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THE Carbon Dioxide (CO2) Thread Pt. 6

Re: THE Carbon Dioxide (CO2) Thread Pt. 6

Unread postby Tanada » Wed 15 Mar 2017, 11:44:29


Week beginning on March 5, 2017: 406.10 ppm
Weekly value from 1 year ago: 403.75 ppm
Weekly value from 10 years ago: 383.47 ppm
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Re: THE Carbon Dioxide (CO2) Thread Pt. 6

Unread postby Tanada » Sun 19 Mar 2017, 11:40:23

March 18: Unavailable
March 17: Unavailable
March 16: 406.46 ppm
March 15: 407.62 ppm
March 14: 407.29 ppm
I should be able to change a diaper, plan an invasion, butcher a hog, design a building, write, balance accounts, build a wall, comfort the dying, take orders, give orders, cooperate, act alone, solve equations, pitch manure, program a computer, cook, fight efficiently, die gallantly. Specialization is for insects.
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Re: THE Carbon Dioxide (CO2) Thread Pt. 6

Unread postby Tanada » Sun 19 Mar 2017, 11:42:35


Week beginning on March 12, 2017: 407.06 ppm
Weekly value from 1 year ago: 404.69 ppm
Weekly value from 10 years ago: 384.39 ppm
I should be able to change a diaper, plan an invasion, butcher a hog, design a building, write, balance accounts, build a wall, comfort the dying, take orders, give orders, cooperate, act alone, solve equations, pitch manure, program a computer, cook, fight efficiently, die gallantly. Specialization is for insects.
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Re: Huge pits forming in Arctic permafrost

Unread postby Cid_Yama » Wed 22 Mar 2017, 18:17:50

Seems you are arguing about the barn door after the horse is already gone.

In fact, we started warming the planet with the advent of civilization itself. Irrigation, dams, agriculture all contributed.

Fossil Fuels may have accelerated the process, but once we broke the natural cycle of warming and cooling, what is happening became inevitable.

Due to orbital cycles we should be in a cooling phase but we are not. We have overwhelmed that natural cycle.

And now we are in an Extinction Level Event initiated thousands of years ago, but only now coming to fruition. It's not a matter of just moving north.

Temperatures will exceed the ability of warm blooded creatures to lose metabolic heat. Even a period of a few hours of such temperatures will make a place uninhabitable.

Also, other processes kick in. Above 426 ppm CO2, your kidneys start compensating for elevated CO2. Your bones start losing calcium in an attempt to reduce the acidity in the blood. This is a temporary compensation allowing a person to survive an environment of elevated CO2 until they get back to fresh air.

Once the atmosphere is above 426 ppm, the compensation never ends as there will be no fresh air to get back to. This compensation process over time will kill you.

With elevated CO2 comes a decrease in O2. Marine creatures have no ability to compensate, creating dead zones in the ocean. Only surface waters will contain oxygen, and the deep ocean becomes euxinic, with high concentrations of hydrogen sulfide, deadly to life, brought to the surface by upwelling oceans.

And yes, we are beyond the point we can do anything about it. We have been on this path since long before we had any idea. It is doubtful that at any time within the last century we would have been able to do anything, other than postpone it for a few decades, had we known. Even Arrhenius' warning in 1896 would have been too late.

Stop laying blame. Sometimes you just don't know until it's too late.

And we only just found out over the last decade the full extent of what is happening. (Not that some people didn't work really hard to keep people in the dark. But since we can't do anything about it, maybe it's best people don't know. Ignorance is bliss.)

Make the best of the time you have left.
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Re: Huge pits forming in Arctic permafrost

Unread postby rockdoc123 » Wed 22 Mar 2017, 21:27:25

Also, other processes kick in. Above 426 ppm CO2, your kidneys start compensating for elevated CO2. Your bones start losing calcium in an attempt to reduce the acidity in the blood. This is a temporary compensation allowing a person to survive an environment of elevated CO2 until they get back to fresh air.

Once the atmosphere is above 426 ppm, the compensation never ends as there will be no fresh air to get back to. This compensation process over time will kill you.


