Carbon monoxide poisoning

[Jhanananda]

Long term carbon monoxide poisoning has been one of the possible causal agents that I have been looking into regarding my declining health.  I had speculated that carbon monoxide might accumulate in the bottom of the bowl that forms the Prescott basin.

Today I was looking through a thrift store for needed items.  There I came across a carbon monoxide detector.  It was only $3, so I bought it.  I plugged it into the inverter in my van and drove to the park to spend the rest of the day.  On the way I noticed that carbon monoxide levels inside my van rose from 0 to 15 parts per million.

I know the doghouse over the engine in my van leaks, and the engine has not been doing well for 2 months now.  So, it looks like I may have been poisoning myself with monoxide coming from the engine of my old van all along.

Carbon monoxide (CO) is a colorless, odorless, and tasteless gas that is slightly less dense than air. It is toxic to hemoglobic animals (including humans) when encountered in concentrations above about 35 ppm, although it is also produced in normal animal metabolism in low quantities, and is thought to have some normal biological functions. In the atmosphere, it is spatially variable and short lived, having a role in the formation of ground-level ozone.

Carbon monoxide consists of one carbon atom and one oxygen atom, connected by a triple bond that consists of two covalent bonds as well as one dative covalent bond. It is the simplest oxocarbon and is isoelectronic with the cyanide anion, the nitrosonium cation and molecular nitrogen. In coordination complexes the carbon monoxide ligand is called carbonyl.

Carbon monoxide is produced from the partial oxidation of carbon-containing compounds; it forms when there is not enough oxygen to produce carbon dioxide (CO2), such as when operating a stove or an internal combustion engine in an enclosed space. In the presence of oxygen, including atmospheric concentrations, carbon monoxide burns with a blue flame, producing carbon dioxide.[5] Coal gas, which was widely used before the 1960s for domestic lighting, cooking, and heating, had carbon monoxide as a significant fuel constituent. Some processes in modern technology, such as iron smelting, still produce carbon monoxide as a byproduct.[6]

Worldwide, the largest source of carbon monoxide is natural in origin, due to photochemical reactions in the troposphere that generate about 5×1012 kilograms per year.[7] Other natural sources of CO include volcanoes, forest fires, and other forms of combustion.

In biology, carbon monoxide is naturally produced by the action of heme oxygenase 1 and 2 on the heme from hemoglobin breakdown. This process produces a certain amount of carboxyhemoglobin in normal persons, even if they do not breathe any carbon monoxide. Following the first report that carbon monoxide is a normal neurotransmitter in 1993,[8][9] as well as one of three gases that naturally modulate inflammatory responses in the body (the other two being nitric oxide and hydrogen sulfide), carbon monoxide has received a great deal of clinical attention as a biological regulator. In many tissues, all three gases are known to act as anti-inflammatories, vasodilators, and promoters of neovascular growth.[10] Clinical trials of small amounts of carbon monoxide as a drug are ongoing.[11] Nonetheless, too much carbon monoxide causes carbon monoxide poisoning.

Toxicity
Main article: Carbon monoxide poisoning

Carbon monoxide poisoning is the most common type of fatal air poisoning in many countries.[27] Carbon monoxide is colorless, odorless, and tasteless, but highly toxic. It combines with hemoglobin to produce carboxyhemoglobin, which usurps the space in hemoglobin that normally carries oxygen, but is ineffective for delivering oxygen to bodily tissues. Concentrations as low as 667 ppm may cause up to 50% of the body's hemoglobin to convert to carboxyhemoglobin.[28] A level of 50% carboxyhemoglobin may result in seizure, coma, and fatality. In the United States, the OSHA limits long-term workplace exposure levels above 50 ppm.[29] Within short time scales, carbon monoxide absorption is cumulative, since the half-life is about 5 hours in fresh air.

The most common symptoms of carbon monoxide poisoning may resemble other types of poisonings and infections, including symptoms such as headache, nausea, vomiting, dizziness, fatigue, and a feeling of weakness. Affected families often believe they are victims of food poisoning. Infants may be irritable and feed poorly. Neurological signs include confusion, disorientation, visual disturbance, syncope (fainting), and seizures.[30]

Some descriptions of carbon monoxide poisoning include retinal hemorrhages, and an abnormal cherry-red blood hue.[31] In most clinical diagnoses these signs are seldom noticed.[30] One difficulty with the usefulness of this cherry-red effect is that it corrects, or masks, what would otherwise be an unhealthy appearance, since the chief effect of removing deoxygenated hemoglobin is to make an asphyxiated person appear more normal, or a dead person appear more lifelike, similar to the effect of red colorants in embalming fluid. The "false" or unphysiologic red-coloring effect in anoxic CO-poisoned tissue is related to the meat-coloring commercial use of carbon monoxide, discussed below.

