Archive for the ‘oxygen’ Category
the photosynthesis challenge
c’est bien simple…
So I wrote last time about my non-career in science, with a promise to myself that I might try to get my head around photosynthesis. So, years ago I read Oliver Morton’s fiendishly difficult book, Eating the Sun, and all I clearly remembered about it was that there were two types, simply named type 1 and type 2, and that the processes are very very very complex, and took decades to unravel. And a feeling that it was all over my head. Or that one had to be there, in those labs, or chatting at science conferences with the experts, as Morton no doubt was, to have a chance of getting my dull head around it all. And yet, never say never…
So I’m rereading Morton’s book (published in 2007 – has more been nailed down about the processes since?), having nothing better to do – and that isn’t meant as an insult – and I’m currently about a quarter of the way through. What I note is that Morton intermixes the undeniably complex science with interesting character sketches of the major researchers and theorists, and descriptions of the mostly mid-twentieth century background of war and conflict (at least in this early part of the book). My aim here though is self-education, so I’ll be focussing entirely on the science as far as I can grapple with it. So there will be no names, just a lot of ‘this breakthrough led to a new avenue of research’, etc.
So, photosynthesis is about using sunlight as sustenance. Of course, water is also required, and CO2. The devil’s in the detail, and there’s an awful lot of it..
So, where to begin. Chlorophyll, I suppose. That’s the green pigment in the chloroplasts of plants and algae. They absorb light, mostly from the sun. But what does this mean? And how did we come to know this?
Chloophyll is green because the green area of the light spectrum is reflected, while blue and red light is trapped, mostly. So, though plants ‘eat’ sunlight, they don’t eat the green part of that light, which is fascinatingly counter-intuitive.
As to these chloroplasts, these key sub-cellular elements in plants and algae, they’re a product of endosymbiosis, the colonisation of eukaryotic cells by earlier microbes – bacteria or their ancestors. Mitochondria, the engines of ATP through oxidative phosphorylation (wateva), are another such product.
Which brings me to photophosphorylation in plants, as useful and interesting a starting point as any. This process, originally called photosynthetic phosphorylation, might be expected to be carried out by mitochondria in plants, as it is in mammals, but plant biologists noted that ‘the leaf cells with the greatest number of chloroplasts – the cells that do the bulk of the photosynthesis – contain remarkably few mitochondria’ (Morton, p76).
Phosphorylating, as I understand it, involves adding a phosphate to ADP (adenosine diphosphate) to create adenosine triphosphate (ATP), the principal ‘energy molecule’. Another such molecule is NADPH (Nicotinamide Adenine Dinucleotide Phosphate), of which more later, perhaps. They are both important in plants, and are key to what became known as the Calvin-Benson cycle, a set of chemical reactions (independent of light) within chloroplasts as a part of photosynthesis. These reactions convert CO2 from the atmosphere into sugars for energy.
There are apparently two main stages to photosynthesis, the light-dependent stage and the light-independent stage (aka the Calvin-Benson cycle, or even the Calvin-Benson-Bassham cycle). The light-dependent stage occurs inside the thylakoid membranes of the chloroplasts. Here’s Wikipedia:
Thylakoids are membrane-bound compartments inside chloroplasts and cyanobacteria. They are the site of the light-dependent reactions of photosynthesis. Thylakoids consist of a thylakoid membrane surrounding a thylakoid lumen. Chloroplast thylakoids frequently form stacks of disks referred to as grana (singular: granum). Grana are connected by intergranal or stromal thylakoids, which join granum stacks together as a single functional compartment.
In thylakoid membranes, chlorophyll pigments are found in packets called quantasomes. Each quantasome contains 230 to 250 chlorophyll molecules.
So that’s something about thylakoid structure. Now to function. Or maybe not – it’s all so complex. The thylakoid proteome (set of individual proteins) consists of at least 335 protein types, of which 89 are in the lumen or central cavity. At this stage it’s calculated that about 42% of these proteins are involved in photosynthesis.