:shock: :?

my understanding is that submarines have a guideline of operating at no higher than 8,000 ppm Co2 for extended periods (weeks) and that the average concentration in all of the US submarines monitored is around 4,000 ppm.

health organization recommendations focus on such high limits:
In terms of worker safety, Occupational Safety and Health Administration (OSHA) has set a permissible exposure limit (PEL) for CO2 of 5,000 parts per million (ppm) over an 8-hour work day, which isequivalent to 0.5% by volume of air. Similarly, the American Conference of Governmental Industrial Hygienists (ACGIH) TLV (threshold limit value) is 5,000 ppm for an 8 hour workday


https://www.blm.gov/style/medialib/blm/wy/information/NEPA/cfodocs/howell.Par.2800.File.dat/25apxC.pdf
Last edited by Tanada on Thu 23 Mar 2017, 06:52:46, edited 1 time in total.
Reason: fixed broken quote
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Re: Huge pits forming in Arctic permafrost

Unread postby Cid_Yama » Thu 23 Mar 2017, 00:17:35

Those limits were set at least 40 years ago while the research in chronic respiratory toxicity of CO2 has only been within the last decade.

You want to go with what (we thought) we knew a half a century ago over what we know now, be my guest. Can't do anything about it anyway.

Chronic Respiratory Carbon Dioxide Toxicity: a serious unapprehended health risk of climate change
The earth’s atmosphere has already reached CO2 levels that are outside the range breathed by humans throughout their evolution. As well, in earlier pre-primate epochs, elevated atmospheric CO2 has been found to be a cause of mass extinction events (Knoll et al. 1996)

Despite significant documentation of health issues due to CO2 in indoor environments, there is minimal awareness in the community. For spacecraft and submarines there are practical considerations that influence the recommended safe levels. Initial safe limits for the International Space Station were partly decided by engineering requirements (Cronyn et al. 2012) and submarine limits were balanced by the ability to surface and renew air quality. It seems that there has been little concern about low-level toxicity of CO2 because we have always had the back-up of an ambient atmosphere with low levels of CO2.

As mentioned previously the body compensates for high levels of CO2, through a combination of increased breathing, blood pH buffering, kidney and bone adaptations depending on the length of continuous exposure, until we can resume breathing lower levels of CO2.

One author suggests that blood pH would be reduced to dangerous levels, if there were no physiological compensation, at CO2 levels as low as about 430 ppm (Robertson 2006) implying that compensation would occur at this level. Ambient conditions may already be dangerously close to CO2 levels that will induce continuous body compensation. Moreover, there is strong evidence that, with chronic activity, compensation mechanisms can produce serious health issues such as kidney calcification and bone loss.

It is conceivable that these problems might appear at much lower levels of CO2 if compensation persisted for a much longer periods, for example living a whole lifetime in an elevated CO2 atmosphere of a climate changed future. In the final paper of the US Navy CO2 research program, Schaefer (1982) indicated that this issue had “become the concern of the Department of Energy and other US government agencies” although it appears to have been largely forgotten (or classified) since.

If allowed to persist, problems such as kidney calcification could lead to renal failure. In the extreme case lifespans could become shorter than the time required to reach reproductive age. This could threaten the viability of human and animal species without interventions such as the creation of artificial living environments.

The human species is already impaired in indoor environments and this is likely to get worse as rising outdoor levels of CO2 contribute to increased indoor concentrations. Furthermore, the incidence and prevalence of human kidney calcification (i.e. stones) is increasing globally with the rate highest for males (Romero et al. 2010). Although this may not be related, it is possible that rising office levels of CO2 is a contributing cause. As well there is evidence that CO2 toxicity contributes to a range of serious health issues including cancer, neurological diseases and sleep disorders, and is being experienced by individuals at the current ambient levels which are now 40% higher than pre-industrial levels. It seems likely that CO2 toxicity related to human-induced climate change is already having an unrecognised impact on population health.

From the evidence presented here, there appears to be current health impacts of rising CO2 levels and a significant risk of serious health issues arising in the human population at some time in this century.

This means that most humans could at this time be experiencing persistent body compensation for acidosis effects resulting in serious health problems. The risk for human and animal population health in the near-future is extremely high and should be communicated since global awareness of this issue may enable a change in CO2 emission activities.

link


Health effects of increase in concentration of carbon dioxide in the atmosphere


Because it's medical researchers who are first to recognize this, the awareness is not high among those concerned with climate change. But it is soundly based on human physiology.

It's another case of finding out too late how serious our predicament is.
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Re: Huge pits forming in Arctic permafrost

Unread postby GregT » Thu 23 Mar 2017, 01:20:18

Thanks for that link Cid. Very sobering indeed. At current rates of CO2 increase, we should reach 430ppm within 15 years time.

