ELEMENT 5 HYDROGEN SULFIDE INSTRUCTOR& TECHNICIAN COURSE HSI005

ELEMENT FIVE

How does H2S Affect Individuals?

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5.1 PHYSIOLOGICAL EFFECTS OF H2S

How exactly does H2S affect and possibly kill an individual?

H2S is a toxic, transparent, flammable gas that is also heavier than air. The slightest
presence of H2S in the air is normally detectable by its characteristic rotten egg odor.
It is dangerous; however, to rely on odor as a means of detecting excessive
concentrations as the olfactory nerve, which controls the sense of smell, is rapidly
paralyzed at higher concentrations. As a result, lethal concentrations may accumulate
without adequate warning.

When a person breathes H2S, it goes directly through the lungs and into the blood
stream. To protect itself the body oxidizes (breaks down) the H2S as rapidly as
possible into a harmless compound. If the individual breathes in so much H2S that the
body can’t oxidize all of it, the H2S builds up in the blood and poisons the individual.
The nerve centers in the brain, which control breathing, are paralyzed; the lungs stop
working, and the person dies due to respiratory failure and asphyxiation.

Because H2S is oxidized quite rapidly to sulfates within the body, permanent after-
effects rarely occur in any cases of recovery, due to acute exposures, unless
deprivation of the nervous system is prolonged. However, in cases of acute exposures
there is the possibility that pulmonary edema may develop. Reports indicate that
symptoms such as nervousness, dry non-productive cough, nausea, headaches, and
insomnia lasting up to three days, have occurred following acute exposure to H2S. At
low concentrations, the predominant effect of H2S is on the eyes and respiratory tract.
Eye irritation, eye inflammation, pain, excessive tearing and painful sensitiveness to
strong light may persist for several days. Respiratory tract symptoms include
coughing, painful breathing, and pain in the nose and throat.

There is no evidence that repeated exposures to H2S result in accumulative poisoning.

Effects such as eye irritation, respiratory tract irritation, slow pulse rate, fatigue,
digestive disturbances, and cold sweats may occur, but these symptoms disappear in a
relatively short time after removal from the exposure. Repeated exposures do appear
to cause some increase in susceptibility to this gas. The paralyzing effect on the sense
of smell is a significant property. This paralysis may create a false sense of security.
A worker can be overcome by H2S after the odor has disappeared. Some victims of
acute overexposure have reported a brief, sickening sweet odor just prior to
unconsciousness. The concentration required to deaden one’s sense of smell may not
affect another worker.

Individuals who have consumed alcohol within 24 hours of exposure have been
overcome by unusually small concentrations of H2S. Alcohol and H2S do not mix,
making these people hyper susceptible to H2S.

What is pulmonary edema?

When H2S is breathed in, the gas burns the lung tissue and forms a fluid similar to the
fluid that forms under a burn blister. If this fluid is not removed, the victim will
drown. Pulmonary edema is the build-up of fluid in the lungs.

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5.2 HOW DOES H2S AFFECT INDIVIDUALS? HEALTH EFFECTS

When a person breathes H2S, it goes directly through the lungs and into the blood
stream. The body oxidizes the H2S as rapidly as possible to a harmless compound.
Below 50ppm, the main effect apart from odor is irritation, principally in the eyes but
also of the nose, throat and lungs, symptoms include headache, nausea, cough and
dizziness.

From about 50 to 250ppm the lung irritation can lead to pulmonary edema – fluid
accumulating in the lung – which is a serious and potentially life threatening situation.
At concentrations above 250ppm, pulmonary edema is common.

When the concentration is too high for the body to neutralize, the H2S builds up and
poisons the individual. Between 500 to 1000ppm, Hydrogen Sulfide interferes with
the oxygen usage in the body (similar to Hydrogen Cyanide).

At concentrations about 1000 to 2000ppm, the nerve that controls breathing is

paralyzed, the lungs stop working and the person is asphyxiated.

Most effects are all acute.

In rare cases, a person who has been exposed to high levels of H2S develops an
asthma-like response to respiratory irritants from then on.

5.3 FACTORS THAT DETERMINE THE AFFECT OF H2S ON

INDIVIDUALS
Duration:
• The length of time the individual is exposed.
Frequency:
• How often the individual has been exposed.
Intensity:
• How much (concentration) the individual was exposed to.
Individual Susceptibility:
• The individuals psychological makeup. These factors are body mass, physical
condition, smoker/non-smoker, age and personal biochemistry.

