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"It was found that when the proportion of CO2 in the air rose to about
3% and the oxygen fell simultaneously to about 17% "... the breathing
began to be noticeably increased ... until with about 6% CO2 and 13% of
oxygen the panting was very "great ...
Page 16 in J S Haldane & J G Priestley "Respiration" New edition.
(Oxford University Press, 1935)
Probably from 2 articles in J.Path. Bact. (1893) 1: 168 & 318
Adrian Smith
Leeds University Library
UK
-----Original Message-----
From: * Biomechanics and Movement Science listserver
[mailto:BIOMCH-L@NIC.SURFNET.NL] On Behalf Of McFarlane, David
Sent: 15 November 2006 00:59
To: BIOMCH-L@NIC.SURFNET.NL
Subject: [BIOMCH-L] The Carbon Dioxide level that initiates
Hyperventilation
Dear all,
Does anyone know the level of carbon dioxide in air that initiates
hyperventilation? I have looked at my old industrial hygiene studies on
the sick building syndrome I have found that some organizations have
given recommended maximum figure for CO2.
According to my records the seminar edition of the publication "Managing
Indoor Air Quality" (BOMA, 1991) cited the NHMRC (Australian "National
Health and Medical Research Council) and Worksafe Australia
recommendations. Worksafe Australia (1990) had recommended a figure of
5,000 ppm for long-term exposure to CO2 at that time. On the basis of
anecdotal evidence (from deep sea diving, mining disasters and submarine
mishaps) that figure looks rather pessimistic (a modest colleague tells
me that he survived 15, 000 ppm for 15 minutes after a mine disaster
with no obvious ill effects and the U Boat crews of WW2 supposedly
endured levels up to nearly 2%; "Das Boot" et cetera).
Incidentally I often wonder what sort of data these long-term exposure
thresh-holds were based on (I have not found any recent examples of good
scientific research papers on this topic yet). Does anyone have any
idea?
Are there any work physiologists out there who are still researching
this topic? Back in the seventies when I was ay uni physiologists had
supposed that the blood vessels of the lungs contained CO2-sensitive or
acidosis-sensitive sensors that regulated the rate and depth of
breathing (rather than a direct response to anoxia). Can anyone tell me
what science has found in the meanwhile? If not is anyone looking for a
PhD thesis?
Regards,
David McFarlane
Ergonomist, WorkCover NSW
References
1. Building Owners and Managers Association of Australia, (1991),
"Managing Indoor Air Quality", section 9.3, page 66.
2. Worksafe Australia Standard, (1990), "Exposure contaminants for
atmospheric contaminants in the occupational environment".
Disclaimer
Any recommendation concerning the use or representation of a particular
brand of product in this document or any mention of them whatsoever
(whether this appears in the text, illustrations, photographs or in any
other form) is not to be taken to imply that WorkCover NSW approves or
endorses the product or the brand.
************************************************** **********************
************************************************** **************
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addressee named and may contain confidential
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notify the sender. Any views expressed in this
message are those of the individual sender and are not necessarily the
views of WorkCover NSW.
************************************************** **********************
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3% and the oxygen fell simultaneously to about 17% "... the breathing
began to be noticeably increased ... until with about 6% CO2 and 13% of
oxygen the panting was very "great ...
Page 16 in J S Haldane & J G Priestley "Respiration" New edition.
(Oxford University Press, 1935)
Probably from 2 articles in J.Path. Bact. (1893) 1: 168 & 318
Adrian Smith
Leeds University Library
UK
-----Original Message-----
From: * Biomechanics and Movement Science listserver
[mailto:BIOMCH-L@NIC.SURFNET.NL] On Behalf Of McFarlane, David
Sent: 15 November 2006 00:59
To: BIOMCH-L@NIC.SURFNET.NL
Subject: [BIOMCH-L] The Carbon Dioxide level that initiates
Hyperventilation
Dear all,
Does anyone know the level of carbon dioxide in air that initiates
hyperventilation? I have looked at my old industrial hygiene studies on
the sick building syndrome I have found that some organizations have
given recommended maximum figure for CO2.
According to my records the seminar edition of the publication "Managing
Indoor Air Quality" (BOMA, 1991) cited the NHMRC (Australian "National
Health and Medical Research Council) and Worksafe Australia
recommendations. Worksafe Australia (1990) had recommended a figure of
5,000 ppm for long-term exposure to CO2 at that time. On the basis of
anecdotal evidence (from deep sea diving, mining disasters and submarine
mishaps) that figure looks rather pessimistic (a modest colleague tells
me that he survived 15, 000 ppm for 15 minutes after a mine disaster
with no obvious ill effects and the U Boat crews of WW2 supposedly
endured levels up to nearly 2%; "Das Boot" et cetera).
Incidentally I often wonder what sort of data these long-term exposure
thresh-holds were based on (I have not found any recent examples of good
scientific research papers on this topic yet). Does anyone have any
idea?
Are there any work physiologists out there who are still researching
this topic? Back in the seventies when I was ay uni physiologists had
supposed that the blood vessels of the lungs contained CO2-sensitive or
acidosis-sensitive sensors that regulated the rate and depth of
breathing (rather than a direct response to anoxia). Can anyone tell me
what science has found in the meanwhile? If not is anyone looking for a
PhD thesis?
Regards,
David McFarlane
Ergonomist, WorkCover NSW
References
1. Building Owners and Managers Association of Australia, (1991),
"Managing Indoor Air Quality", section 9.3, page 66.
2. Worksafe Australia Standard, (1990), "Exposure contaminants for
atmospheric contaminants in the occupational environment".
Disclaimer
Any recommendation concerning the use or representation of a particular
brand of product in this document or any mention of them whatsoever
(whether this appears in the text, illustrations, photographs or in any
other form) is not to be taken to imply that WorkCover NSW approves or
endorses the product or the brand.
************************************************** **********************
************************************************** **************
This message, including any attached files, is intended solely for the
addressee named and may contain confidential
information. If you are not the intended recipient, please delete it and
notify the sender. Any views expressed in this
message are those of the individual sender and are not necessarily the
views of WorkCover NSW.
************************************************** **********************
************************************************** **************