Wonderful.
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Re: Huge pits forming in Arctic permafrost

Unread postby Cid_Yama » Thu 23 Mar 2017, 06:49:48

The lowest value at which the atmospheric concentration of carbon dioxide could be stabilized by reduction of additions made by human activity (fossil fuel-burning, etc.) is estimated as 550 ppm. To achieve this, severe limitations are required on the latter activities. The most often quoted desirable/attainable stable concentration is 750 ppm. This concentration level is not related in any way to health considerations and is above the estimated dangerous level of 426 ppm. The value is also above the 600 ppm level, which results in the ‘stuffy room’ conditions described above. At the very least, 600 ppm of carbon dioxide in the atmosphere will be unpleasant and there will be no readily available means of reversing the changes giving rise to the above symptoms. Such a situation is unlikely to be tolerable for a lifetime by humans (and other mammals with the possible exception of seals) without deterioration in general health along with serious curtailing of physical activity presently taken as normal.
It is likely that when the concentration of carbon dioxide in the atmosphere reaches 426 ppm in less than two generations from the present date(2005), the health of at least some sections of the world population will deteriorate, including those of the developed nations. It is also obvious that if the extremes of conditions described above come to pass, then the biosphere and humankind are seriously threatened.

link
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Re: Huge pits forming in Arctic permafrost

Unread postby Tanada » Thu 23 Mar 2017, 06:58:53

Cid_Yama wrote:Those limits were set at least 40 years ago while the research in chronic respiratory toxicity of CO2 has only been within the last decade.

You want to go with what (we thought) we knew a half a century ago over what we know now, be my guest. Can't do anything about it anyway.

Chronic Respiratory Carbon Dioxide Toxicity: a serious unapprehended health risk of climate change
The earth’s atmosphere has already reached CO2 levels that are outside the range breathed by humans throughout their evolution. As well, in earlier pre-primate epochs, elevated atmospheric CO2 has been found to be a cause of mass extinction events (Knoll et al. 1996)

Despite significant documentation of health issues due to CO2 in indoor environments, there is minimal awareness in the community. For spacecraft and submarines there are practical considerations that influence the recommended safe levels. Initial safe limits for the International Space Station were partly decided by engineering requirements (Cronyn et al. 2012) and submarine limits were balanced by the ability to surface and renew air quality. It seems that there has been little concern about low-level toxicity of CO2 because we have always had the back-up of an ambient atmosphere with low levels of CO2.

As mentioned previously the body compensates for high levels of CO2, through a combination of increased breathing, blood pH buffering, kidney and bone adaptations depending on the length of continuous exposure, until we can resume breathing lower levels of CO2.

One author suggests that blood pH would be reduced to dangerous levels, if there were no physiological compensation, at CO2 levels as low as about 430 ppm (Robertson 2006) implying that compensation would occur at this level. Ambient conditions may already be dangerously close to CO2 levels that will induce continuous body compensation. Moreover, there is strong evidence that, with chronic activity, compensation mechanisms can produce serious health issues such as kidney calcification and bone loss.

It is conceivable that these problems might appear at much lower levels of CO2 if compensation persisted for a much longer periods, for example living a whole lifetime in an elevated CO2 atmosphere of a climate changed future. In the final paper of the US Navy CO2 research program, Schaefer (1982) indicated that this issue had “become the concern of the Department of Energy and other US government agencies” although it appears to have been largely forgotten (or classified) since.

If allowed to persist, problems such as kidney calcification could lead to renal failure. In the extreme case lifespans could become shorter than the time required to reach reproductive age. This could threaten the viability of human and animal species without interventions such as the creation of artificial living environments.

The human species is already impaired in indoor environments and this is likely to get worse as rising outdoor levels of CO2 contribute to increased indoor concentrations. Furthermore, the incidence and prevalence of human kidney calcification (i.e. stones) is increasing globally with the rate highest for males (Romero et al. 2010). Although this may not be related, it is possible that rising office levels of CO2 is a contributing cause. As well there is evidence that CO2 toxicity contributes to a range of serious health issues including cancer, neurological diseases and sleep disorders, and is being experienced by individuals at the current ambient levels which are now 40% higher than pre-industrial levels. It seems likely that CO2 toxicity related to human-induced climate change is already having an unrecognised impact on population health.

From the evidence presented here, there appears to be current health impacts of rising CO2 levels and a significant risk of serious health issues arising in the human population at some time in this century.

This means that most humans could at this time be experiencing persistent body compensation for acidosis effects resulting in serious health problems. The risk for human and animal population health in the near-future is extremely high and should be communicated since global awareness of this issue may enable a change in CO2 emission activities.

link


Health effects of increase in concentration of carbon dioxide in the atmosphere


Because it's medical researchers who are first to recognize this, the awareness is not high among those concerned with climate change. But it is soundly based on human physiology.