5.4 TARGET ORGANS SUBJECT TO THE EFFECTS OF H2S

• Olfactory nerves
• Lungs
• Eyes
• Brain
• Respiratory control center

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ELEMENT 5 HYDROGEN SULFIDE INSTRUCTOR& TECHNICIAN COURSE HSI005

5.5 SIGNS AND SYMPTOMS OF H2S EXPOSURE

Acute Toxicity Chronic Toxicity

Eye irritation Eye irritation
Headaches Headaches
Nausea Nausea
Irritates respiratory tract Irritates respiratory tract
Dizziness Sleep disturbances
Confusion Anorexia
Sneezing Corneal blistering
Diarrhea Pulmonary oedema
Olfactory paralysis Corneal pitting
Excitement
Staggering gait
Pulmonary oedema
Photophobia
Respiratory arrest
Cardiac arrest
Brain damage

5.6 ENTRY INTO THE BODY

In discussing toxicity, it is necessary to describe how a material gains entrance into

the body and then into the bloodstream. A material cannot produce systemic injury
unless it gains entry into the bloodstream. Common routes of entry are ingestion,
injection, skin absorption and inhalation. Depending on the substance and its specific
properties, however, entry and absorption can occur by more than one route. For
instance, inhaling a solvent that can penetrate the skin. Where absorption into the
bloodstream occurs, a toxicant may elicit general effects or, more than likely, the
critical injury will be localized in specific tissues or organs.

Ingestion

Anything eaten or drunk gets into the intestine and may be absorbed into the blood
and thereafter prove to be toxic. In general, the term “toxicity” is associated by most
people with things taken by mouth. The problem of ingesting chemicals is not
widespread in industry.

Oral toxicity is generally lower than the inhalation toxicity for the same material due
to the relatively poor absorption of many materials from the intestines into the
bloodstream. After absorption from the gastrointestinal system into the bloodstream,
the toxic material goes to the liver, which can further metabolically alter, degrade, or
detoxify many substances. Basically, detoxification involves a sequence of reactions;
deposition in the liver, conversion to a nontoxic compound, transportation to kidney
via the bloodstream, and excretion through the kidney and urinary tract.

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ELEMENT 5 HYDROGEN SULFIDE INSTRUCTOR& TECHNICIAN COURSE HSI005

Injection

A material can be injected into any part of the body or directly into the bloodstream.
The effects produced vary with the route of administration. Injection is not too
important as a route of worker exposure.

In the laboratory, toxic substances may be injected into animals because it is far more
convenient and less costly than establishing blood levels by inhalation exposure.
Additionally, intravenous injection short-circuits protective mechanisms in the body
which prevent substances from entering the blood.

Skin absorption

An important route of entry in terms of occupational exposure is absorption through

either intact or abraded skin. Contact of a substance with skin results in four possible
actions: (1) the skin can act as an effective barrier, (2) the substance can react with the
skin and cause local irritation, (3) the substance can produce skin sensitization, and
(4) the substance can penetrate the blood vessels under the skin and enter the
bloodstream.

Inhalation

For industrial exposures to chemicals, the most important route of entry is usually
inhalation. Nearly all materials that are airborne can be inhaled.

The respiratory system is composed of two main areas: (1) the upper respiratory tract
airways – the nose, throat, trachea, and major bronchial tubes leading to the various
lobes of the lungs; and (2) the alveoli where the actual transfer of gases across thin
cell walls takes place. Only particles smaller than about 5 micrometers in diameter
are likely to enter the alveolar sac.

The total amount of a toxic compound absorbed via the respiratory pathways depends
upon its concentration in the air, the duration of exposure, and pulmonary ventilation
volumes, which increase with higher work loads.
Gases and vapors having low water solubility but being highly soluble in fats pass
through the alveolar lining into the blood and are distributed to organ sites for which
they have special affinity. In the course of inhalation exposure at a uniform level, the
concentration of the compound in the blood reaches an equilibrium value between
absorption, on the one hand, and metabolism and elimination, on the other.

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ELEMENT 5 HYDROGEN SULFIDE INSTRUCTOR& TECHNICIAN COURSE HSI005

5.7 DOSE-RESPONSE RELATIONSHIP

All toxicological considerations are based on the dose-response relationship. A dose

is administered to test animals, and, depending on the outcome, is increased or
decreased until a range is found where at the upper end of all animals die and, at the
lower end, where all animals survive. The data collected are used to prepare a dose-
response curve relating to percent mortality to dose administered.

A single large dose of a toxic substance can be expected to produce a greater response
than the same total dose administered in small amounts over a long period of time.
Each of the small amounts may be detoxified quickly but a large dose may produce its
detrimental action before appreciable detoxification can occur. A toxic substance that
is detoxified or excreted at a rate that is slower than the rate of intake of the substance
becomes a cumulative poison.

Lethal Dose
If a number of animals are exposed to a toxic substance, when the concentration
reaches a certain level, some, but not all, of those animals will be killed. Results of
such studies are used to calculate the lethal dose (LD) of toxic substances.

The LD50 is the calculated dose of a substance that is expected to cause the death of
50% of a defined experimental animal population, as determined from the exposure to
the substance, by any route other than inhalation.

Lethal Concentration
When considering inhalation exposures, the LD50 is not too useful; the dose by
inhalation is needed. A similar designation, lethal concentration (LC) is used for
airborne materials.

Time becomes very important because a half-hour exposure might produce one effect,
a few minutes’ exposure another, and 24 hours’ exposure would produce other effects.