Jumping away from all this, it’s important to note that for us mammals, the essential value of photosynthesis is that it creates, or releases, oxygen. Think of the great oxygenation event, mainly involving oceanic cyanobacteria, ‘about 2.4 billion years ago, shortly after the end of the Archaean’, according to Morton (p175). So how does that oxygenising aspect of photosynthesis work?
But I was going to write about the light-dependent part of photosynthesis, requiring sunlight and water. It’s called photosystem 1, and Wikipedia calls it ‘a vital membrane protein complex that uses light energy to transfer electrons from plastocyanin to ferredoxin, producing NADPH and helping generate ATP.’ So, digging slightly deeper, plastocyanin is ‘a small copper-containing protein that acts as a mobile electron carrier in the photosynthetic electron transport chain of plants, green algae and cyanobacteria’, and ferredoxins are ‘small iron-sulphur proteins that act as electron carriers in a wide variety of biological redox reactions’.
Now, NADPH is, of course, ‘the reduced form of nicotinamide adenine dinucleotide phosphate’ which acts as ‘a key electron donor and energy carrier’ in various processes, including photosynthesis. So, my guess is that these movements of electrons create chemical changes, and a moment’s research tells me that’s what redox reactions are all about. In oxidation, electrons are lost, which takes the oxidation number up (the substance is oxidised), and in reduction they’re gained, which takes it down, and the substance is reduced.
In oxidation, electrons are lost, which takes the oxidation number up (the substance is oxidised), and in reduction they’re gained, which takes it down, and the substance is reduced.
Ok so that’s enough for now, there’s so much more to explore – rubisco, the z scheme… I cannot help but feel that it’s not light yet, but it’s getting there, to non-paraphrase Dylan….
References
Oliver Morton, Eating the Sun, 2007
covid19: corticosteroids, male susceptibility, evaluating health, remdesivir, coagulation factors
from The Lancet, ‘the four horsemen of a viral apocalpse’
Canto: So short-course use of some steroids was being advocated in the medcram update 88, though without thorough RCT evidence.
Jacinta: Well, data was presented from the Oxford RCT on those on oxygen or on ventilators showing a statistically significant reduction of mortality from short-course (up to 10 days) low dosage of dexamethasone, a freely-available steroid medication. The study involved some 2000 patients, but only those severely afflicted were helped by the medication.
Canto: An interesting aside to the data is that in the study males outnumbered females by almost 2 to 1, and that accords with the overall ratio of male to female covid19 patients Dr Seheult is finding, which rather shocked me. Why would more males be coming down with the disease? Presumably that’s not the infection rate, but the rate at which they need to be hospitalised.
Jacinta: Yes, you’re right, according to this Australian site (unfortunately undated):
Reports continue to emerge that men are significantly more vulnerable to COVID-19 than women. The commonly held perception that more men smoke and this makes them more susceptible along with other lifestyle factors does not tell the whole picture. White House COVID-19 Task Force director Dr Deborah Birx highlighted a “concerning trend” that men in all age brackets were becoming seriously ill from the virus at a higher rate than women, including younger males.
They’re suggesting more research needs to be done on this gender difference, for health issues in general. Some are claiming that estrogen makes a difference. In any case I think cardiovascular problems are more common in males – but maybe not so much in younger males.
Canto: So update 89 is fairly short, and deals with US data about cases and deaths, most of it out of date now, and more on corticosteroids and the dangers of unsupervised use. Update 90 introduces us to a tool I’ve never heard of called ‘Discern’. Very useful for we autodidacts in helping us, for example, to enlighten our doctors as to our condition. Discern is a tool for evaluating internet health info, such as medcram’s updates on youtube, or anything else on youtube. The instrument asks you to evaluate the material according to 16 different criteria. Interestingly, this tool has been tested on covid19 material by a study out of Poland done in March. The results weren’t so good, especially for news channels.
