution complaints related to dead and dying blue mussels washing up on shorelines throughout Narragansett Bay and in Point Judith Pond. I strongly suspected that these events were caused by prolonged periods of low dissolved oxygen in the Bay. Until this article, though, there was little scientific evidence of a causal link between dead musssels and nutrient pollution.
It makes sense. So many of the major pollution problems we have observed throughout Narragansett Bay in recent years are rooted in the same cause- too much nitrogen from wastewater is polluting the Bay. That nitrogen causes excessive algae to bloom, turning the water a murky green and blocking the sunlight from penetrating the Bay's water. As this algae dies and settles on the bottom, it forms a stinky muck. As bacteria break down the muck and as the algae goes through its nightly respiration, these processes consume all the dissolved oxygen in the water.
Low dissolved oxygen can cause fish kills if it happens suddenly, as it did in Greenwich Bay in August, 2003. It has also caused massive numbers soft-shelled clams to wash up dead, as well as sea stars, oysters, and blue mussels. It is this same algae that piles up on the Warwick and Cranston shorelines causing rotting egg odor so strong it drives people from their homes.
What are the lessons to be drawn from this? First, we have to adopt advanced wastewater treatment practices at all the Bay's major wastewater facilities. This can be done equitably, and no single plant or company is solely responsible. Rhode Island has established nitrogen limits for some wastewater plants, but much of the treated wastewater flowing into the Bay still has very high nitrogen levels. Passing the clean water bond issue in November will help the state raise money for these sorely-needed upgrades.
Second, we need to eliminate cesspools entirely and get coastal communities to upgrade septic systems wherever it is practicable. It's shameful that we still have so many raw pits of sewage and clogged septic systems discharging directly into the Bay.
Third, we have to do a better job monitoring the Bay. Last year, the Rhode Island legislature failed to appropriate any money for Bay monitoring. Without standardized and comprehensive monitoring, we're not getting the information we need to accurately measure the health of the Bay. Lacking complete science is no excuse, though, for delaying decisive action where it is clearly needed.
Independent and unbiased scientific reports like this one provide clear and irrefutable evidence of the problem. In the face of facts like this, it's difficult to comprehend how anyone can still doubt the extent and obvious causes of nutrient pollution in the Bay. -JT
Ecology: Vol. 87, No. 3, pp. 717–730.
LOCAL EXTINCTION OF A FOUNDATION SPECIES IN A HYPOXIC ESTUARY: INTEGRATING INDIVIDUALS TO ECOSYSTEM
Andrew H. Altieri and Jon D. Witman
Department of Ecology and Evolutionary Biology, Box G-W, Brown University, Providence, Rhode Island 02912 USA
Abstract.We integrated across individual, population, community, and ecosystem levels to understand the impact of environmental stress by tracking the foundation species Mytilus edulis in the hypoxic estuary Narragansett Bay, Rhode Island, USA. Our initial surveys revealed that the mussels occurred in nine extensive (2–28 ha) dense (814–9943 individuals/m2) subtidal reefs that attracted a diverse suite of predators (sea stars, crabs, gastropods). Hypoxia occurred in the summer of 2001, and a mussel transplant experiment revealed overall reduced growth rates of individuals, and higher mortality rates among larger mussels. At the population level, large decreases in densities and cover of mussels were correlated with dissolved oxygen concentrations, leading to extinction at one site and reductions of over an order of magnitude at others. Within one year, seven of the eight remaining populations were edged to extinction, and the previously extinct population was recolonized. At the community level, a predator exclusion experiment indicated that predation was an unimportant source of mussel mortality during the hypoxic period, in part due to the emigration of sea stars, as predicted by the Consumer Stress Model. However, mussels were too intolerant to hypoxia to have a net benefit from the predation refuge. The seasonal (summer) occurrence of hypoxia allowed sea stars to return following a lag, as predicted by a stress return time model, and the resumption of predation contributed to the subsequent extinction of mussel populations. At the ecosystem level, the initial filtration rate of the mussel reefs was estimated at 134.6 × 106 m3/d, equivalent to filtering the volume of the bay 1.3 times during the 26-d average residence time. That function was reduced by >75% following hypoxia. The effect of hypoxia on each level of organization had consequences at others. For example, size-specific mortality and decreased growth of individuals, and reduced filtration capacity of reefs, indicated a loss of the ability of mussels to entrain planktonic productivity and potential to control future eutrophication and hypoxia. Our study quantified patterns of loss and identified pathways within an integrative framework of feedbacks, summarized in a conceptual model that is applicable to similar foundation species subjected to environmental stress.
Key words:Asterias forbesi; benthic–pelagic coupling; bivalve; dissolved oxygen; disturbance;; environmental stress; eutrophication; filtration; mussel; Mytilus edulis; predation; refuge.
Manuscript received 8 February 2005; revised 12 July 2005; accepted 1 August 2005; final version received final version 16 August 2005.. Corresponding Editor: P. T. Raimondi.