DARWIN, DYSOX, AND OUR FERMENTING PLANET-ESSAY
4:
OXYGEN DEFICIT IN PLANETARY WATERS AND CLIMATIC CHAOS:
Times are desperate for most forms of life on the
planet Earth. In the man-microbe conflicts, microbes are winning. That also is
the case for butterflies, bees, and bats. In my view, the reason is the changing
"oxygen conditions" of planetary life. In this series of essays on the
fermenting planet, I present my hypothesis that the primary result of the
changing oxygen conditions is impairment of oxygen-driven energy systems of
humans, animals, and plants. The oxygen-shunning species are thriving at the
expense of the oxygen-loving species. This trend has far-reaching significance
for all planetary life.
There are two predominant groups of life forms on
our planet: oxyphils that thrive in oxygen-rich environments and oxyphobes that
flourish in oxygen-poor conditions. Oxyphils include humans, all animals, and
most plants while oxyphobes comprise fungi and anaerobic bacteria. The changing
oxygen conditions are altering the balance between these groups by favoring
oxyphobes over oxyphils.
Evolution created two primary modes of cellular
energetics: low-efficiency non-oxygen-driven metabolism designated as
fermentation and a high-efficiency oxygen-driven metabolism called respiratory
mode of energy generation. The oxygen deficit over land masses and in planetary
waters fosters the growth of the fermenters as it threatens the oxygen-utilizing
species.
Darwin, Dysox, and Our
Fermenting Planet - Essay 1
Hypoxia is oxygen deficit. Hypoxic waters are
bodies of water with deficiency of oxygen. Anoxia is absence of oxygen. Anoxic
waters are bodies of water with an absence of oxygen. Hypoxia develops in
aquatic environments as the amount of dissolved oxygen (molecular oxygen
dissolved in the water) falls to a level that is detrimental to fishes and other
forms of oxygen-breathing aquatic species.56-59 The temperature and
salt content (salinity) of bodies of water determine the amount of oxygen
dissolved in the water. So, the value of dissolved oxygen is expressed as a
percentage of the amount of oxygen that would dissolve in the water at the
prevailing temperature and salinity. An aquatic ecosystem without dissolved
oxygen (0% saturation) is designated as an anoxic aquatic system. Dissolved
oxygen is measured in standard solution units of millimoles O2 per liter (mmol/L),
milligrams O2. At 20
°C
under sea level atmospheric pressure, the value of dissolved oxygen in
freshwater is 9.1 mg/L, a value that is designated as 100% saturation. The U.S.
Geological Service (USGS) offers at its web site solubility tables showing the
values, in milliliters per liter [ml/L], based upon temperature and corrected
for different salinities and pressures.
It is
noteworthy that most species of fish cannot survive in waters with dissolved
oxygen saturation of less than 30%. For optimal sustenance of oxygen‑utilizing
life forms, an aquatic ecosystem must not develop oxygen deficits that allow the
dissolved oxygen levels to fall below 80%.
Are natural bodies of water sometimes
supersaturated? Can excess dissolved oxygen in water can sometimes be harmful
for fish, aquatic animal species, and aquatic vegetaion? Not much has been
documented in this area. However, it is known that oxygen supersaturation does
develop under certain conditions and causes decompression damage to aquatic
life.
Algae and
related aquatic vegetation called phytoplankton in the water mass release oxygen
by spliting water into hydrogen and oxygen in the process called photosynthesis.
On the other side of the equation, oxygen is picked up and metabolized by
bacteria, fish, and organisms included in the category. This is the essential
"oxygen balance," not only in aquatic ecosystems, but on land masses as well. In
oceans, seas, and large lakes, the equilibrium between the two mechanisms for
the release and consumption of oxygen determine the amount of oxygen dissolved
in the water which, in turn, determines the aquatic biomass (the total mass of
living species, vegetative as well as animal species). I might add here that the
difference between the amount of oxygen in the water (theoretical concentration
if there were no living organisms) and the actual amount (concentration) of
oxygen is designated as the biological demand of oxygen.
The climatic changes documented so far are deepening the "oxygen crisis" in most
bodies of water in the world. If the current trends hold, the predicted climatic
chaos will dangerously enlarge the bodies of anoxic waters with dire
consequences for life within them. There are several mechanisms by which global
warming, incremental carbonization of oceans and land masses, and
chemicalization of the planet decreases the amount of dissolved oxygen
saturation in water. Specifically, such mechanisms include the following.60-62
-Warm
water holds less oxygen;
-Eutrophication
(increased growth of plankton and algae due to addition of nitrogen,
phosphorus, and potassium in water) reduces the amount of oxygen
dissolved in water;
-Persistence
of stratification in large bodies of water, as described earlier, disrupts
oxygenation of deep waters;
-Higher
air temperature intensifies the density stratification of water making it less
dense and relatively anoxic;
-Solar
warming of the surface water reduces water density and causes anoxia;
-Saltier
water increases the density of water;
-Change
of direction of the wind can cause significant local upwelling of the anoxic
bottom water (wind can actually drag the surface water away from shore,
replacing it with deeper water);
-Increasing
anthropogenic nitrogen input;
-Stratification;
-Energetic
tidal circulation; and
-The pycnocline effect (a rapid
change in water density with depth).