Jacinta: Yes, physicians’ information did best – but of course we don’t go to news channels for health information, and we’d advise against anyone else doing so. The study evaluated the Discern tool itself and found it excellent, then used the tool to evaluate health information, specifically on youtube. Of course know that there’s ‘viral misinformation’ from various news outlets that gets posted on youtube. And good to see that the medcram updates were some of the most highly rated using the Discern tool.
Canto: So we’re now into reporting from early July with update 91. It starts by looking at a ‘covid risk calculator’ in which you can type in your age, gender, BMI, underlying conditions, waist circumference, and other data which you might need a full medical checkup to find out about (and that’s overdue for me), including, for example, %FMD, a measure I’ve never heard of, but which has to do with endothelial function.
Jacinta: FMD stands for fibromuscular dysplasia. The Johns Hopkins medicine site describes it as a rare blood vessel disease in which the cells of some arteries become more stiff and fibrous and less flexible. This leads to weakness and damage. Not sure how it relates to covid19 but surely any pre-existing blood vessel damage is a danger for those contracting the virus.
Canto: Right, so it’s unlikely anyone will know offhand their percentage of FMD. I don’t even know my HDL and LDL levels, never mind my HbA1c or lipids. I’d love to be able to take measures of all these myself, without visiting a doctor.
Jacinta: Typical male control freak. So all of this is to measure your risk of covid19 hospitalisation, ICU admission or mortality. Fun times. So next the update looks at Gilead, the makers of the antiviral remdesivir, who donated all their supplies of the drug to the USA in early May. But of course they kept manufacturing the drug and have to recoup the money they spent researching, developing and trialling it etc. The Wall Street Journal reports that a typical course of the drug will cost over $3000 per patient. Interestingly the Trump administration is wanting the drug to stay in the USA as much as possible, rather than be available overseas, and is spending money to that effect.
Canto: Hmm. Is that protectionism?
Jacinta: Yes I suppose. It’s not surprising that a country wants to look after its own first, especially via a product produced within its own borders. But I suspect this government would’t be interested in helping any other country – unless there was a quid pro quo. And there’s another antiviral, favipiravir, currently being trialled in Japan and the USA (I mean as of early July), and a vaccine, developed in China, is being used on the Chinese military in what seems a rather rushed and somewhat secretive fashion – we don’t know if they got the soldiers’ permission on this seemingly untried vaccine. At least at the phase 3 level.
Canto: Very CCP.
Jacinta: So onto update 92, and we revisit the electron transport chain, with four successive electron transfers converting molecular oxygen into water. Problems within this chain can produce reactive oxygen species (ROS) such as superoxide, hydrogen peroxide and hydroxy radicals, which are destructive in excess. We also look, yet again, at covid19’s impact on angiotensin and particularly the production of superoxide, which in turn causes endothelial dysfunction, increased von Willebrand factor activity, which leads to thrombosis. People were presenting as ‘happy hypoxics’, looking and feeling fine but with very low oxygen levels, and autopsies revealed ‘microthrombi in the interalveolar septa’ of victims’ lungs. All this leading to a paper published in The Lancet which looked at factors in this process of coagulation and thrombosis:
We assessed markers of endothelial cell and platelet activation, including VWF antigen, soluble thrombomodulin [a marker of endothelial cell activation], soluble P-selectin [a marker of endothelial cell and platelet activation], and soluble CD40 ligand [a marker of platelet and T-cell activation], as well as coagulation factors, endogenous anticoagulants, and fibrinolytic enzymes.
So this was about getting to the bottom of the increased clotting. And the results were hardly surprising, but the final discussion section is worth quoting at length, as it seems to capture much that we know about covid19’s effects (at least short-term effects) at the moment:
We therefore propose that COVID-19-associated coagulopathy is an endotheliopathy that results in augmented VWF release, platelet activation, and hypercoagulability, leading to the clinical prothrombotic manifestations of COVID-19-associated coagulopathy, which can include venous, arterial, and microvascular thrombosis. The factors responsible for this endotheliopathy and platelet activation are uncertain but could include direct viral infection of endothelial cells, collateral damage to the tissue as a result of immune infiltration and activation, complement activation, or any number of inflammatory cytokines believed to play a role in COVID-19 disease.