It's another case of finding out too late how serious our predicament is.



I call BS. My younger brother served as a nuclear submariner as have quite literally tens of thousands of sailors over the last century. Even in its current shrunken state the US Navy has about a thousand sailors out to sea 24/7/365 in submarines breathing air with much higher CO2 levels than this so called researcher uses to draw their conclusions. Many of those same sailors serve out 20 year careers of which roughly half the period is in those higher exposure regimes. I am confident that if hundreds of former submariners were suffering severe consequences of that exposure it would be big news, especially given how the MSM likes to sensationalize just about every story they ever hear of that makes the military leadership look bad.
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Re: Huge pits forming in Arctic permafrost

Unread postby dohboi » Thu 23 Mar 2017, 09:39:57

IIRC, we've had this conversation here before...maybe many times. Is this the best thread for a re-do of it?
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Re: THE Carbon Dioxide (CO2) Thread Pt. 6

Unread postby Tanada » Thu 23 Mar 2017, 10:58:04

March 22: 406.56 ppm
March 21: 406.63 ppm
March 20: 406.30 ppm
March 19: 406.74 ppm
March 18: Unavailable
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Re: THE Carbon Dioxide (CO2) Thread Pt. 6

Unread postby Cid_Yama » Thu 23 Mar 2017, 13:18:43

Yes, I know. It's a conspiracy of the medical community now.

The Stress of Global Warming on Human Health: pH Homeostasis, the Linkage between Breathing and Feeding via CO2 Economy.
Significantly, earlier human studies have shown that chronic exposure to CO2 at moderate inspired concentrations alters pH homeostasis, and fosters body CO2 storage at the expense of buffers protein and phosphates in lean body mass, as does higher atmospheric CO2 concentration in the terrestrial biosphere. Increased CO2 stores matching lower bone mineralization characterizes Osteoporosis, a major public health problem whose risks for osteopenia, and non-spine fractures are significantly higher for people with higher percentage of body fat. Increased CO2 storage is present also in obstructive sleep apnea, a prevalent disorder characterized by gradual elevations of the partial pressure of CO2 in the arterial blood, associated with major nocturnal hemoglobin desaturation, higher HbO2 affinity, and repetitive episodes of partial or complete upper airway obstruction. Most individuals with obstructive sleep apnea have metabolic syndrome, term describing the clustering of abdominal obesity with other risk factors for atherosclerotic-cardiovascular disease (ACVD) which show abnormal intracellular ion profile in red blood cells, and sustained cortisol levels as does chronic exposure to increased ambient CO2. Studies suggest that moderately increased endogenous CO2 may oxidize erythrocytes, and promote their suicidal death (eryptosis) which, by fostering the release of pro-inflammatory cytokines throughout systemic circulation, activates hormonal stress response, and results in increased CO2 stores, abdominal fat accumulation, and Metabolic Syndrome. Ominously, Global Warming is an unbearable stress for ecosystems and their member species, just as this cluster of ACVD risk factors is for human health. This review focuses on Metabolic Syndrome and pH homeostasis, the linkage between breathing and feeding via CO2 economy, to disclose the Stress of global Warming on human health.

Earlier human studies have shown that chronic, continuous exposure to CO2 at 0.5-3% inspired concentrations for more than one month alters pH homeostasis and raises body CO2 storage [15,16,17], as does higher atmospheric CO2 concentration in the terrestrial biosphere. Mostly during CO2 exposure, ion profile changes in red blood cells (RBCs); hemoglobin-O2(HbO2) affinity increases with RBCs oxidation; the adrenal cortical response is activated, as measured by increased blood corticosteroid level and lymphopenia; and the partial pressure of CO2 in the arterial blood (PaCO2) rises as CO2 is stored as HCO3- in the extracellular fluid (ECF), and as CO3-2 in bone, at the expense of buffer protein and phosphate in the lean body mass (LBM) [15,16,17]. Continuous CO2 inhalation is commonly thought to be tolerated at 3% inspired concentrations for at least one month, and 4% inspired concentrations for over a week. The effects produced seem reversible, decrements in performance or in normal physical activity may not happen at these concentrations [18].

