Researchers have not found any toxins or harmful algae inside the harbor, however, and they're still attributing the die-off to a nearly complete lack of oxygen in the water.
In an e-mail sent early today to other scientists, members of the media and other interested folks, USC professor David Caron said it's not clear how the domoic acid poisoning may have contributed to conditions causing the fish kill:
Domoic acid can cause a variety of neurological disorders, and death, of animals consuming fish contaminated with the neurotoxin. Research also indicates that domoic acid poisoning can cause abnormal swimming behavior in some fish. It is possible that high levels of domoic acid in the sardines in King Harbor may have exacerbated physiological stress of the fish brought on by oxygen depletion of the water, or may have been a contributing explanation for them congregating in the harbor at very high abundances, but this has not been confirmed.The toxic algae consumed by the fish likely came from a huge bloom that's been present at least since Monday off the coast -- stretching from Point Conception to San Diego, according to researchers who've tracked the greenish-brown mass by satellite.
After the jump is the extended and fascinating email from Caron on what's been learned so far. Sampling was continuing today.
On Tuesday, March 8, 2011, King Harbor in the City of Redondo Beach experienced a massive fish kill (estimates are in the millions of fish killed), apparently mostly Pacific sardine. This event has received national and global attention. My research group at the University of Southern California has been actively working and monitoring King Harbor as a site of recurrent algal blooms since a massive fish kill occurred there in 2005. The exact cause of the 2005 event was never clearly determined, but it coincided with a large microalgal bloom. Thus, the buildup of algae and perhaps toxins produced by harmful algal species, were implicated as playing a role in the fish mortality.
In response to the 2005 mortality event, we established a monitoring program there in 2006 to characterize the algal species at the site, and subsequently a suite of instruments to measure water quality in 2007, and we have maintained those instruments and characterized the microalgae in the water through the present time. These instruments, and additional measurements made at the time of the event on March 8th and immediately following the mortality event, are summarized below:
Our sensor packages in the water recorded pertinent environmental parameters (temperature, salinity, dissolved oxygen, and chlorophyll fluorescence which is a proxy for microalgal biomass) prior to and during the event. These instruments indicated a precipitous drop in dissolved oxygen coincident with the mortality event. Based on the information collected by the sensor packages, we conclude that depletion of dissolved oxygen was unquestionably the immediate cause of the mortality event.
Profiles of dissolved oxygen made in and around King Harbor on March 8 indicated exceptionally low dissolved oxygen concentrations within the harbor, with increasing concentrations of oxygen in the outer harbor region. Severely depleted levels of dissolved oxygen persist today (March 10) in parts of the harbor in the wake of the mortality event.
It is not clear at this time whether the oxygen depletion in King Harbor on the 8th occurred solely due to respiration by the very large population of sardines that entered the harbor days prior to the mortality event. It is possible that an influx of coastal water with a low concentration of oxygen may have occurred, contributing to the low oxygen conditions. We are continuing to examine this possibility.
Our continuously-recording instruments measured relatively low chlorophyll concentrations leading up to, during, and immediately following the event (<2 ug/l). Therefore, we have ruled out the possibility of a massive buildup of algal biomass as a factor contributing to the mortality event (high algal biomass was a presumed contributor to the 2005 mortality event).
In addition, analysis of water samples collected on the day of the event in King Harbor indicated very low microalgal biomass in general, and the virtual absence of potentially harmful or toxic algal species in the water.
Despite the lack of toxic algal species in the water at King Harbor during this event, analyses of the gut contents of fish collected on March 8th have tested strongly positive for domoic acid. Domoic acid is a powerful neurotoxin produced by a specific type of microalgae. The algae are strained from the water by plankton-eating fish such as sardines and anchovy, and the toxin is often found concentrated in the stomach contents of these fish during a toxic algal bloom. Domoic acid can cause a variety of neurological disorders, and death, of animals consuming fish contaminated with the neurotoxin. Research also indicates that domoic acid poisoning can cause abnormal swimming behavior in some fish. It is possible that high levels of domoic acid in the sardines in King Harbor may have exacerbated physiological stress of the fish brought on by oxygen depletion of the water, or may have been a contributing explanation for them congregating in the harbor at very high abundances, but this has not been confirmed.
We believe that the fish ingested the toxin offshore (before entering the harbor) because domoic acid was not detected in the water within King Harbor on the day of the event. Additionally, during our 5-year study we have not observed significant concentrations of domoic acid in King Harbor. We have confirmed that plankton collected from the coastal ocean approximately 20 km southwest of Redondo Beach on March 9 had very high concentrations of domoic acid in the plankton. That finding support the idea that the fish ingested the toxin in coastal waters before entering the harbor.
This is the present status of our knowledge on this event. My lab is continuing to analyze for other algal toxins in the fish collected at the time of the mortality event. We are also continuing to monitor the chemical conditions (especially dissolved oxygen) and biological conditions (algal abundance) within the harbor in order to characterize the recovery of the harbor, and/or any response of the microalgal community to the release of nutrients by the decomposing fish.
We are continuing to characterize the toxic bloom now taking place in the adjacent coastal ocean, and we are acquiring oceanographic information that will help determine if a pulse of low-oxygen water from the coastal ocean may have entered King Harbor and contributed to the fish mortality event.
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