Date: Tue, 4 Oct 2011 08:12:29 -0400
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Subject: 5 more RE: [DCHAS-L] H2S Antidotes
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From: Alan Hall 
Subject: RE: [DCHAS-L] H2S Antidotes
Date: October 3, 2011 2:07:03 PM EDT


H2S is indeed very rapidly fatal in concentrations of approximately 1,000 ppm or greater, with one or two breaths resulting in what has been termed the "slaughterhouse sledgehammer effect" with extremely rapid unconsciousness and respiratory arrest.  Basically, the transit time of the poison through the systemic circulation from the lung to the brain or about 22 seconds in most cases.  If the victim is not rapidly moved to fresh air and/or supplemental oxygen and assisted ventilation administered, it can indeed be fatal in these circumstances.  However, with rapid extrication and treatment, most such victims can survive without neurological impairment.  It is only when they remain in the toxic atmosphere until either irreversible brain damage/death or bodily death has occured (brain damage and perhaps death usually follows 5 minutes of more of apnea -- absence of breathing).  Most such exposures occur in enclosed spaces, and NIOSH data and my own experience note that there a!
re approximately 3-5 additional victims after the initial victim as well-meaning persons lacking appropriate respiratory protection enter the enclosed spaces to attempt rescue.  Another very good reason to enforce enclosed space entry rules and the use of all necessary safety equipment.

A good review can be found in:

Guidotti TL:  Hydroen Sulfide, in:  Shannon MW et al (eds), Haddad and Winchester's Clinical Management of Poisoning and Drug Overdose, 4th ed.  Saunders Elsevier, Philadelphia, 2007, pp. 1335-1342.

I also had a fairly extensive section on H2S poisoning in my chapter:

Hall AH:  Systemic Asphyxiant Poisoning, in:  Irwin RS, Rippe JM (eds), Irwin and Rippe's Intensive Care Medicine, 6th ed.  Wolters Kluwer | Lippincot Williams & Wilkins, Philadelphia, 2008, pp. 1699-1706.

Good information documents are also available without charge from the HSDB (Hazardous Substances Data Bank) at the National Library of Medicine ( and ATSDR ( -- look under Case Studies in Environmental Medicine and Toxicological Profiles, and also under Emergency Medical Guidelines).

Hope this information is useful.

Alan H. Hall, M.D.
President and Chief Medical Toxicologist
Toxicology Consulting and Medical Translating Services, Inc.
Laramie, WY

Clinical Assistant Professor
Colorado School of Public Health
University of Colorado-Denver
Denver, CO

From: Alan Hall 
Subject: RE: [DCHAS-L] 7 RE: [DCHAS-L] H2S Antidotes
Date: October 3, 2011 2:50:50 PM EDT
I agree with Neal Langerman that the ATSDR Toxicological Profile on H2S is an excellent document, having peer reviewed it myself in several iterations over the years.  The problem with H2S is not only the rapid knockdown at an airborne concentration of about 1,000 ppm or greater with 1-2 breaths, but the fact that exposure to about 250 ppm for prolonged periods results in delayed-onset non-cardiogenic pulmonary edema (fluid in the lungs not because of heart failure) and because the nose becomes "paralyzed" to the rotten-eggs odor after about 5 minutes, workers may wrongly assume that whatever smelled bad is gone and stay in exposure long enough to later become seriously or even fatally ill.  Even at very low concentrations with chronic exposure, keratoconjunctivitis may occur.  One more reason to emphasize unequivocally that detection of odor is a very, very poor way to determine if a working environment is safe.

The issue with antidotes is a complicated one.  The following is not to be construed as medical advice for any particular patient or case, but as some information in general.

Anecdotally, and I will emphasize that this is anecdotal, I have personally seen dramatic clinical recovery following administration of the sodium nitrite portion of the old Lilly/Pasadena/Taylor cyanide antidote kit when extrication from the contaminated breating atmosphere, endotracheal intubation, and assisted ventilation with 100% oxygen had not been efficacious.  There are also anecdotal reports of survival (I was involved in 1 or 2), apparently without any significant brain damage, when treatment with hyperbaric oxygen therapy was given rather rapidly following extrication.  There are, however, no controlled studies of either intervention.

The argument against administration of sodium nitrite in such cases is that the methemogolobin it induces (theoretically active against hydrogen sulfide by forming sulfmethemoglobin) is too short-lived to be efficacious.  However, all such mitochondrial cytochrome oxidase poisons as H2S have great involvement of nitric oxide/nitric oxidase mechanisms and even in cyanide poisoning, many of us who have worked in the field are becoming more and more convinced that methemoglobin formation by sodium nitrite may actually be a side effect and that its nitric oxide mechanism(s) may be the real antidotal action(s).

Then the issue arises, "What about the relatively new cyanide antidote, hydroxocobalamin?"  Published data clearly show that hydroxocobalamin is a nitric oxide scavenger as well as a direct cobalt moiety cyanide chelator.  Could it work in H2S poisoning?  Answer:  "Theoretically, maybe."  But no animal studies or clinical trials have been done to my knowledge and at present, I would not recommend it for the treatment of H2S poisoning until some studies have been done.