Carbon monoxide also binds to other molecules such as myoglobin and mitochondrial cytochrome oxidase. Exposures to carbon monoxide may cause significant damage to the heart and central nervous system, especially to the globus pallidus,[32] often with long-term chronic pathological conditions. Carbon monoxide may have severe adverse effects on the fetus of a pregnant woman.

Occurrence
Carbon monoxide occurs in various natural and artificial environments. Typical concentrations in parts per million are as follows:
Composition of dry atmosphere, by volume[41] ppmv: parts per million by volume (note: volume fraction is equal to mole fraction for ideal gas only, see volume (thermodynamics))
Concentration    Source
0.1 ppmv    Natural atmosphere level (MOPITT)[42]
0.5–5 ppmv    Average level in homes[43]
5–15 ppmv    Near-properly adjusted gas stoves in homes, modern vehicle exhaust emissions[44]
17 ppmv    Atmosphere of Venus
100–200 ppmv    Exhaust from automobiles in the Mexico City central area in 1975[45]
700 ppmv    Atmosphere of Mars
5,000 ppmv    Exhaust from a home wood fire[46]
7,000 ppmv    Undiluted warm car exhaust without a catalytic converter[44]

Urban pollution

Carbon monoxide is a temporary atmospheric pollutant in some urban areas, chiefly from the exhaust of internal combustion engines (including vehicles, portable and back-up generators, lawn mowers, power washers, etc.), but also from incomplete combustion of various other fuels (including wood, coal, charcoal, oil, paraffin, propane, natural gas, and trash).

Large CO pollution events can be observed from space over cities.

Indoor pollution

In closed environments, the concentration of carbon monoxide can easily rise to lethal levels. On average, 170 people in the United States die every year from carbon monoxide produced by non-automotive consumer products.[53] However, according to the Florida Department of Health, "every year more than 500 Americans die from accidental exposure to carbon monoxide and thousands more across the U.S. require emergency medical care for non-fatal carbon monoxide poisoning"[54] These products include malfunctioning fuel-burning appliances such as furnaces, ranges, water heaters, and gas and kerosene room heaters; engine-powered equipment such as portable generators; fireplaces; and charcoal that is burned in homes and other enclosed areas. The American Association of Poison Control Centers (AAPCC) reported 15,769 cases of carbon monoxide poisoning resulting in 39 deaths in 2007.[55] In 2005, the CPSC reported 94 generator-related carbon monoxide poisoning deaths.[53] Forty-seven of these deaths were known to have occurred during power outages due to severe weather, including Hurricane Katrina.[53] Still others die from carbon monoxide produced by non-consumer products, such as cars left running in attached garages. The Centers for Disease Control and Prevention estimates that several thousand people go to hospital emergency rooms every year to be treated for carbon monoxide poisoning.[56]
Presence in blood

Carbon monoxide is absorbed through breathing and enters the blood stream through gas exchange in the lungs. It is also produced in hemoglobin metabolism and enters the blood from the tissues, and thus is present in all normal tissues, even if not inhaled.

Normal circulating levels in the blood are 0% to 3%,[clarification needed][citation needed] and are higher in smokers. Carbon monoxide levels cannot be assessed through a physical exam. Laboratory testing requires a blood sample (arterial or venous) and laboratory analysis on a CO-Oximeter. Additionally, a noninvasive carboxyhemoglobin (SpCO) test method from Pulse CO-Oximetry exists and has been validated compared to invasive methods.

The cheapest Pulse CO-Oximeter I was able to find on Google was the Pronto Pulse CO-Oximeter - 9167 for $556.76.  It is out of my budget, so I will just monitor the background levels of CO for now.

[Alexander]

My car is quite old and I'm checking it for CO this weekend. I've been feeling drowsy or dizzy while driving for some time but took till now to inspect it. I've been keeping my window open now winter's over. It's certainly something you have to be aware of.

[Jhanananda]

Thank-you, Alexander, for your reply.  Yes, if your car is old, and you find yourself getting tired driving, then your car may very well have an exhaust leak into the interior.