Acute Effects
Acute exposures and acute effects involve short-term high concentrations and
immediate results of some kind; illness, irritation, or death. Acute exposures are
usually related to an accident.

Chronic Effects
In contrast to acute effects, chronic effects or illness is characterized by symptoms or
disease of long duration or frequent recurrence. Chronic effects often develop slowly.
The term chronic relates to continued exposure to substances presumably throughout
a working lifetime. Chronic poisoning assumes that some level of material will be
continuously present in the tissues.

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ELEMENT 5 HYDROGEN SULFIDE INSTRUCTOR& TECHNICIAN COURSE HSI005

Exposures
Levels of exposure to air contaminants can also be referred to in terms of acute and
chronic exposure. Acute exposure generally refers to exposure to very high
concentrations during very short time periods; chronic exposure involves repetitive or
continuous exposure during long time periods.

Do not assume that chronic effects of air contaminants are less serious than acute
effects simply because they result from exposure to lower concentrations of toxic
materials. In fact, the opposite may be true; although the onset of damage to health
can be slow, the ultimate effect can be quite serious and irreversible.

An effect is local if it harms only that part of the body it comes in contact with, as
with an acid burn of the skin. A systemic effect is generalized and changes the
normal functioning of related organs operations as a system.

5.8 MEDICAL CONSIDERATIONS IN THE TREATMENT OF H2S

EXPOSURES

Hydrogen sulfide is a toxic and irritant gas whose major effects are exerted on the
nervous system, the eyes and the respiratory tract. The type of poisoning whether
acute, sub-acute or chronic, depends on the duration and level of exposure to the gas,
frequency and individual susceptibility.

Acute Poisoning:
Acute poisoning has, in general, been used to describe episodes of systemic poisoning
that have been of rapid onset and in which the central nervous system effects have
prevailed. Although H2S is an irritant, the general systemic effects of acute poisoning
predominate over the local irritant effects of sub-acute poisoning.

The threshold for acute poisoning is between 700 mg/m3 and 1000 mg/m3 (1 mg/m3
= 0.717ppm or 1ppm = 1.394 mg/m3). Exposure levels of 1400 – 2100 mg/m3
stimulate the nervous system and are fatal within 30 minutes and levels above 3800
mg/m3 bring instantaneous death by means of nervous system paralysis. The
symptoms usually present include sudden fatigue, dizziness and intense anxiety, with
paralysis manifesting itself in the immediate loss of olfactory function, collapse and
respiratory arrest terminating in death.

Cardiac failure usually follows in 5 – 10 minutes after respiratory paralysis.

Asphyxiation is indicated as the immediate cause of death.

Recovery, if it occurs, is generally rapid and without sequelae.

The sequelae are reported, they are either neurasthenic or otoneurological in character
and may include fatigue, gastrointestinal disturbance, convulsion, anxiety and
depression, and peripheral acoustic neuritis.

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ELEMENT 5 HYDROGEN SULFIDE INSTRUCTOR& TECHNICIAN COURSE HSI005

Sub acute poisoning:

The phenomenon of sub acute poisoning is mainly attributed to the direct local
irritative action if H2S on the mucous membranes of the eyes and respiratory tract.
Sub acute effects are generally experienced within several hours of exposure. The
severity of sub acute poisoning increased directly with the concentration and duration
of H2S exposure but doesn’t terminate in acute poisoning if continued.

Since the eyes are exposed more directly to the surrounding air, they are subject to
greater irritation. Thus, irritation of the conjunctiva and/or corneal epithelium is the
most common symptoms of sub acute poisoning. Concentrations from 7 – 100ppm
most commonly cause eye irritation, and conjunctivitis has been observed at less than
15ppm and in varying higher concentrations. The most serious consequence to the
eyes are:

• Conjunctivitis
• Keratitis and rupture of the corneal vesicles
• Temporary loss of vision

Increased humidity is an important contributory factor that increases these irritative

effects, which may not appear as severe during the exposure as after due to the
anesthetic effect of hydrogen sulfide on the nerves supplying the corneal membrane.
Symptoms preceding these painful conditions include lacrimation, hyperemia, averted
eyelids, retro orbital arching, blepharospasm, distorted and blurred vision,
photophobia and rainbow around lights.

Respiratory tract irritation in the form of bronchitis, rhinitis and pharyngitis has
occurred after prolonged exposure to 50-200ppm of H2S. These effects have
occasionally occurred after 5 – 10 minutes exposure to 500 – 600ppm. Pulmonary
edema usually does not appear until some time after the exposure, and thus constitutes
important and sometimes fatal sequelae of sub acute poisoning.

Recovery from sub acute poisoning is often slow, sometimes requiring several days.
This prolonged course is due to the inflammatory processes which follow irritation.
Coughing is often persistent for some time following exposure.

The ability of hydrogen sulfide to induce serious respiratory tract irritation is due to
its relatively insoluble nature. This property enables the irritative effects of the gas to
extend uniformly throughout the entire respiratory tract, so that deeper structures such
as the atria and alveoli are involved.