They suggest anti-platelet therapy and endothelial cell modification treatments as well as anticoagulation treatments, and they suggest some agents ‘which might have therapeutic potential’.
Canto: Potential? You’d think they’d be onto all this by now.
Jacinta: Well there’s also potential for untried medications – at least untried in this context – to go terribly wrong. And it’s also likely that some hospitals are already onto using the safer forms of treatment. Dr Seheult speaks of the antioxidant N-acetylcysteine (NAC) in this context, as it has been shown to be a thrombolytic when used intravenously. There are studies pending on the effects of NAC in treating covid19 patients.
Canto: Now, I’ve just been watching something on monoclonal antibodies as perhaps the most promising treatment yet, short of a vaccine. Can you explain….
Jacinta: Yes I’ll try, maybe next time.
References
Coronavirus Pandemic Update 88: Dexamethasone History & Mortality Benefit Data Released From UK
Coronavirus Pandemic Update 89: COVID 19 Infections Rising in Many States; Dexamethasone Cautions
Coronavirus Pandemic Update 90: Assess The Quality of COVID-19 Info With A Validated Research Tool
Coronavirus Pandemic Update 91: Remdesivir Pricing & Disparities in Drug Availability
Coronavirus Pandemic Update 92: Blood Clots & COVID-19 – New Research & Potential Role of NAC
amhf.org.au/covid_19
https://www.thelancet.com/journals/lanhae/article/PIIS2352-3026(20)30216-7/fulltext
more Covid-19 gleanings from MedCram updates 67-69
I’m continuing my self-education re everything Covid-19 thanks to Dr Seheult’s updates and other useful sites. Update 67 carries on from where we left off, summarising again how SARS-CoV2 induces endothelial dysfunction, before focusing on thrombosis. So we repeat again that a key molecule in normal endothelial function and in the working of AT-1,7 is nitric oxide (NO). Endothelial function (and, to be clear, the endothelium lines the vasculature, which means the body’s blood vessels) is also dependent on the various other enzymes mentioned in the last post, e.g. superoxide dismutase (SOD), and glutathione peroxidase (GPx).
So how does Covid-19 bring about oxidative stress and how does this effect thrombosis? Seheult discusses an article from April this year which addresses this. It describes a previously healthy elderly male admitted to hospital with fever and respiratory symptoms. After rapid deterioration he was sent to ICU, having developed ARDS, acute renal insufficiency and other health problems. Among various measures noted was a ‘massive elevation of von Willebrand factor (VWF), as well as ‘factor VIII of the coagulation cascade’. To quote from the article:
The increased VWF points toward massive endothelial stimulation and damage with release of VWF from Weibel-Palade bodies. Interestingly, endothelial cells express ACE-2, the receptor for SARS-CoV2, thus possibly mediating endothelial activation.
To explain some of these terms: Weibel-Palade bodies are found only in epithelial cells, and they contain VWF, which are released when required for haemostasis and coagulation. VWF is a stringy material of amino acid proteins which combine with platelets (aka thrombocytes) to coagulate the blood. When endothelial cells suffer serious damage, Weibel-Palade bodies inject large amounts of VWF into the bloodstream. Dr Seheult presents the abstract from a 2017 article on the topic:
The main function of VWF is to initiate platelet adhesion upon vascular injury. The hallmark of acute and chronic inflammation is the widespread activation of endothelial cells which provokes excessive VWF secretion from the endothelial cell storage pool. The level of VWF in blood not only reflects the state of endothelial activation early on in the pathogenesis, but also predicts disease outcome. Elevation in the blood level of VWF occurs either by pathologic increase in the rate of basal VWF secretion or by increased evoked VWF release from dysfunctional/activated endothelial cells. The increase in plasma VWF is predictive of prothrombotic complications and multi-organ system failure associated with reduced survival in the context of severe inflammatory response syndrome, type 2 diabetes mellitus, stroke and other inflammatory cardiovascular disease states.