In the large bodies of fresh water, the density change is essentially caused
by changes in the temperature, while in the oceanic waters the density
change is caused by changes in water temperature and/or salinity. For
further information on the above subjects and specific data concerning the
extent and duration of harmful algal blooms (Microcystis aeruginosa)
in the Potomac River, the reader is referred to
www.marine.unc.edu/modmon
Anoxia develops in sea waters under natural conditions. Anoxic sea water is
generally found in regions of restricted water exchange. In general, oxygen
does not reach the depths of the sea area due to a physical barrier, such as
silt and extended periods of density stratification. Such conditions allow
bacteria to increase their rates of the oxidation of organic matter, thus
increasing oxygen utilization beyond the supply. For example, the occurrence
of markedly anoxic conditions have been documented in the geological history
of the Baltic Sea. Recent evidence shows that increasing degrees of
eutrophication have increased the degrees of the anoxic regions in the
Baltic Sea and the Gulf of Mexico.
Anoxic states are created by water stagnation, density stratification,
influx of organic matter, thermoclines, and bacterial metabolism of sulfide.
Sulfur compounds settle in the sediments and later rise into the surface
waters. Recent reports of anoxic waters are disturbing both for the degrees
of oxygen deficit and for the frequency with which such deficits are
encountered, especially the findings of fatal anoxia in the bodies of water
in which anoxia was not previously present. For example, in February 2008,
severe anoxia was detected for the first time in the northern California
current system, an enormous ecosystem with no previous record of extreme
oxygen deficits.63 The severity of anoxia raises the specter of
rapid and discontinuous ecosystem changes in highly productive coastal
systems that sustain the world's fisheries.
In 1888, Lajos Winkler, a Romanian chemist, developed a method of
determining the level of dissolved oxygen in water samples.64
The test is designated as the Winkler test. It is interesting to note that
the subject of the oxygen content of large bodies of water (and its effects
on life in them) preoccupied a Romanian student as far back as the end of
the nineteenth century. Yet, it holds little, if any, interest for doctors
today, notwithstanding the central importance of oxygen factors in the
pathogenesis of all chronic disorders.
SMOG AND OXYGEN DEFICIT
The story of smog has many interesting faces:
clinical, historical, biochemical, environmental, and political. The
clinical problems associated with poor quality air, first and foremost,
should have been related to problems of oxygen homeostasis in health and
disease. What could be simpler than that? Why do we breathe except to bring
oxygen in and expel the produced waste. It both amused and saddened me when
I read a large number of articles about smog posted by governmental, public,
environmental, and academic groups. For three hours, I read and read without
finding a single reference to smog disrupting oxygen signaling and
oxygen‑driven cellular energetics. Inexplicably, the literature of smog
evolved into a literature of ozone in ambient air.
For public education, the United States Environmental Protection Agency
(EPA) developed an Air Quality index to explain the degrees of air
pollution. For reasons that escape me, it built its entire case around the
eight‑hour average concentration of ozone in the air, as if the sulfur and
nitrogen pollutants do not matter. The EPA promulgated the following
standards:
85 to 104 ppbv (parts per billion by volume):
Unhealthy for Sensitive Groups
105 ppbv to 124:
Unhealthy
125 ppbv to 404 ppbv:
Very unhealthy
Smog, in reality, is much more than just the concentration of ozone in the
air. It is the sum total of all noxious and toxic elements that exist in the
ambient air at any given time. Did the folly of fixating on ozone levels
lead to the disastrous proclamation on September 15, 2001 of Christie
Whittman, the then EPA chief when she declared that air in New York was safe
to breathe, following the inferno of collapsed World Trade Centers (WTC).
That comment stirred me to action and culminated in the publication in early
2002 of my book September Eleven,2005 (2002),65a volume
of predictions written in a fictionalized past tense. I had three primary
reasons for writing that book:
1.
To predict that more than 250,000 people exposed to the poisons released
from the WTC inferno would become chronically ill due to 9/11‑related causes
in September 2005;
2. To assert that at the levels of
oxygen signaling and oxygen‑driven cellular energetics, terror turns into
toxicity, and toxicity into terror;
3.
All patterns of chronic illness triggered by 9/11‑related events would be
fundamentally caused by disruptions of the oxygen signaling and
oxygen‑driven cellular energetics;
4.
Much of 9/11‑related illness could be prevented by robust integrative
treatment plans that restore deranged oxygen signaling and oxygen‑driven
cellular energetics; and
5.
Regrettably, the fundamental oxygen issues of the 9/11 tragedy would be
ignored by the prevailing one‑disease‑one‑cause‑one‑drug model of thinking.