The microscopic pathology of sub acute poisoning are observed in animals is much
more distinctive than the rather unremarkable findings of acute poisoning. The lungs
show evidence of local congestion, and the cells lining the alveoli are filled with
transudate and blood. Cases of repeated poisoning also show leukocytes in the
alveolar spaces.

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ELEMENT 5 HYDROGEN SULFIDE INSTRUCTOR& TECHNICIAN COURSE HSI005

The degree of lung damage induced by H2S in concentrations greater than 15ppm
reduces vital lung capacity by 5.3% on the average. This effect appears to involve the
autonomic nervous system although, as yet, no precise mechanism has been set forth.

Although sub acute poisoning mainly involves local irritation, slight systemic
intoxication resulting in headache, fatigue, irritability, insomnia, mild depression, and
gastrointestinal disturbances may be caused by exposure to low concentrations of H2S
for several hours.

Chronic Poisoning:
Chronic poisoning may be defined as a prolonged state of symptoms or a debilitated
condition which results from a single or repeated long-duration exposure to
concentrations of H2S that, in themselves, do not produce symptoms of acute or sub
acute poisoning. The occurrence of neurasthenic symptoms which cannot be
explained otherwise have usually constituted the meager basis of the diagnosis of
chronic H2S poisoning does not exist, and there is wide disagreement concerning the
very existence of the pathological state defined as chronic poisoning.

High Risk Populations:

Knowledge of the toxicology of H2S permits the identification of individuals who,
because of some disease process, metabolic disorders or psychological disturbance,
cannot tolerate H2S or its by-products and therefore possess enhanced sensitivity to
the gas. In terms of evidence in the literature, however, the identification of “high
risk” groups within the population appears similar to the characterization of chronic
poisoning, i.e., the evidence if sparse, without stringent controls or reproduced results.
Having stated this qualification, we have undertaken to identify those individuals
whose capacity to tolerate H2S is reduced.

First, individuals with eye or respiratory tract problems would seem especially
vulnerable to the caustic and irritant, and sometimes-fatal action of the gas at these
sites. Conjunctivitis, eye irritation, emphysema, TB viral pneumonia and bronchitis
would seem to aggravate the irritative property of H2S in individuals with such
problems. Reports of studies investigating sensitivity of H2S of people with these
chronic disabilities are limited.

Second, individuals with anemia would appear to constitute another vulnerable

segment, since the detoxification of H2S relies on the presence of O2 is dependent on
both the amount of Hb in the red cells and on the number of red cells. Again, no
report of the increased susceptibility of this group have been found.

Third, alcoholics or individuals who have consumed alcohol within 24 hours of

exposure have been overcome by unusually small concentrations of H2S
indicating that alcohol and H2S do not mix. In community terms, alcoholics may
constitute a hyper susceptible population.

Fourth, persons having psychiatric problems are a poor risk at any H2S level.
Individuals with schizoid or paranoid tendencies become markedly worse following
exposure. Neurotic individuals have developed innumerable bizarre symptoms, many
of which remain for a long time as after-effects of the exposure.

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Pharmacology of Hydrogen Sulfide:

The physiological effects of H2S are dependent upon duration, frequency, and
intensity of exposure and upon individual susceptibility. The principal route of
absorption of H2S into the bloodstream is through the lungs. Although absorption
through the skin and intestinal wall have been reported, these routes of entry are
insignificant both in terms of the amount absorbed and the consequent toxic effects.

The detoxification of H2S, the body’s defense mechanism, is dependent upon the
oxygen content of the blood. Existing only momentarily in the blood as dissolved
H2S, the vast proportion of the gas reacts with oxygenated hemoglobin (HbO2) to
produce such compounds as thiosulfate or sulfate, which are eliminated through the
kidneys.

The present evidence suggests that neither enzyme or cofactor are important catalysts
in this reaction which occurs primarily in the blood and, to a minor degree, in muscle
where H2S reacts with myoglobin. The remaining trace amount of unoxidized and
dissolved H2S is eliminated by the lungs. The detoxification process is very rapid,
preventing H2S from acting as a cumulative poison. This fact is demonstrated by
the finding that slow intravenous injection several times the lethal dose of Na2S has
no apparent effect whereas a rapid injection of a lower dosage is fatal.

The portion of the gas which first comes into contact with moist tissues such as the
eyes and the respiratory mucosa undergoes an additional reaction prior to oxidation by
hemoglobin. The gas combines with the alkali in the tissues to form sodium sulfide, a
caustic irritant responsible for the irritative effects of H2S and the following
hydrolysis presumably occurs:

Na2S (2H2O)=(H2S + 2NaOH)

The H2S liberated by this reaction is then oxidized as before.

The systemic effects result from absorption of H2S into the bloodstream at a rate
faster than it cam be detoxified and the consequent perfusion of the central nervous
system by unoxidized H2S. Various investigations indicate that the systemic effects
are attributable to H+2S blocking action on certain enzyme systems, some of which
are directly involved in the oxidative processes of cells. Respiratory paralysis, as a
particularly acute systemic effect, has been attributed by others to the reflexes
resulting from the irritative action of the gas on the carotid sinus.