The article points out that an over-production of VWF in highly elongated form is an indication of pathology. This is apparently being seen in serious Covid-19 patients. On the molecular level, the VWF is able to remodel itself from its usual globular conformation when it senses shear forces – note this definition from Science Direct: Shear stress is defined as the frictional force generated by blood flow in the endothelium, that is, the force that the blood flow exerts on the vessel wall, expressed in force-area unit (typically dynes/cm2). The VWF, under this stress, ‘turns into an extended chain format that forms ultra-large strings to which platelets bind to initiate clot formation at sites of vascular damage’. When the shear stress reaches a certain level, factor VIII is released. All of this can be essential for haemostasis, but too much of the multimeric, elongated form of VWF will lead to thrombosis, as appeared to be occurring in the patient described above.
So, as Seheult summarises, SARS-CoV2 binds to ACE-2 receptors and reduces ACE-2 production. This reduction has the effect of increasing AT-2 production and reducing AT-1,7. This results in an increase in superoxide production, oxidative stress and endothelial dysfunction. This in turns leads to an increase in VWF activity in the bloodstream, and local thrombosis. There is evidence from autopsies that thrombosis is a feature of Covid-19 mortality.
In his update 68 Dr Seheult looks at the predisposition of some ethnic groups (in the USA) to the more severe symptoms associated with Covid-19. He discussed a May CDC MMWR (morbidity and mortality weekly report) on 580 hospitalised Covid-19 patients which found that 45% were white, as far as they could ascertain, compared to 55% in that region’s community. 33% were black, compared to 18% in the community, and 8% were Hispanic compared to 14% in the community. A smallish sample, but suggestive. The CDC also reported on New York figures showing that Covid-19 death rates among black/African Americans and Hispanic/Latino persons were substantially higher than in the white population. Many possible reasons – work and living conditions, lower access to care – all generally related to relative poverty. There may also be other, purely physiological grounds for the disparity. A 16-year-old research article published in Circulation describes the results of placing nanosensors in isolated human umbilical vein endothelial cells (HUVECS) from blacks and whites (pardon the over-simplification, I’m only the messenger), as an attempt to measure endothelial oxidative stress. I can’t follow the details of the research, but what they found was that blacks expressed much more NADPH oxidase than whites (that’s bad). Nitric oxide, a reducer of oxidative stress, was produced in greater quantities in whites than in blacks, and the bad superoxides were produced in greater quantities in blacks. I won’t go further into the complex biochemistry, but I must say I find these apparent racial differences very surprising.
Update 68 also looks at increasing hospitalisations (at least in May) of young children due to Kawasaki disease, or something similar. The disease is characterised by inflammation of blood vessels. Symptoms include fever, high heart rate and possibly sepsis. There are a number of similarities to Covid-19, including ‘systemic vascular lesions’. Kawasaki disease is normally rare, and believed to be viral, or a response to a virus. A ten-year-old research paper on the disease hypothesises that the infection enters through the respiratory or gastro-intestinal systems, and so unsurprisingly there are similarities to the reaction to SARS-CoV2. Whether there’s a connection between Covid-19 and an uptick in Kawasaki disease has yet to be confirmed (but I’m behind the times on the research on this).