Thus, it should be noted not only that CO2 levels in poorly ventilated spaces can be found even higher than this range of 3-4%, but also that humans may be chronically exposed to intermittent, not continuous CO2 inhalation, a condition that by inducing mildly increased endogenous CO2 may cause pathological adaptations. In fact, studies show that because of the greater concentration of buffer base, acclimatization to CO2 results in desensitization of dyspnea and in changes of set point for central respiratory controllers such that, on return to “outdoor” air breathing, ventilation may decline below control values even in individuals intermittently exposed to CO2 increase for 13 hours per day [15,19]. Furthermore, chronic exposure to intermittent, mild ambient CO2 increase results also in changes of set point for central feeding controllers which may lead to obesity. In fact, it has been shown that during chronic inhalation of CO2 at 1.5% inspired concentration for more than one month, food intake decreases significantly, by ~30%, but body weight does not change [17]. On return to “normal” air breathing, food intake rises and body weight is gained [20]. Actually, stress is a well known inducing factor of both transient and chronic loss of appetite or overeating [21].

Inhaled CO2 induces the same physiological effects as does metabolically produced CO2, the key chemical messenger gas in the linking of respiration, systemic circulation, and local vascular response, to body’metabolic demands both at rest and exercise [18]. Increased CO2 needs to be removed as quickly as possible because its lowering of blood pH can denature enzymes. A major portion of the physicochemical defenses of neutrality by the buffer systems of the whole body takes place in muscle and bone [24]. Protein from muscle can be released to bind with acids in the blood. This can contribute to LBM loss. Calcium and phosphorus in bones can bind to acidic substances to neutralize them, thereby contributing to bone mineral loss. Suggestively, greater CO2 stores matching reduced bone mineralization characterizes Osteoporosis, a major public health problem whose risks for osteopenia, and non-spine fractures have been shown to be significantly higher for people with higher percentage of body fat [25]. Increased CO2 storage is present also in obstructive sleep apnea (OSA), a prevalent disorder characterized by gradual PaCO2 elevations, associated with major nocturnal hemoglobin desaturation, higher HbO2 affinity, and repetitive episodes of partial or complete upper airway obstruction [26]. Most individuals with OSA have metabolic syndrome (MetS), a common, condition consisting of a constellation of metabolic risk factors for atherosclerosis and cardiovascular disease (ACVD) associated with abdominal obesity, namely, increased plasma glucose values, higher blood pressure levels, higher triglycerides levels, and lower high-density lipoprotein cholesterol (HDL-C) levels [27]. The MetS presents abnormal intracellular ion profile in RBCs, and sustained cortisol levels [28,29] as does exposure to CO2 at 1.5% inspired concentrations for more than one month [17,30].

As stated, CO2 acclimatization to chronic exposure to CO2 at 1.5% inspired concentration results in greater concentrations of buffer base, with the consequent reduction of minute volume ventilation, forced vital capacity, and PaO2 [15]. Beyond that, food intake rises, and body weight is gained, on return to “normal” air breathing [20], as compared to exposure to moderately increased ambient CO2 in which lower (~30%) food intake, without body weight changes, matches increased ventilation [17]. Accordingly, adaptations to chronic exposure to intermittent, mildly increased ambient CO2 may result in lower O2 uptake, reduced metabolic rate, and excess feeding, as it occurs in MetS. Food intake may rise because mildly increased endogenous CO2 enhances the expression of TNF-α and IL-6, which further glucocorticoids release, with consequent higher expression of the oroxigenic NPY. Hence, CO2 does not only determine the need for alveolar ventilation, but it is also the “stress” ruler of both transient and chronic overeating or loss of appetite [21], to normalize/oppose pH changes.

With moderately increased endogenous CO2, as soon as RBCs oxidation threatens pH homeostasis, TNF-α may induce the coincident appearance of MetS ACVD risk factors [97] to restore the lost balance. In essence, TNF-α inhibits auto-phosphorylation of tyrosine residues of insulin receptors and promotes serine phosphorylation of insulin receptor substrate-1; this, in turn, triggers serine phosphorylation of insulin receptors in adipocytes, prevents the normal tyrosine phosphorylation, and interferes with transduction of the insulin signal. Hence, insulin resistance results in Akt (protein-kinase-B) inhibition and subsequent
inhibition of NO-synthase (NOS) [97]. Accordingly, TNF-α promotes adaptations such as insulin resistance-hyperglycemia, NOS inhibition, reoccurrence of glycolysis, and decreased O2 uptake whose joined effects overall reduce RBCs oxidation and maintain blood O2 release. Inflammation is, indeed, a fundamental survival mechanism but it is dangerous when its transient, physiological adaptations are converted to a long-lasting, pathological state. Potential causes for steady CRH activation and glucocorticoids release include environmental stresses, which as explained, result in higher HbO2 affinity and mildly increased endogenous CO2 [23]. Ominously, as atmospheric CO2 increases, Global Warming may threaten human health. Thus, the following reviews the mechanism through which intermittent exposure to mildly increased ambient CO2 may lead to MetS and/or osteoporosis.