So what would I recommend as of today if my advice were sought for a seriously H2S-poisoned patient who has been extricated from the contaminated breathing atmosphere by rescuers with suitable personal protective equipment (note NIOSH data on additional deaths amongst well-intentioned would-be rescuers without appropriate PPE and some of my own publications on the same topic)?  First, I would administer 100% supplemental oxygen and provide assisted/mechanical ventilation and airway management as clinically necesssary.

If that didn't bring the patient around and I had sodium nitrite available, I would administer one 300 mg dose intravenously over no less than 5 minutes to avoid its dangerous hypotensive vasodilating effects.  Half an hour later, I might try a second dose at half that amount with the same precautions.  That didn't work and I had a hyperbaric chamber available without the necessity to transfer a critically ill, unstable patient just for HBOT, I would give it a try as a last-ditch effort.  Others might differ in their approach and there is no "gold standard" of treatment as of today.  Might work, might not.  Personally, I have always believed in giving critically ill patients, particularly otherwise healthy workers, the benefit of the doubt until it becomes medically futile.

Alan H. Hall, M.D.
President and Chief Medical Toxicologist
Toxicology Consulting and Medical Translating Services, Inc.
Laramie, WY

Clinical Assistant Professor
Colorado School of Public Health
University of Colorado-Denver
Denver, CO
Alan H. Hall, M.D.

==From: Ray Cook 
Subject: RE: [DCHAS-L] H2S Antidotes
Date: October 3, 2011 6:31:43 PM EDT

Greetings All,

The interesting thing about hydrogen sulfide is that it quickly paralyzes the phrenic nerve resulting in cessation of respiration.  Due to this, the build-up of hydrogen sulfide in the system is slight in high concentrations, since it does not build up and bind the hemoglobin as cyanide does.  Because of this, if you can get artificial respiration to a victim quickly, they can be revived, although we all know there are time limits involved regarding brain damage.  Also because of this, one breath at about 1,000 ppm or above will stop the respiration immediately.

When I started in the HSE field many years ago, my former boss would put a mouse in an airtight chamber when we were teaching employees about the dangers of hydrogen sulfide.  He would then release H2S into chamber and the mouse would apparently "die." After about 30 seconds, he would flood the chamber with oxygen at a pressure slightly greater than ambient, and within about a minute the mouse would "return to life."  This was to emphasize the importance of immediate resuscitation of anyone that had been overcome, once they were moved to a safe area.  Obviously that is not a practice that would be considered today, but it does illustrate the properties and the ability for resuscitating a person that has encountered the gas at a high concentration.

Another insidious property of the gas is that it also paralyzes the olfactory nerve at a concentration of about 100 ppm for most people.  The danger here is that if you are not properly protected by a personal alarm monitor, you might walk into a gas concentration of 200 ppm and briefly think you smell the gas, but suddenly the odor is gone (at least to you), which would make you think it was safe to remain, when in fact, the exposure continues.  I hope this was helpful.


Raymond L. Cook, Jr.,  MSIH, CIH, CSP
President & Principal Consultant

1 Cor 1:18
==From: Stephen Stepenuck 
Subject: H2S Exposures [was: H2S antidotes]
Date: October 3, 2011 10:20:41 PM EDT
To: DCHAS-L Discussion List 
I tend to agree with Al:
In my first teaching job, I was required to charge several Kipp generators as sources of H2S for the Qualitative Analysis lab.  They were in hoods, but as Al says, those did not work very well in those days.  The orders were to recharge them each day, but when I realized that they were good for more than one day, I sometimes let them go for two to minimize my exposures.  One day,  I was in the college library, when I was reamed out in front of several dozen students by the department chair, who had had one of the generators run out during his lab section.  [Rather than recharge it, he had apparently scoured the campus to find me...]
Anyway, I was required to return to the department and immediately recharge all the generators [three, I think].  Since those were quite tall glass apparatus, I probably had to have the hood door mostly open in order to do the work. When I opened one of those to remove the contents, I was blasted with a large dose of hydrogen sulfide.  The exposure probably lasted several seconds.  I did get a headache, but no other symptoms that I can recall.
[My lung function has been very poor for many years.  Maybe I have a case?   ;-)  ]

In no way do I wish to minimize the danger of H2S exposures.

Around that time, I was told that a well-endowed eastern university used to have H2S piped in to its labs for the „Qual‰ course, but after a student death, removed that system.

Stephen J. Stepenuck, Ph.D.
Professor of chemistry emeritus
Keene State College
Keene NH 03435-2001
==From: Mr John David Turner 
Subject: Re: [DCHAS-L] H2S Antidotes
Date: October 3, 2011 11:43:39 PM EDT
I was reading the E-mail string associated with your comment regarding hydrogen sulfide.  Although it may not be entirely pertinent, I thought I would provide an anecdotal aside.

As a long time analytical chemist responsible for testing materials for the presence of heavy metals according to USP method <231>, I made and used saturated solutions of hydrogen sufide (In a working fume hood of course).  I would make the saturated H2S by passing a stream of the gas through chilled DI water in an ice bath.  As a rule of thumb, I was told that as long as I could smell it, I was safe.  When I could no longer smell the H2S, close the hood sash and get out into fresh air.  I managed to survive for over 35 years and, as far as I know, so have the entry level chemists I trained.

John D. Turner, CHMM, QC Manager

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