I have been monitoring the CO concentration in my van when I burn candles and cook on my propane stove, and drive.  It turns out there is significant levels of CO accumulating in my van, which might at least be one of the causal agents in my diabetes.  So, I plan to keep monitoring CO levels and blood sugar levels to see if I can find a correlation.

[Jhanananda]

On the CO causes diabetes hypothesis, I checked my blood sugar yesterday after almost a week without blood sugar test strips, and found my blood sugar was almost 200, which is on a continuous ultra-low-carb diet.  I have not driven my van for a few days, because it is dead right now, so I have not been exposed to high levels of CO since then.  However, according to studies it can take about 5 days for CO to be removed from the blood stream.  Nonetheless, I did recall that my van had been dead for 2 months last year, and my blood sugar was quite high.  So, I believe that I can conclude that elevated CO exposure surely leads to ill-health, but does not seem to be causal in my diabetes.  If I am ever able to get my van running again I will most definitely work on sealing up the leaks to the engine compartment from the passenger compartment of my van.

[Jhanananda]

Here is some research on CO and it reducing arthritis. Inhalation of carbon monoxide ameliorates collagen-induced arthritis in mice and regulates the articular expression of IL-1beta and MCP-1.

Abstract

Carbon monoxide (CO), long considered a toxic gas, has recently been shown to mediate anti-inflammatory effects in various animal models. The aim of this study was to investigate whether the inhalation of CO ameliorated collagen-induced arthritis (CIA) in mice. CIA was induced in female DBA/1 mice by the injection of an anti-type II collagen antibody and lipopolysaccharide. The CO treatment group was exposed to CO gas at a concentration of 200 ppm in a closed cage starting on the day of the injection with an anti-type II collagen antibody and throughout the remaining study period. The clinical arthritis scores was examined daily for swelling of the paws as a sign of arthritis. For histopathology, the sections of the hind legs were evaluated by hematoxylin-eosin staining. Moreover, we evaluated the expression of interleukin (IL)-1beta and monocyte chemoattractant protein-1 (MCP-1) mRNA in the hind paws. Both clinical arthritis scores as well as histological findings of joint inflammation were significantly reduced in mice treated with CO gas inhalation compared to untreated mice. Further, CO significantly inhibited the increased expression of IL-1beta and MCP-1 mRNA in paws at day 3 after the induction of arthritis. In conclusion, the inhalation of CO protected mice from the synovial inflammation of CIA. Based on these data, the beneficial effects of CO in murine RA model may be attributed to its anti-inflammatory properties.

Please note: 200 ppm of CO exposure to humans is a lethal dose.  Research on humans has shown that 15PPM CO is safe, and reduces inflammatory conditions, such as arthritis.

Considering the hunter-gatherer model of human evolution places humans around a fire pit on a regular basis, does explain to me why we made actually depend upon low levels of CO for our health.

[Jhanananda]

Reciprocal regulation of carbon monoxide metabolism and the circadian clock. Klemz R1, Reischl S1, Wallach T1, Witte N2, Jürchott K1, Klemz S1, Lang V1, Lorenzen S3, Knauer M2, Heidenreich S2, Xu M4, Ripperger JA5, Schupp M2, Stanewsky R4, Kramer A1. Nat Struct Mol Biol. 2017 Jan;24(1):15-22. doi: 10.1038/nsmb.3331. Epub 2016 Nov 28.

Abstract

Circadian clocks are cell-autonomous oscillators regulating daily rhythms in a wide range of physiological, metabolic and behavioral processes. Feedback of metabolic signals, such as redox state, NAD+/NADH and AMP/ADP ratios, or heme, modulate circadian rhythms and thereby optimize energy utilization across the 24-h cycle. We show that rhythmic heme degradation, which generates the signaling molecule carbon monoxide (CO), is required for normal circadian rhythms as well as circadian metabolic outputs. CO suppresses circadian transcription by attenuating CLOCK-BMAL1 binding to target promoters. Pharmacological inhibition or genetic depletion of CO-producing heme oxygenases abrogates normal daily cycles in mammalian cells and Drosophila. In mouse hepatocytes, suppression of CO production leads to a global upregulation of CLOCK-BMAL1-dependent circadian gene expression and dysregulated glucose metabolism. Together, our findings show that CO metabolism is an important link between the basic circadian-clock machinery, metabolism and behavior.

Now that is interesting