The precise mechanism by which H2S exerts its toxic properties via enzymic
inhibition has not been firmly established, but is generally agreed that it occurs by the
formation of sulfide of numerous cations. This reactivity essentially removes at
whatever degree, enzymic metal cofactors that are necessary for optimal activity.
Such inhibitory effects due to the presence of H2S have been reported for the
dehydrogenases (succinic), phosphatases (ATPase), oxidases (DOPA oxidase),
carbonic anhydrase, dipeptidase, benzamidase and such iron-containing enzymes as
the catalases, peroxidases and cytochromes (respiratory enzymes).
The foregoing information is quoted from a study made by the State of Illinois
Institute of Environmental Quality, Document NO. (IIEQ Doc. No. 74-24) entitled

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ELEMENT 5 HYDROGEN SULFIDE INSTRUCTOR& TECHNICIAN COURSE HSI005

Hydrogen Sulfide Health Effects and Recommended Air Quality Standards,

March, 1974.

5.9 REGULATIONS
There are a number of institutions involved in the compiling and enforcing of safety
regulations in the workplace, here are some of the regulatory institutions you will get
familiar with during the course of your training and field experience:
• OSHA - Occupational Safety & Health Administration (USA)
• MMS - Minerals Management Services (USA)
• DOT – Department of Transportation (USA)
• ANSI – American National Standards Institute (USA)
• API - American Petroleum Institute (USA)
• ISA – Instrument Society of America (USA)
• ACGIH – American Council of Governmental Industrial Hygienists (USA)
• NACE - National Association of Corrosion Engineers (USA)
• NIOSH - National Institute of Occupational Safety & Health (USA)
• CEN - European Committee for Standardization
• BSI - British Standards Institution (UK)
• EN - European Standard
• COSHH – Control of Hazardous to Health Regulations (UK)

Here are some of the regulatory terms you will need to be familiar with
• TLV – Threshold Limit Value
• TWA – Time-Weighted Average
• PEL – Permissible Exposure Limit
• STEL – Short Term Exposure Limit
• TLV-C - Threshold Limit Value – Ceiling
• IDLH – Immediately Dangerous to Life and Health
• LEL/LFL – Lower Explosive/Flammable Limit
• UEL/UFL – Upper Explosive/Flammable Limit
• REL – Recommended Exposure Limit ( NIOSH )

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5.10 DEFINITIONS:

Threshold Limit Value (TLV)

• The maximum concentration of an airborne contaminant a person, with no
respirator, can be repeatedly exposed to without any adverse effects.
Time-Weighted Average (TWA)
• The average concentration of an airborne contaminant during a specific time
period.

Permissible Exposure Limit (PEL)

• The designated level of an airborne contaminant which a person may be exposed
to, with no respirator.
Short Term Exposure Limit (STEL)
• The maximum concentration of an airborne contaminant a person, with no
respirator, can be exposed to for up to 15 minutes without any adverse effects.
Threshold Limit Value – Ceiling (TLV-C)
• This is the concentration that should never be exceeded, even instantaneously.
Immediately Dangerous to Life and Health (IDLH)
• Any condition that poses an immediate hazard to life that may couse immediate
irreversible debilitating effects on health.or that would interfere with an
individual’s ability to escape from a dangerous atmosphere.

Lower Explosive Limit/Lower Flammable Limit (LEL/LFL)

• The minimum concentration which a gas or vapor, when mixed with air, will
produce a flame or explosion when in contact with a source of ignition. The gas
or vapor will not burn or explode below this point because it is now too lean.
Upper Explosive Limit/Upper Flammable Limit (UEL/UFL)
• The maximum concentration which a gas or vapor, when mixed with air, will
produce a flame or explosion when in contact with a source of ignition. The gas
or vapor will not burn or explode beyond this point because it is now too rich.
There is no differential made between the terms “flammable” and “explosive” as
applied to the lower and upper limits of flammability.

5.11 THRESHOLD LIMIT VALUES

Threshold limit values are based on the best available information from industrial
experience, from experimental human and animal studies, and when possible a
combination of the three. The basis on which the values are established may differ
from substance to substance.

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5.12 ACCEPTABLE H2S CONCENTRATIONS

The acceptable eight hour Threshold Limit Value/Time-Weighted Average

(TLV/TWA) as recommended by the ACGIH – To avoid discomfort, the 8 hour
threshold limit value/time weighted average concentration of H2S shall not exceed
10ppm in the USA / 5ppm in the UK / 7ppm in Kazakhstan.

The Permissible Exposure Limit (PEL) as recommended by OSHA – The PEL for
H2S is 10ppm. This is the amount you can safely breathe, based on an 8 hour day
over a 5 day work week
.
The Short Term Exposure Limit (STEL) as recommended by OSHA – The STEL
for H2S is 15ppm. This is the amount you can be safely exposed to averaged over a
15 minute period four times a day, with at least a 1 hour period between each 15
minute exposure. The STEL should be considered the maximal allowable
concentration, or absolute ceiling, which is not to be exceeded at any time during the
15 minute exposure.