Overall, during exposure to mildly raised ambient CO2 levels, slow adaptive processes in electrolyte exchange and pH regulation results in higher PaCO2 due to reduction in forced vital capacity. Presumably, food intake decreases much to reduce PaCO2, and body weight does not change [17] due to the water retention required to hydrate and store the inhaled CO2 as ECF HCO3-, and as bone CO3-2. Basically, with CO2 acclimatization, compensatory processes for respiratory acidosis result in metabolic alkalosis [107] which, on return to “normal” air breathing, constantly triggers glucocorticoids release. In fact, with abdominal accumulation, a lower compliance of the respiratory system causes the decline of forced vital capacity, minute volume ventilation, and PaO2 [15], with ensuing chronic lactate accumulation. This, by raising HbO2 affinity, results in higher PaCO2[49], and RBCs oxidation with TNF-α and IL-6 release from phagocytic cells. Besides, the relentless LBM loss coupled to the body fat gain arisen during exposure to CO2 implies not only that HbO2 affinity rises, and O2 release falls because the loss of body phosphate impairs 2-3DPG synthesis [53], but also that adipocytes release TNF-α and IL-6. Presumably, on return to normal air breathing, food intake rises, and insulin resistance persists until an ampler number of adipocytes release enough leptin which lowers bone formation and food intake without respiratory depression. In few words, with chronic exposure to intermittent, mildly increased CO2, body buffers loss sets a vicious cycle in which the more CO2 is inhaled and stored, the more food is eaten to raise PaCO2, foster ventilation, and save pH homeostasis.
With time, however, steady activation of the stress response leads to the loss of bone and muscle which, due to parallel abdominal fat accumulation, causes shallow, rapid breathing (not conscious tachypnea), turns up the set point for central feeding controllers, and induces overeating with its chronic pathological consequences, namely, MetS and osteoporosis.

Chronic exposure to CO2 at 0.5-3% inspired concentrations alters pH homeostasis and fosters body CO2 storage in humans [15,16, 17], as does increased atmospheric CO2 in the terrestrial biosphere. Increased CO2 stores in bone are present in osteoporosis, whose risks for osteopenia, and non-spine fractures have been shown to be significantly higher for subjects with higher percentage body fat, independent of body weight [25]. Fat accumulation and increased CO2 stores characterize also MetS which, despite lifestyle changes and the use of pharmacologic approaches to lower plasma cholesterol levels, continues to be, and it is expected to become the major cause of disability and death in the world by 2020 [108]. So far, it seems undeniable that pH homeostasis, the linkage between breathing and feeding via CO2 economy, discloses the stress of Global Warming on human health.

link

Actually you HAVE heard about the increase in cardiovascular disease, kidney disease, diabetes, osteoporosis and obesity but not the connection to chronic exposure to elevated CO2 levels.

This research has been conducted and the link elucidated only within the last decade. We now know what we didn't know then.

And it isn't just submariners who have been exposed to chronic elevated levels, but 9-5ers in office buildings and classrooms.

These diseases, though they have become 'normalized' in modern society, are pathological. And increasing with increased CO2 levels.
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Re: THE Carbon Dioxide (CO2) Thread Pt. 6

Unread postby rockdoc123 » Thu 23 Mar 2017, 14:35:58

1.5% ,which is the CO2 chronic exposure referenced in most of the studies in the paper equates to 15,000 ppm, about 35 times the current level in atmosphere. RCP 8.5, which is believed to be an over the top projection of CO2 levels by 2100 given current rates of increase, a notion of peak oil and demand shift to alternatives suggests a level of around 1300 ppm less than a tenth of what the experiments referenced were done at.

And one also has to always keep in mind the limitations of medical experiments. In the past decade coffee has been first bad for us, then good for us and then bad for us. Some medical researchers suggest alcohol in small amounts is good for humans whereas others suggest alcohol in any amount is bad, some claim asparatame is a carcinogen others suggest it is harmless. Such is the nature of experiments with humans which are difficult to control at the best of times and worse when double blind tests are not utilized. This is why Tanada mentioned the real world example of submariners exposed to very high levels of CO2 for prolonged periods with no apparent issues.
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Re: THE Carbon Dioxide (CO2) Thread Pt. 6

Unread postby Cid_Yama » Thu 23 Mar 2017, 18:02:15

No, 1.5% is 1500ppm and .5 is 500ppm. Noticed you ignored the low end and only mention the high end then inflated it by a factor of 10. Don't miss a trick do you.

