Tuesday, May 15, 2012


cc: sandy.tudhope@ed.ac.uk, k.briffa@uea.ac.uk, mhughesatXYZxyzr.arizona.edu
date: Tue, 15 May 2001 10:41:54 -0700
from: Julia Cole <jcoleatXYZxyz.arizona.edu>
subject: Re: comments?
to: Keith Alverson <keith.alversonatXYZxyzes.unibe.ch>, "Raymond S. Bradley" <rbradleyatXYZxyz.umass.edu>

<x-rich>Hi Keith and all,

I was away late last week and did not have a chance to look at the
newsletter article until today. A few comments on the coral section, if
it isn't too late -

- The comment on Urvina Bay implies that the reef from which the
published long record came was destroyed in 1982 - in fact that reef
was uplifted tectonically (above sea level) in 1954 or so....
additional living corals from the Bay itself may have been killed by
that event however. Maybe better to say that the 1982-3 ENSO event
caused coral mortality throughout the Galapagos. We saw this clearly in
a 1989 visit.

- Recent studies are confirming that corals and other calcifying marine
organisms are under geochemical threat from rising CO2. As atmospheric
CO2 increases, oceanic CO2 rises and carbonate drops, making the oceans
more acidic and removing the CO3 needed for skeletal formation.
Carbonate supersaturation is maintained, but even a drop in the
supersaturation level appears to influence the ability of corals and
other organisms to form calcium carbonate skeletons (Marubini and
Atkinson 1999; Kleypas et al. 1999; Langdon et al. 2000). This effect
is strictly a geochemical phenomenon - it is not a consequence of how
much the oceans warm or whether circulation changes. It is likely to
augment additional stresses currently affecting coral reefs,
particularly where CO3 is already naturally low.

- Corals are also under threat from more localized stresses. Dynamite
and cyanide fishing, nutrient overloading, the disruption of grazing
fish populations (which allow algal overgrowth), coastal pollution, and
unregulated development all contribute to coral mortality, particularly
in populated regions of the tropics. The combination of these
localized stresses with background warming and increasing CO2 means
that corals are experiencing multiple stresses on many fronts -
physical, ecological, geochemical - and are increasingly vulnerable to
mass mortality.

- on the Moore et al. citation - I read this paper; thanks for sending
it Keith. The message of your paper is clear - teleconnections with
this site can change through time, even reverse. So how do you go from
that conclusion to saying that it provides a record of ENSO? It sounds
like you are trying to have it both ways.... you can't reconstruct ENSO
unless you know what direction the teleconnections are working in the
past. A better ref for this statement might be Henderson et al. 1999
(below), although this one hasn't been tested against long records

- I'd use speleothems rather than either stalagmites or stalactites...

Hope this isn't too late to be of use,

cheers, Julie

<fontfamily><param>Geneva</param><smaller>Henderson, K. A., L. G.
Thompson and P.-N. Lin (1999). "Recording of El Ni�o in ice core d18O
records from Nevado Huascaran, Peru." <underline>Journal of Geophysical
Research</underline> <bold>104</bold>: 31,053-31,065.

Kleypas, J. A., R. W. Buddemeier, D. Archer, J. P. Gattuso, B. N.
Opdyke, C. Langdon and M. Frankignoulle (1999). "Geochemical
consequences of increased atmospheric CO2 on corals and coral reefs."
<underline>Science</underline> <bold>284</bold>: 118-120.

Langdon, C., T. Takahashi, C. Sweeney, D. Chipman, J. Goddard, F.
Marubini, H. Aceves, H. Barnett and M. Atkinson (2000). "Effect of
calcium carbonate saturation state on the calcification rate of an
experimental coral reef." <underline>Global Biogeochemical
Cycles</underline> <bold>14</bold>: 639-954.

Marubini, F. and M. Atkinson (1999). "Effect of lowered pH and elevated
nitrate on coral calcification." <underline>Marine Ecology Progress
Series</underline> <bold>188</bold>: 117-121.


Dr. Julia Cole

Dept. of Geosciences

Gould-Simpson Bldg.

1040 E. 4th St.

University of Arizona

Tucson AZ 85721

phone 520-626-2341

fax 520-621-2672



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