[Kirk]

A friend who goes to SIO forwarded me this email from David Caron at USC.

Following is a synopsis of the state of knowledge that my lab has
acquired regarding the massive fish kill that took place this week in
King Harbor, City of Redondo Beach. This is fairly general because I
am sending this to a fairly wide audience, but feel free to pass this
along to individuals or groups that you feel should be made aware of
this, and feel free to give me a call or drop an email if you need
further information or have questions.
David Caron



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.