The fire effluent toxicology simulation equation derived by David Purser in this reference:

Purser, D. (2012). Validation of additive models for lethal toxicity of fire effluent mixtures. Polymer Degradation and Stability, 97(12), 2552–2561. https://doi.org/10.1016/j.polymdegradstab.2012.07.009

has an additive correction factor for hypercapnia caused acidosis, the 'A' in the equation below.

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FED = { } x V CO2 + A + 1/H

FED = Fractional Effective Dose where FED = 1 = LD50

V CO2 = 1 + (exp (0.14[CO2])-1)/2. ----- The factor caused by hypercapnic hyperventilation

A = ([CO2] x 0.05) - 0.02 ----- Acidosis term in the equation

In the { } are the Haber's Rule fractions for items present that are toxic, such as HCl or CO or whatever may be present in the fire/baby's crib, depending on the application for the equation.

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In Purser's use of the equation, the V CO2 predominates by multiplicatively increasing the toxicity of that which is in the braces { }. The acidosis term lags 2% behind the 5 percent of the concentration of the carbon dioxide present. Acidosis only begins to play a part [speculation] when CO2 itself becomes toxic at 6.5% and above. Below 6.5% CO2 is where only hypercapnic hyperventilation plays a part in toxicity. Rebreathing when bedsharing was measured up to about 4.7% CO2.

Thinking about the pathology findings in SIDS, which ones could be caused by acidosis?

Pulmonary edema = Yes

Thymal petechiae = probably not

Cardiac conduction system deterioration = No

Myocardial vacuolization = No

Shock = I don't know on this one

Postmortem liquid blood in the heart = No

Frothy pink oronasal secretions = No

Pulmonary lymphocytic infiltrations = Probably

Thanks for that impressive and thorough answer! To add to your list at the end, "abnormal muscle contractions" (similar to exercise induced muscle spasms). I have reason to believe the diaphragm goes into spasm causing respiratory arrest and death.

Thank you for that additional finding. I believe that is what causes the petechiae, a terminal contraction.

A parallel symptomatology to SIDS is found with phosphine poisoning as found in mostly the Iranian, Indian, and Pakistani Medical literature.

Yes, absolutely: diaphragmatic spasm → effective paralysis of diaphragm → inspiratory arrest → struggle to breathe against the effective airway resistance of diaphragmatic failure + pliable chest wall (infantile) = intrathoracic petechiae

The historical writings on diaphragmatic issues you've posted and SIDS stated the diaphragm relaxes and that it occurs in REM (Active Sleep).

From our discussion last month above we both are of the view there is a seizing of the thoracic cavity instead of a relaxation. The consensus of SIDS literature say SIDS occurs in NREM (Quiet Sleep) at a higher threshold of arousal.

Is your novelty in that your postulate deviates from the past expressions of the diaphragmatic failure?

PS: Reading the symptoms list above on SIDS I gave; they are all accurate and associated with SIDS, but whether acidosis causes that particular finding, is completely subjective on my part. I would use your better judgment there!!

I will need to look at that claim in the literature, re: during non-REM. Thanks for bringing that to my attention Paul.

To clarify, I am stating the diaphragm goes into spasm paroxysmally during sleep in infants and children due to a combination of factors, but salient among them is acidosis (from a combination of respiratory and metabolic acidosis). [Conjecture] Prone sleep position putatively causes worsening rebreathing and respiratory acidosis. It also causes diaphragmatic shortening-thickening. We all know from life experience that muscles are prone to spasm during exercise, an acidotic state (from lactate buildup in tissues).

[Conjecture]:

In REM sleep in an infant, the consequent respiratory arrest would be worsened bc the accessory muscles are shut down (via centrally mediated skeletal muscle inhibition during REM). However, the child would then wake up in distress, unable to breathe in, thereby recruiting the respiratory accessory muscles. But without the diaphragm functioning to expand the thoracic cavity and generate lung expansion, respiratory arrest ensues, followed quickly by cardiac arrest.

[Conjecture]:

Alternatively, if the acute diaphragmatic spasm mechanism happens during non-REM sleep, the accessory muscles would be immediately available. However, the issue persists where the accessory muscles cannot overcome the resistance posed by lung compliance. So, whether in REM or not, the outcome is the same.

I agree almost all of this is subjective, including, "The terminal struggle to breathe in could also explain the origin of the intrathoracic petechiae found on most SIDS autopsies". I base that claim on pathophysiology knowledge and therefore is only conjecture. Thank you for reminding me I need to be careful to separate facts from suppositions. It's tricky work at this point.

I need to be careful just as well on the fact vs. supposition aspect of my statements.

I am of the impression that any postulate on SIDS, must take into a unified account nearly all of the SIDS risk factors, as well as the facts known about SIDS.

I listed some pathology items above.

SIDS risk factors I can enumerate are:

• SIDS occurs during the sleep
• SIDS occurs towards the end of the sleep, early morning hours, most frequently
• Anecdotally: Day care centers are more risky
• Same room sharing with the parents is safer than sleeping the infant alone in another room
• Male to female infant SIDS case ratio is roughly 60/40
• Occurs most frequently between 2 and 4 months and 90% of the time before 6 months of age in full term infants. Preterm infants' SIDS cases are at later postnatal age and earlier post conceptual age than full term infants
• Prone sleeping is more dangerous than supine
• Level of arousal threshold during sleep parallels the SIDS risk and inversely the protective factors
• Breastfeeding reduces SIDS risk
• Sleeping on sofas, couches, and recliners have a very severe SIDS risk (OR 60+)
• Bedsharing with parents and immunizations are disputed as to their SIDS risk
• Practice of bedsharing with siblings is a greater risk
• Native Americans and African Americans in the USA, Maori in New Zealand, and Indigenous peoples in Australia have a higher risk of SIDS cases.
• Firm mattresses are safer than soft mattresses, bedding and pillows

This is not an exhaustive list of SIDS risks, but the best I can recollect.

My Respiratory Rate (RR) postulate incorporates all of these to some greater or lesser degree for each. Problem is that a postulate is not scientific fact just on correlations and that all fits into the concept.

An experiment/study must be run that verifies the postulate by having repeatable results showing it is valid.

I am thinking that phosphine poisoning in my theory doesn't occur directly by the nerve gas toxicology itself, but by slowly lengthening the QT interval in sleep, where it is already longer, such as with acquired LQTS, to bring on Tordes de Pointes and your diaphragmatic contraction to create the petechiea, but only in the thoracic cavity. [How is that paragraph all for conjecture?]

Thanks Paul. Great stuff re: SIDS risk factors. Yes, phosphine toxicity, similar to nicotine, increases effect of acetylcholine in skeletal muscles such as the diaphragm but also cardiac. "There is evidence that phosphine increases acetylcholine neurotransmission by suppressing acetylcholine esterase." So yes, the ADS mechanism could be triggered by such exposures. The question then becomes, how do infants get exposed to phosphine in sleep? By contrast, nicotine exposure is certainly not uncommon in households, particularly worse in hot bedrooms located UPSTAIRS (thermal gradient).

Article Mechanisms of Phosphine Toxicity

Phosphine is extremely toxic, but any gas that might prolong the QT interval, or as you quote, might be an acetylcholine esterase inhibitor. Possibly ammonia.

Final answer: YES, rebreathing CO2 leads to respiratory acidosis. Acidosis does contribute to muscle cramps, typically from lactate though. .