In 2008, anyone who reads September Eleven, 2005 will recognize the
utter logic and predictability of events that I foresaw. In September 2001,
I knew that the EPA and the mainstream medicine would stubbornly refuse what
Londoners of the Roman times knew: Pollutants in the air sicken the people
who breathe it. Indeed, The New England Journal of Medicine
considered the 9/11 events "not necessarily medical significant"66
and advised its readers not to "medicalize"67 them (see
September Eleven, 2005 for full details).
The English claim the origin of the term "smog"and attribute it to Dr.
Henry Antoine Des Voeux in his 1905 paper entitled "Fog and Smoke" presented
at a meeting of the Public Health Congress.68 On July 27, 1905,
the London newspaper Daily Graphic celebrated the paper, writing that
Des Voeux had done a public service in coining a new word for the London
fog. Californians challenge that claim, citing the use of the word "smog" by
Los Angeles Times on January 19, 1893. The English need not feel
up‑ended since the Times attributed it to "a witty English writer."
The Londoners have sound reasons for amusing themsleves with the assertions
of Angelos. Since the Roman times, they have recognized this distinction. In
1306, King Edward I briefly banned coal fires in the city. In 1661, John
Evelyn's Fumifugium blamed burning coal for what people considered to be
London cough. In 1952, The Great Smog darkened the city sreets and killed
approximately 4,000 people in four days, claiming another 8,000 during the
days and weeks that followed it. Some readers might find the following text
I found in Transcultural Psychiatry69 interesting in the
current context:
Reports of occupational mass psychogenic
illness (OMPI) in the scientific literature were examined to describe
underlying presentation patterns and explain their sporadic appearance in
the literature. Three distinct patterns were identified: (i) mass anxiety
hysteria is precipitated by the sudden appearance of an anxiety generating
stimulus following the redefinition of an innocuous or imaginary odour or
agent that is perceived as an immediate threat; (ii) mass motor hysteria is
characterized by internalized conflict which fosters dissociation,
histrionics and psychomotor agitation. Episodes are typified by an
atmosphere of pre existing tension and employee dissatisfaction with
restrictive management practices coupled with inhibited negotiation
channels; (iii) a third presentation pattern involves the relabelling of
endemic symptoms and the occasional appearance of conversion reactions,
which are reinforced by a hypervigilant medical community and exacerbating
factors. Social factors may explain the irregular appearance of reports.
Notice, the author does not recognize any oxygen‑related issues in his
discourse on what he designates occupational mass psychogenic illness.
Simple tests done to measure the urinary excretion of the metabolites of
Krebs cycle and glycolytic pathways, mycotoxins, and hippuric acid in the
subjects of his study would have shed much light on what was observable and
documentable in the chemistry of those afflicted by the putative
occupational mass psychogenic illness.
Please see essay 5 of the Darwin, Dysox, and Our Fermenting Planet series
for continuation of this discussion.
References
57. Fenchel T,
Bland J. (1995) Ecology and Evolution in Anoxic Worlds (Oxford Series in
Ecology and Evolution). 1995. Oxford University Press.
58. Fischer P., K.
Rademacher, and U. Kils. 1992. In situ investigations on the respiration and
behaviour of the eelpout Zoarces viviparus under
short term hypoxia. Mar
Ecol Prog Ser. 1992; 88: 181 184.
59. Zilli M.,
Guarino C., Daffonchio D., Borin S., Converti A. (2005) AThe enigma of
prokaryotic life in deep hypersaline anoxic basins. Science.
2005.307:121
123.
60. West TG, 1 and
R. G. Boutilier RG. Metabolic suppression in anoxic frog muscle . Journal of
Comparative Physiology B: Biochemical, Systemic, and Environmental
Physiology. 1998; 168:273‑280 .
61. Richards, F.A.
(1965) Anoxic basins and fjords@, in Riley, J.P., and Skirrow, G. (eds)
Chemical Oceanography, London, Academic Press, 611 643.
62. Sarmiento J.L.,
Herbert T.D., Toggweiler J.R. Causes of anoxia in the world ocean@. Global
Biochemical Cycles, 1988A;2: 115 128.
63. Chan F, Barth
JA, Lubchenco J, et al. Emergence of Anoxia in the California Current Large
Marine Ecosystem. Science. 2008;319: 920.
64. Winkler,
1888 (Ber. Deutsch Chem. Ges., 21, 2843).
65. Ali M. September
Eleven, 2005. 2003. New York, Aging Healthfully Books.
66. Letter to the
Editor. N Eng J Med. February 21, 2002.
67. Letter to the
Editor. N Eng J Med. February 21, 2002.
68.
http://en.wikipedia.org/wiki/Smog
69. Bartholomew RE.
Occupational Mass Psychogenic Illness: A Transcultural Perspective.
Transcultural Psychiatry. 2000;37:495 524.
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