Immediately Dangerous to Life and Health (IDLH) – The IDHL limit shall not
exceed 100ppm.

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5.12 FACIAL HAIR ( Not Allowed with SCBA units )

Respirators will not be worn when conditions prevent a good face seal. Facial hair
lying between the sealing surface of a respirator facepiece and the wearer’s skin will
prevent a good seal. ( Examples above ). It is very important, especially on an
offshore location, that all personnel practice good grooming tips such as, shaving
daily, keeping moustaches trim, etc. Any person who refuses to cooperate must be
reported to his supervisor and the Company Man, which could result in drastic
measures being taken such as being removed from the job site, or even being
terminated.

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5.13 PULMONARY FUNCTION TEST (PFT)

Under the new OSHA regulations, any worker who is required to wear a respiratory to
perform his job or duties must now participate in a medical questionnaire and a
pulmonary function test. The pulmonary function test provides measures of lung
function, lung capacity, airway resistance, etc. The test will be performed by an
accredited, certified technician. The results of the test will then be examined by a
medical physician or licensed health care professional who will determine if the
worker, who has taken the PFT, is able to wear a respiratory in his duties. The new
law went into effect April 8, 1998.

1. How does any fit test system attempt to determine respirator fit?
By trying to assess the degree of respirator leakage while respirators are worn.
The assessment is made either quantitatively by measuring challenge agent
penetration, or qualitatively through sensory detection of challenge agent
penetration into the mask.
2. What are the major sources of respirator leakage when a mask is worn? How
should the following sources of respirator leakage be ranked (most to least) in
general? Which source is the most difficult to control during respirator use?
1) Faceseal leakage
2) valve leakage
3) air purifying media penetration
3. If you had to make a decision about respirator fit based a measurement of only
one of the following types of respirator leakage, which one would you use?
Basic Leakage - related to fundamental fit achieved when the respirator is
donned; affects every breath taken in the workplace. This is the one I would use
Positional Leakage - related to a head or face position that opens a break in the
faceseal; leakage occurs through break during inhalation; duration of ? sec;
assumed to affect every breath taken while head is in that position
Transient Leakage - related to transient breaks in the faceseal during
movement that result in leakage if coupled with an inhalation; duration of ?
millisec
Shift in basic leakage (shift in fundamental fit) - may be caused by vigorous
movement; affects every breath taken in workplace after the shift occurs

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4. Based on available data, what are the capabilities of the following QNFT methods
to measure the following types of respirator leakage?

Fit Test System Type Of Leak

Basic Positional Transient Shift

Generated poor poor unknown poor

Aerosol

Ambient Aerosol poor poor unknown* poor

CNP good good none good

*Based on a fit factor of 1,000 and an ambient aerosol concentration of 5,000

particles/cc, a Portacount detector sees about 0.06 particles/millisec assuming no in-
mask sampling biases .
5. Since air is the medium that carries contaminants or challenge agents into
respirators through leakage paths, how should aerosol-based measurements of
respirator leakage compare to CNP-based measurements of respirator leakage?
Difference in leakage measurements should reflect aerosol losses during
penetration of challenge agent through leakage paths into respirators. Ambient
aerosol losses during penetration are presumably very low. The real problem
lies in the ability of the aerosol particle to migrate to the aerosol detector after it
leaks into the mask. Comparing inhalation flow rates (about 50,000 ml/min)
with Portacount sample flow rates (700 ml/min) indicates that most particles
move to the lungs instead of the sampling probe during inhalation. This can be
confirmed by observing particle counts during inhalation vs. exhalation. Be sure
to account for Portacount sampling lag time while observing phenomenon in
count mode. Penetration occurs during inhalation, but particle counts are
usually higher during exhalation.
6. As currently implemented, CNP systems cannot measure transient leakage as
defined in question #4 above. If transient leakage plays a significant role in
respirator fit testing or protection, why do CNP fit test systems using static head
positions consistently measure so much more respirator leakage than aerosol-
based systems, which use dynamic exercises?
The current OSHA fit test protocol is primarily designed to try to measure
transient respirator leakage associated with the many dynamic exercises
included in the protocol (exercises consume the vast majority of time allocated to
fit testing). Analyses of the effects of exercises on measured fit have not shown
significant differences in leakage of respirators as a function of test exercises.
(Note that the difference between a fit factor of 5,000 and a fit factor of 10,000
may look like a big difference in fit, but it represents only a 0.01% change in
respirator leakage, equivalent to about 5 ml/min).

