Oxygen Toxicity and Special Operations Forces Diving: Hidden and Dangerous

Abstract

In Special Operations Forces (SOF) closed-circuit rebreathers with 100% oxygen are commonly utilized for covert diving operations. Exposure to high partial pressures of oxygen (PO2) could cause damage to the central nervous system (CNS) and pulmonary system. Longer exposure time and higher PO2 leads to faster development of more serious pathology. Exposure to a PO2 above 1.4 ATA can cause CNS toxicity, leading to a wide range of neurologic complaints including convulsions. Pulmonary oxygen toxicity develops over time when exposed to a PO2 above 0.5 ATA and can lead to inflammation and fibrosis of lung tissue. Oxygen can also be toxic for the ocular system and may have systemic effects on the inflammatory system. Moreover, some of the effects of oxygen toxicity are irreversible. This paper describes the pathophysiology, epidemiology, signs and symptoms, risk factors and prediction models of oxygen toxicity, and their limitations on SOF diving.

Full text

MINI REVIEW
published: 25 July 2017
doi: 10.3389/fpsyg.2017.01263
Frontiers in Psychology | www.frontiersin.org 1July 2017 | Volume 8 | Article 1263
Edited by:
Costantino Balestra,
HE2B - Haute Ecole
Bruxelles-Brabant, Belgium
Reviewed by:
Jacek Kot,
Gda ´
nsk Medical University, Poland
Peter Germonpre,
Centre for Hyperbaric Oxygen
Therapy, Belgium
Guy Louis Vandenhoven,
Sports Medical Centre, Belgium
*Correspondence:
Thijs T. Wingelaar
tt.wingelaar@mindef.nl
Specialty section:
This article was submitted to
Movement Science and Sport
Psychology,
a section of the journal
Frontiers in Psychology
Received: 17 May 2017
Accepted: 11 July 2017
Published: 25 July 2017
Citation:
Wingelaar TT, van Ooij P-JAM and van
Hulst RA (2017) Oxygen Toxicity and
Special Operations Forces Diving:
Hidden and Dangerous.
Front. Psychol. 8:1263.
doi: 10.3389/fpsyg.2017.01263
Oxygen Toxicity and Special
Operations Forces Diving: Hidden
and Dangerous
Thijs T. Wingelaar 1, 2*, Pieter-Jan A. M. van Ooij1and Rob A. van Hulst 2
1Diving Medical Center, Royal Netherlands Navy, Den Helder, Netherlands, 2Department of Anaesthesiology, Academic
Medical Center, Amsterdam, Netherlands
In Special Operations Forces (SOF) closed-circuit rebreathers with 100% oxygen are
commonly utilized for covert diving operations. Exposure to high partial pressures of
oxygen (PO2) could cause damage to the central nervous system (CNS) and pulmonary
system. Longer exposure time and higher PO2leads to faster development of more
serious pathology. Exposure to a PO2above 1.4 ATA can cause CNS toxicity, leading to
a wide range of neurologic complaints including convulsions. Pulmonary oxygen toxicity
develops over time when exposed to a PO2above 0.5 ATA and can lead to inflammation
and fibrosis of lung tissue. Oxygen can also be toxic for the ocular system and may have
systemic effects on the inflammatory system. Moreover, some of the effects of oxygen
toxicity are irreversible. This paper describes the pathophysiology, epidemiology, signs
and symptoms, risk factors and prediction models of oxygen toxicity, and their limitations
on SOF diving.
Keywords: oxygen toxicity, CNS-toxicity, pulmonary toxicity, diving, closed-circuit rebreather
INTRODUCTION
Military diving, especially within the domain of the Special Operations Forces (SOF), is one of
the most extreme forms of diving. Depending on the task, this type of diving demands different
equipment, procedures and training and, therefore, it is totally unlike commercial or civilian diving.
For SOF divers, range and endurance, high mobility and stealth, are of utmost importance. To
facilitate these requirements, the most commonly used equipment is the closed-circuit oxygen
rebreather (O2-CCR): a comprehensive overview of the historic aspects of CCR diving is already
published (Donald, 1992; Acott, 1999; Butler, 2004).
A CCR is fundamentally different from any open-circuit or semi-closed diving system. Instead
of releasing exhaled air to the surrounding environment, it is recirculated within the apparatus.
Any exhaled carbon dioxide (CO2) is “scrubbed” by a chemical mixture, often various hydroxides,
for instance NaOH and Ca(OH)2. The efficacy of scrubbers is beyond the scope of this review,
but factors like granule size, ambient temperature, and humidity greatly affect and sometimes limit
scrubber efficiency. CCRs can be used with air, mixed gas, or pure oxygen. There is no exhaled
gas under the form of bubbles and gas consumption is very much limited, increasing the possible
autonomous dive time. In case of a breathing gas composed of pure oxygen, a second substantial
difference compared to a regular SCUBA or mixed gas rebreather can be noted: the oxygen diver
has no accumulation of nitrogen or other inert breathing gas and, therefore, no decompression
limits. To facilitate recirculation, the breathing gas is temporarily stored in a “counter lung” before
inspiration. The volume of this counter lung limits the tidal volume (TV) and maximum minute