Robertson has determined chronic physiological compensation begins at 426 ppm. That is when the damage starts.

Feel free to poo poo the research. No skin off my ass. I'm old enough to be gone before things get really nasty.

Just out of curiosity, are you suggesting this research be ignored? Why, because it's recent? Because we thought differently a half century ago and didn't recognize the long-term damage being done?

Or maybe because it would be cost prohibitive for buildings and businesses and devastating for the fossil fuel industry?

Always the shill.

Medicine has for a long time understood the metabolic pathways involved from Chronic Respiratory Acidosis and hypercapnia. The only thing recent is the connection between chronic exposure to low-level elevated CO2 and these diseases being the result of chronic physiological compensation for that exposure.

Not much you can argue against, except try to dismiss it whole cloth as you just attempted.
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Re: THE Carbon Dioxide (CO2) Thread Pt. 6

Unread postby rockdoc123 » Thu 23 Mar 2017, 19:49:54

No, 1.5% is 1500ppm and .5 is 500ppm. Noticed you ignored the low end and only mention the high end then inflated it by a factor of 10. Don't miss a trick do you.


ppm means parts per million.....hence 15000 ppm is 15000/1000000 which equals = 0.015 which is 1.5%

but don't believe me, I'm just a scientist:

http://www.co2meter.com/blogs/news/15164297-co2-gas-concentration-defined

Parts-per-million (abbreviated ppm) is the ratio of one gas to another. For example, 1,000ppm of CO2 means that if you could count a million gas molecules, 1,000 of them would be of carbon dioxide and 990,000 molecules would be some other gases.

When you start counting over 10,000ppm, most manufacturers move from ppm to percent concentration. So instead of describing a 50,000ppm CO2 sensor, we talk about a 5% CO2 sensor instead. (50,000/1,000,000 = 0.05) – the terms are synonymous. In other words, 1ppm = 0.0001% gas.


Robertson has determined chronic physiological compensation begins at 426 ppm. That is when the damage starts.


did you read that paper? Apparently not because he offers no studies done for long periods of time at low CO2 concentrations. From what I could tell all he is doing is listing off studies done at high concentrations and then speculating. He does show a plot of blood PH verus CO2 levels but doesn't bother to mention that CO2 is quickly converted and expelled as a means of the body buffering Ph. I see no mention of a study which suggests this natural buffering shuts down at low concentrations nor that the body can build up concentrations of CO2 over time unless something else has gone wrong to offset the natural buffering system. Not a medical doctor so perhaps I missed it though.

Medicine has for a long time understood the metabolic pathways involved from Chronic Respiratory Acidosis and hypercapnia. The only thing recent is the connection between chronic exposure to low-level elevated CO2 and these diseases being the result of chronic physiological compensation for that exposure.

Not much you can argue against, except try to dismiss it whole cloth as you just attempted.


I suspect most of them got the conversion between percentage concentration and ppm correct though. :roll:
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Re: THE Carbon Dioxide (CO2) Thread Pt. 6

Unread postby Cid_Yama » Fri 24 Mar 2017, 01:05:33

You are, of course, correct on the percentage to ppm, brain fart, sorry.

Robertson, if you followed the footnote, refers back to a previous paper, which is why you don't see it here. I have requested access and will post it when I get it.

What you missed it that it is the physiological compensation itself, when it becomes chronic, that leads to the diseases mentioned. This compensation becomes chronic at atmospheric levels around 426 ppm and there are indications that such compensation is already taking place at current levels.

These papers are warning about chronic exposure to levels below 1000 ppm, levels expected to be reached this century. And chronic exposure to even higher levels in buildings. And that some people are already experiencing health impacts.

The human species is already impaired in indoor environments and this is likely to get worse as rising outdoor levels of CO2 contribute to increased indoor concentrations. As well there is evidence that CO2 toxicity contributes to a range of serious health issues including cancer, neurological diseases and sleep disorders, and is being experienced by individuals at the current ambient levels which are now 40% higher than pre-industrial levels. It seems likely that CO2 toxicity related to human-induced climate change is already having an unrecognised impact on population health.

From the evidence presented here, there appears to be current health impacts of rising CO2 levels and a significant risk of serious health issues arising in the human population at some time in this century.

This means that most humans could at this time be experiencing persistent body compensation for acidosis effects resulting in serious health problems. The risk for human and animal population health in the near-future is extremely high.


That's from the paper you pulled the 1.5% from, referring to one study looking at higher concentrations.