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If aerosol-based systems do in fact measure transient leakage well, then

transient leakage must not be a major contributor to total respirator leakage
since CNP fit test systems consistently detect much more respirator leakage than
aerosol systems.
7. Which fit test exercise generally produces lower fit factors during ambient-
aerosol fit tests?
The talking exercise. At first this may seem logical because of all the face and
mouth movement associated with talking. However, respirator leakage occurs
during inhalation when the facepiece is negatively pressurized. It is extremely
difficult to inhale and talk at the same time. Talking occurs during exhalation,
when the mask is positively pressurized. The reason that talking produces lower
fit factors is that the exhalation period is much longer when we talk. Since the
Portacount detects more particles during exhalation (when particle streamlining
is much less predominant), and exhalation occurs for a much longer period
during talking, we have a better chance of detecting the leakage that occurred
during inhalation when the mouth was not moving. In other words, the lower fit
factors that we see during the talking exercise are more an artifact of the
measurement system than significantly increased mask leakage associated with
talking.
A recent paper has identified higher peak inspiratory flow rates associated with
the talking exercise as a possible explanation for the lower Portacount fit factors
associated with talking. If this were true, we would expect to also see
significantly lower fit factors for the deep breathing exercise, which also involves
higher inspiratory flow rates. Unlike the talking exercise, the deep breathing
exercise has not been shown to produce significantly lower aerosol fit factors.
8. If a fit test system cannot measure respirator leakage effectively when the head is
not moving, how does moving the head help?
The leak measurement capability of aerosol-based systems has never been
validated. Most studies that can be traced to primary measurement standards
show that they do not. You should make sure that you can accurately measure the
basic parameter of interest (respirator leakage) before getting too carried away
with trying to measure variations of that parameter.
9. A number of people have recommended a fit factor of 5,000 as a minimum
passing level for Portacount fit tests. The US Marine Corps currently uses a fit
factor of 6,667 as it pass/fail criterion. How does a fit factor of 5,000 compare to
the maximum penetration allowed for a HEPA filter?
A fit factor of 5,000 is higher. 1 - 99.97% minimum removal efficiency = 0.03%
maximum allowable filter penetration = 3,333 equivalent fit factor. Although
HEPA filters typically do much better, is it reasonable to expect respirator
faceseals to perform better than minimal HEPA filter performance?

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10. What correlation has been found between workplace protection factor studies and
measured fit factors?
None
11. When was the generated aerosol “Gold Standard” fit test method validated?
Generated aerosol system has never been validated.
12. How do the results of workplace protection factor studies compare with the
results of fit testing in general? Are there logical explanations for this
phenomenon?
Aerosol-based fit factors in general are much higher than reported WPFs. Since
WPF values are calculated from workplace aerosol concentrations that are
typically orders of magnitude lower than those used to measure fit factors, it is
not surprising that WPFs are typically orders of magnitude lower than typical
aerosol fit factors. It is interesting to note that CNP fit factors are consistently
much lower than aerosol-based fit factors.
13. Mark Nicas, Ph.D., CIH of the University of California at Berkeley prepared a
document on assigned protection factors for OSHA in regard to its update of the
Respiratory Protection Standard. What did Nicas say about the relationship
between fit factors and workplace protection factors?
“To begin, the QLFTs in the OSHA lead standard were "validated" using a QNFT
result as the gold standard, which is to say, a QNFT fit factor was treated as the
true measure of respirator fit.(21,22,23) However, as noted by Nelson, "fit factors
have not been shown to be a predictor of WPF's."(18) One appropriate reference
is cited for this statement,(10) but other respirator researchers have made the
same observations.(11) It logically follows that a QLFT protocol cannot be
validated against QNFT fit factors if the latter fail to predict WPF values. It is
somewhat surprising that over the past decade of respirator research, no one has
recognized fundamental inconsistency in trying to validate a screening test (a
QLFT) against a second screening test (a QNFT) that fails to predict the
outcome of interest (the WPF value).”
14. Which has the greater impact on respirator fit -- mask donning or fit test
exercises?
Based on a limited number of data sets, mask donning seems to have a much
greater effect on mask fit than test exercises. It seem ironic that we typically
base our determinations of respirator fit on a single mask donning, with the
presumption that the mask will be donned the same way in the workplace.

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16. What role should fit test systems play in respirator selection?
According to OSHA, the determination of fit should play a major role in
respirator selection. However, based on ANSI Z88.10 Committee deliberations
to date, it seems that respirator selection (based primarily on feel?,
appearance?, comfort?) is accomplished prior to the fit test. The fit test is used
as some sort of final exam. This approach emphasizes avoidance of failure
rather than selection of the best fitting respirator.
Total Safety uses a Portacount® in most areas of operation for fit testing.

PORTACOUNT Universal Fit Test System Model 8028 can fit test any tight-fitting
respirator.
The Model 8028 Universal Fit Test System consists of a PORTACOUNT® Plus
Model 8020 and an N95-Companion™ Model 8095 together as one line item. It is
available at a reduced price compared to the two instruments when ordered separately.
(Computer not included.)