I’m moving now to update 69, and I’m going to follow Dr Seheult through the whole oxidative stress process again. It’s about reduction of oxygen – the adding of electrons. Adding an electron to oxygen, mediated by NADPH oxidase, produces superoxide. Add another electron and you get hydrogen peroxide. Another electron produces hydroxyl, and yet another produces water, moving from most oxidised to most reduced, and adding electrons also brings on protons. So at both ends of this chain you have neutral or positive molecules, but in between you have, I think ROS, reactive oxygen species, which are a problem. The body’s defence against these include the enzyme superoxide dismutase (SOD), which converts superoxide into hydrogen peroxide and also back into oxygen, and catalase which converts hydrogen peroxide into water and oxygen. Another important enzyme which protects against oxidative damage is glutathione peroxidase (GPx). It takes reduced glutathione (2GS-H, called a sulph-hydryl group) and uses it to reduce hydrogen peroxide into water, in the process oxidising the glutathione into a form of disulphide G-S-S-G. This oxidised form is in turn ‘regenerated back’ by taking the reduced form of NADP+ (NADPH) and converting it via glutathione reductase to NADP+.
So the point is that the accumulation of superoxide in people with diabetes, hypertension, coronory disease etc will be exacerbated by Covid-19. And going through that once more, Covid-19 blocks the ACE-2 receptor, causing an accumulation of AT-2 which stimulates superoxide production, and also a deficiency of AT-1,7, which, mediated by nitric oxide, inhibits superoxide production. The SARS-CoV2 virus also attracts PMNs (polymorphonuclear leukocytes – immune cells including neutrophils), which boost superoxide production, with attendant endothelial damage.
I’ll be continuing this series, and no doubt getting further behind, over the next few weeks.
References
Coronavirus pandemic update 67, presented by Dr Roger Seheult, as with all other updates
Coronavirus pandemic update 68
Coronavirus pandemic update 69 (first 5 minutes or so)
https://www.verywellhealth.com/polymorphonuclear-leukocyte-2252099
about ozone, its production and depletion
People will remember the ‘hole in the ozone’ issue that came up in the eighties I think, and investigators found that it was all down to CFCs, which were quite quickly banned, and then everything was hunky dory….
Or that’s how I vaguely recall it. Time to take a much closer look.
I take my cue from ‘An ancient ozone catastrophe?’, chapter 4 of David Beerling’s The emerald planet, in which he looks at the evidence for a previous ozone disaster and its possible relation to the great Permian extinction of 252 millions years ago. I’ll probe into that matter in another post. In this post I’ll try to answer some more basic questions – what is ozone, where is the ozone layer and why does it have a hole in it?
Ozone is also known as trioxygen, which gives a handy clue to its structure. Oxygen can exist in different allotropes or molecular structures which are more or less stable. O3, ozone, is much less stable than O2 and has a very pungent chlorine-like odour and a pale blue colour. It’s present in minute quantities throughout the atmosphere but is most concentrated in the lower part of the stratosphere, 20 to 30 kilometres above the Earth’s surface. This region is called the ozone layer, or ozone shield, though it’s still not particularly dense with ozone, and that density varies geographically and seasonally. Ozone’s instability means that it doesn’t last long, and has to be replenished continually.
In 1928 chlorofluorocarbons (CFCs) were developed as a seemingly safe form of refrigerant, which, under patent as Freon, came to be used in air-conditioners, fridges, hair-sprays and a variety of other products. As it turned out, these CFCs aren’t so harmless when they reach the upper atmosphere, where the chlorine reacts with ozone to form chlorine monoxide (ClO), and regular O2. This reaction is activated by ultraviolet radiation, which then breaks up the unstable ClO, leaving the chlorine to react with more ozone in a continuing cycle.
By the eighties, it had become clear that something was going wrong with the ozone layer. Studies revealed that a gigantic hole in the layer had opened up over Antarctica, and without going into detail, CFCs were found to be largely responsible. There was the usual fight with vested business interests, but in 1987 the Montreal protocol against the use of ozone-depleting substances (ODS) was drawn up, a landmark agreement which has been successful in starting off the long and far from completed process of repair of the ozone shield.
As a very effective oxidant, ozone has many commercial applications, but the same oxidising property makes it a danger to plant and animal tissue. Much better for us to keep most of it up above the troposphere, where its ability to absorb UV radiation has made it virtually essential for maintaining healthy life on Earth’s surface.