We are talking about a problem that is taking place now and will progressively get worse.

And there is no place to go to get some fresh air.
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Re: THE Carbon Dioxide (CO2) Thread Pt. 6

Unread postby Tanada » Fri 24 Mar 2017, 06:46:27

The basic problem I have with these claims is twofold. First studies of human being are notoriously difficult to preform for moral, ethical, and expense reasons. You don't get good data from journals or proxy studies when the group in the study has free access to do things outside the bounds of the study.

The second issue is, human have been living in both natural and artificial shelters for 250,000 years more or less with fire a constant factor during that entire period. Leaky building or not for at least the last 50,000 northern people have lived in structures with cooking and heating fires and for at least the last 3,000 years flame based light sources inside structures. When you cook over a fire pit or with a fire place or cast iron stove you breath air with very high CO2 concentration. When you are boiling clothes or making beer or forging metal the same applies. When your family gathers around the table in the evening to tell stories or play games and the light comes from a candle or a flame lamp burning grease or oil or petroleum you are all breathing high CO2 concentrations.

The buffering capacity of the human body is extremely efficient. Blood acidosis only takes place at extreme levels, and if you are eating anything near a balanced diet your body will uptake the chemicals it needs to buffer far more than you think. There has been this whole Acid vs Alkaline diet craze for at least the last 20 years trying to get people to eat certain ways, but the fact is what you eat is not the key, what your gut absorbs and how quickly your kidneys and liver remove it from your blood is the key. Your kidneys and liver work together in concert to keep your blood Ph right at the optimum level.
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Re: THE Carbon Dioxide (CO2) Thread Pt. 6

Unread postby Cid_Yama » Fri 24 Mar 2017, 07:35:53

You are missing the point. Perhaps because I am using the term compensation (which covers a slew of metabolic changes that take place during chronic acidosis) instead of buffering.

The problem isn't whether we can buffer and maintain ph homeostasis, it is when that buffering (and all the other metabolic changes) becomes continuous.

It is the continuous compensation for elevated CO2, that causes the damage. Our physiology evolved these mechanisms as a temporary compensation for elevated CO2. But that exposure has always been temporary. Low levels of CO2 in the atmosphere we evolved in allowed our bodies to expel that CO2. We just had to get some fresh air. Step outside. In fact we lived most of our days outside.

But we have lost the atmosphere we evolved in. And CO2 levels continue to increase, forcing our bodies into continuous compensation, which is literally killing us.

The mechanisms by which it is doing this, the metabolic pathways, and physiological changes we are experiencing are detailed in the last paper I posted.

It shows that the chronic compensation, and the storing of CO2 in our bodies, is directly responsible for Metabolic Syndrome, a cluster of metabolic changes leading to Arteriosclerotic-Cardiovascular Disease, Osteoporosis, Diabetes, Chronic Kidney Disease and Obesity. This is the damage being done as the result of chronic compensation for elevated CO2. It is damaging our heart, bones, pancreas, kidneys, and brain. It is causing permanent detrimental physiological changes. Even so far as to damage our DNA, causing cancers and vascular changes in the brain leading to neurological disorders.

The chronic compensation for elevated CO2 is literally killing us as we enter a world with an atmosphere that causes continuous acidosis. Just like it is acidifying the oceans, it is acidifying our bloodstream. As our bodies destroy themselves trying to compensate.
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Re: THE Carbon Dioxide (CO2) Thread Pt. 6

Unread postby dissident » Fri 24 Mar 2017, 09:03:48

In spite of all the sniping there is a case here. Modern humans showed up in the last several hundred thousand years and most human evolution towards larger brain size has happened in the last 5 million years. CO2 levels were not systematically over 400 ppmv at any time during this period, in fact they were under 320 ppmv aside from a period associated with the closing of the Panama channel. So humans are not biochemically adapted to 400+ ppmv CO2 levels. I can see the rapid hand waving coming that a 50% CO2 increase is basically zero. Prove it! That these studies were done at much higher dosages does not imply zero effect at 400 ppmv. And we are talking about a lifetime integrated effect. Perhaps this additional metabological stress acts as a nucleating agent allowing other processes to get a foothold.

The smug dismissals of this biochemical aspect are obnoxious. Right along the lines that aerosol nanoparticles have no health effects being peddled by corporate shills. Apparently, what you can't see, can't hurt you.
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Re: THE Carbon Dioxide (CO2) Thread Pt. 6

Unread postby kiwichick » Fri 24 Mar 2017, 16:05:00

well said diss
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