Wingelaar et al. Special Operating Forces Oxygen Diving
volume (MMV) of the SOF diver. The limitation of TV and MMV
and possible saturation of the soda lime can cause retention of
CO2(Arieli et al., 2006a,b). This greatly affects the development
of oxygen toxicity (see below).
Although many studies have investigated the toxic effects
of oxygen on both the central nervous system (CNS) and
the pulmonary system, the question remains how applicable
those studies are for SOF divers. Much of the research was
conducted with animals; although this has greatly contributed
to our understanding of physiological processes, the results
cannot always be extrapolated to humans (Robinson et al., 1974;
Bryan and Jenkinson, 1988; O’Collins et al., 2006). Secondly,
much of the available data on humans is rather old, and many
of these experiments will never be replicated today due to
our current viewpoint on research ethics. Nevertheless, these
historical studies give some insight into the (life-threatening)
dangers that oxygen poses for man (Donald, 1992; Acott, 1999).
Since technological advances (such as, the capacity of “scrubbing”
CO2) influence the occurrence of oxygen toxicity, many of these
older studies cannot be used to determine the threshold or safe
limits or oxygen exposure. Lastly, most human experiments were
performed in rest in a recompression chamber, the so-called
“dry dives.” Although dry dives enable researchers to administer
oxygen in partial pressures above 1 ATA (equal to 101.3 kPa), the
effects of oxygen are not the same as in an actual dive. Several
studies have shown that submersion can alter the physiologic
reaction to breathing gases (Donald, 1992; Kerem et al., 1995; van
Ooij et al., 2011).
However, even when taking these limitations into
consideration, some relevant data on oxygen toxicity in
diving are still available. The aim of this paper is to summarize
the pathologic effects of oxygen (mainly on the CNS and
pulmonary system) and their operational consequences for SOF
divers.
CENTRAL NERVOUS SYSTEM TOXICITY
The phenomenon of CNS toxicity is commonly referred to as
the Paul Bert effect, named after the French physiologist who
first described it (Bert, 1878). In many dry dive experiments,
Bert showed that oxygen is toxic and potentially lethal for many
organic species including seeds, fungi, insects, and several small
mammals. Others published similar results, showing that CNS
toxicity was dependent on the inspired partial pressure of oxygen
(PO2) and the time exposed. In 1910 Bornstein was probably
the first to expose two human volunteers in a dry dive setting to
hyperbaric oxygen at a PO2of 2.8 ATA (equal to 283.7 kPa) for
30 min without any complaints (Acott, 1999).
The tolerance for oxygen in dry dives is much higher
than in wet dives (Donald, 1992). In an immersed setting, a
PO2above 1.4 ATA can lead to nausea, numbness, dizziness,
twitching, hearing and visual disturbances, unconsciousness and
convulsions (Harabin et al., 1995). In humans, no oxygen induced
convulsions have been described with a PO2lower than 1.3,
although susceptibility to oxygen toxicity has a high interpersonal
and intra-individual variability (Donald, 1992; Arieli et al., 2008).
While convulsions can occur without any prior symptoms, visual
disturbances generally precede convulsions (Curley and Butler,
1987; Arieli et al., 2006a). Reports on the incidence of CNS
toxicity vary greatly, ranging from 1 in 157,930 CCR dives to
approximately 3.5% of the CCR dives (Harabin et al., 1995;
Walters et al., 2000; Arieli et al., 2002). This may be attributed to
different exposures in time and depth, or to different definitions