So here are some questions. Why does ozone proliferate particularly at the top of the troposphere, in the lower stratosphere? If it’s so reactive, how does it maintain itself at a particular rate? Has the thinning or reduction of that layer seriously influenced life on Earth in the past? From my reading, mainly of Beerling, I think I can answer the first two questions. The third question, which Beerling explores in the above-mentioned chapter of his book, is more speculative, and more interesting.
Sidney Chapman, a brilliant geophysicist and mathematician of the early twentieth century, essentially answered the first question. He realised that ozone was both formed and destroyed by the action of sunlight, specifically UV radiation, on atmospheric oxygen. He calculated that this action would reduce and finally stop at a point approximately 15 km above sea level, because the reactions which had produced the ozone higher up had absorbed the UV radiation in the process. No activation energy to produce any more ozone. That explained the lower limit of ozone. The upper limit was explained by the lack of oxygen in the upper stratosphere to produce a stable layer – for production to exceed destruction. This was interesting confirmation of observations made earlier by the meteorologist and balloonist Léon-Phillippe Teisserenc de Bort, who noted that, contrary to his expectations, the air temperature didn’t fall gradually with altitude but reached a point of stabilisation where the air even seemed to become warmer. He named this upper layer of air the stratosphere, and the cooler more turbulent layer below he called the troposphere. It’s now known that this upper-air warming is caused by the absorption of UV radiation by ozone.
Our picture of ozone still had some holes in it, however, as it seemed there was a lot less of it around than the calculations of Chapman suggested. To quote from Beerling’s book:
… there had to be some as-yet unappreciated means by which ozone was being destroyed. The fundamental leap required to solve the problem was taken comparatively recently, in 1970, by a then young scientist called Paul Crutzen. Crutzen showed that, remarkably, the oxides of nitrogen, produced by soil microbes, catalysed the destruction of ozone many kilometres up in the stratosphere. Few people appreciate the marvellous fact that the cycling of nitrogen by the biosphere exerts an influence on the global ozone layer: life on Earth reaches out to the chemistry of the stratosphere.
Now to explain why the hole in the ozone shield occurred above the Antarctic. My understanding and explanation starts with reading Beerling and ends with this post from the USA’s National Oceanic and Atmospheric Administration’s Earth System Research Laboratory (NOAA/ESRL).
The ozone hole over Antarctica varies in size, and is largest in the months of winter and early spring. During these months, due to the large and mountainous land mass there, average minimum temperatures can reach as low as −90°C, which is on average 10°C lower than Arctic winter minimums (Arctic temperatures are generally more variable than in the Antarctic). When winter minimums fall below around −78°C at the poles, polar stratospheric clouds are formed, and this happens far more often in the Antarctic – for about five months in the year. Chemical reactions between halogen gases and these clouds produce the highly reactive gases chlorine monoxide (ClO) and bromine monoxide (BrO), which are destructive to ozone.
Most ozone is produced in the tropical stratosphere, in reactions driven by sunlight, but a slow movement of stratospheric air, known as the Brewer-Dobson circulation, transports it over time to the poles, so that ozone ends up being more sparse in the tropics. Interestingly, although most ozone-depleting substances – mainly halogen gases – are produced in the more humanly-populated northern hemisphere, complex tropospheric convection patterns distribute the gases more or less evenly throughout the lower atmosphere. Once in the stratosphere and distributed to the poles, the air carrying the halogen-gas products becomes isolated due to strong circumpolar winds, which are at their height during winter and early spring. This isolation preserves ozone depletion reactions for many weeks or months. The polar vortex at the Antarctic, being stronger than in the Arctic, is more effective in reducing the flow of ozone from tropical regions.
So – I’ve looked here briefly at what ozone is, where it is, and how it’s produced and destroyed, but I haven’t really touched on its importance for protecting life here on Earth. So that, and whether its depletion may have had catastrophic consequences 250 million years ago, will be the focus of my next post.
References
The Emerald Planet, by David Beerling, Oxford Landmark Science, 2009