Features and Benefits

 Fit test ANY tight-fitting respirator including N95, P2 and P1 disposables

Applications
 Quantitative respirator fit testing (QNFT)
 Disposable filtering-facepiece fit testing (series-95, P1, P2)
 Half-mask fit testing
 Full-face fit testing
 Gas mask fit testing
 PAPR fit testing
 SCBA fit testing

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5.14 CONTACT LENS

Also, under the new regulations, contact lens can now be worn inside respirator face-
pieces. According to medical reports there were no cases of injury because of the use
of contact lens with respirators. Furthermore, a study was done with firefighters. It
showed that far fewer firefighters who wore contact lens with their SCBAs had
problems that necessitated the removal of their facepieces than did firefighters
wearing glasses. OSHA’s review of the record identified no evidence that the use of
contact lens with respirators increases safety hazards.

Keeping in mind, some companies will only allow you to wear soft contact lenses, not
hard contact lenses. So, when under contract and we are getting paid to provide a
service, we must abide by that company’s safety policy.

5.15 HYDROGEN SULPHIDE

IDLH 100ppm

Basis for IDLH Value:

It has been reported that 170 to 300ppm is the maximum concentration that can be
endured for 1 hour without serious consequences (Henderson and Haggard 1943) and
that olfactory fatigue occurs at 100ppm (Poda 1966). It has also been reported that 50
to 100ppm causes mild conjunctivitis and respiratory irritation after 1 hour; 500 to
700ppm may be dangerous in 0.5 to 1 hour; 700 to 1,000ppm results in rapid
unconsciousness, cessation of respiration, and death; and 1,000 to 2,000ppm results in
unconsciousness, cessation of respiration, and death in a few minutes (Yant 1930).

AIHA (1963). Hydrogen sulphide. In: Hygienic Guide Series.

Am Ind Hyg Assoc J 24:93.
Henderson Y, Haggard HW (1943). Noxious Gases, 2nd edition.
New York, NY; einhold Publishing Corporation, p. 245.
Patty FA, ed. (1963). Industrial Hygiene and Toxicology, 2nd
Edition, revised. Vol. II. Toxicology. New York, NY:
Interscience Publishers, p. 899.
MCA (1950). Chemical Safety Data Sheet SD-36, Hydrogen
Sulfide. Washington, DC; Manufacturing Chemists Association,
p. 12.

Threshold Limit Values

Threshold Limit Values (TLV) refer to airborne concentrations of substances and

represent conditions under which it is believed that nearly all workers may be
repeatedly exposed day after day without adverse effect. Because of a wide variation
in individual susceptibility, however, a small percentage of workers may experience
discomfort from some substances at concentrations at or below the threshold limit; a
smaller percentage may be affected more seriously by aggravation of a pre-existing
condition or by development of an occupational illness.

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Threshold Limit Values are based on the base available information from industrial
experience, from experimental and animal studies, and when possible, from a
combination of the three. The basis on which the values are established may differ
from substance to substance; protection against impairment of health may be a
guiding factor for some, whereas reasonable freedom from irritation, narcosis,
nuisance or other forms of stress may form the basis for others.

Definitions. There are three categories of Threshold Limit Values:

Threshold Limit Value – Time Weighted Average (TLV/TWA)

• The time-weighted average concentration for a normal 8 hour work day and a 40
hour work day and a 40 hour work week, to which nearly all workers may be
repeatedly exposed, day after day, without adverse effect.

Threshold Limit Value – Short Term Exposure Limit (TLV/STEL)

• The concentration to which workers can be exposed continuously for a short
period of time without suffering from 1) irritation, 2) chronic or irreversible tissue
damage, or 3) narcosis of sufficient degree to increase the likelihood of accidental
injury, impair self-rescue or materially reduce work efficiency, and provided that
the daily TLV/TWA is not exceeded. It is not a separate independent exposure
limit, rather it supplements the time-weighted average (TWA) limit where there
are recognized acute effects from a substance whose toxic effects are primarily of
a chronic nature. STEL’s are recommended only where toxic effects have been
reported from high short-term exposures in either humans or animals.

A STEL is defined as a 15-minute time-weighted average exposure which should

not be exceeded at any time during the work day even if the eight hour time-
weighted average is within the TLV. Exposures at the STEL should not be longer
than 15 minutes and should not be repeated more than four times per day. There
should be at least 60 minutes between successive exposures at the STEL.

Threshold Limit Value-Ceiling (TLV-C)

• The concentration that should not be exceeded during any part of the working
exposure. ( 50ppm in the USA )

Threshold Limit Values are intended for use in the practice of industrial hygiene as
guidelines or recommendations in the control of potential health hazards and for no
other use. The TLVs should be interpreted and applied only by a person trained in
industrial hygiene. They are not intended for use, or for modification for use, (1) as a
relative index of hazard or toxicity, (2) in the evaluation or control of community air
pollution nuisances, (3) in estimating the toxic potential of continuous, uninterrupted
exposures, or other extended work periods, (4) as proof or disproof of an existing
disease or physical condition, or (5) for adoption by countries in which working
conditions differ from those in the United States and where substances and processes
differ. These limits are not fine lines between safe and dangerous concentrations.

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