of the symptoms or, perhaps, because the covert nature of SOF
diving precludes the reporting of precise incidences.
Pathogenesis and Risk Factors
Although the exact mechanism is not fully understood, currently,
the most plausible explanation is related to an overflow of reactive
oxygen species (ROS) in the brain after an increase of cerebral
blood flow (CBF) (Visser et al., 1996a; Koch et al., 2008). Due to
the increased PO2in plasma there is an auto oxidation of nitric
oxide (·NO) to several ROS, of which peroxynitrite (ONOO−)
is the most important (Goldstein and Czapski, 1995; de Groot
et al., 2004). ROS cause angiotensin-II induced vasoconstriction
via activation of non-phagocytic NAD(P)H oxidase (Weissmann
et al., 2000; de Groot et al., 2004; Nguyen Dinh Cat et al.,
2013). However, at the same time, endothelial and neuronal
nitric oxide synthase (eNOS and nNOS), which are responsible
for vasodilatation, are increased (Hoehn et al., 2003). The net
result of both processes is vasoconstriction and a reduction
of CBF up to a certain “breaking point.” Possibly due to
depletion of the radical oxygen scavenger system, vessels dilate
and increases CBF (Chavko et al., 1998; Demchenko et al.,
2002; Eynan et al., 2014). Simultaneous to this increase in
CBF, the cortical electroencephalography (EEG) activity increases
(Bean and Coulson, 1971; Visser et al., 1996b). This increase
in CBF and cortical EEG activity precedes convulsions (Bean
and Coulson, 1971; Visser et al., 1996a,b; Demchenko et al.,
2001; Koch et al., 2008). The exact mechanism though which
ROS cause convulsions is not entirely clear. ROS are believed
to directly affect various ionic conductance that regulate cell
excitability, as well as disrupting chemical synaptic transmission
(Manning, 2016). The role of superoxide dismutase (SOD),
catalase and other scavengers in the brain, predominantly on
the function of the hippocampus, remains to be elucidated.
However, animal experiments have shown that modulating the
N-methyl-D-aspartate (NMDA) and N-nitro-L-arginine (NNA)
system alters the susceptibility (Eynan et al., 2014; Manning,
2016). When any prodromal symptoms are encountered and the
PO2is lowered, convulsions may be avoided (Arieli et al., 2008).
Despite extensive research to identify risk factors in CNS
toxicity, most studies were on animals and the relevance for
oxygen diving in humans remains unclear. Oxygen toxicity is
dependent on both PO2and time, i.e., the time of onset of
symptoms is shorter when the PO2is higher (Donald, 1992;
Arieli et al., 2002). An increase in end-tidal partial pressure of
carbon dioxide (PetCO2), either by “CO2retainers” (divers with
a delayed or altered response to hypercapnia) or due to exercise,
also increases susceptibility to oxygen toxicity (Arieli et al., 2001;
Koch et al., 2013). Dehydration and starvation prolongs the latent
period to onset of convulsion in rats, but the pathophysiological
mechanism is unclear (Bitterman et al., 1997). In a small study,
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Wingelaar et al. Special Operating Forces Oxygen Diving
a ketogenic diet in divers increased oxygen tolerance, but the
mechanism for neuroprotection remains unknown (Valadao
et al., 2014). Adding nitrogen or helium to the inspired gas, as
well as adding periods of breathing air (commonly called “air
breaks”) to the oxygen exposure, protect against convulsions
in dry dives, but the feasibility in oxygen diving is limited
(Hendricks et al., 1977; Bitterman et al., 1987; Harabin et al.,
1988; Arieli et al., 2005, 2008). An overview of pharmacological
agents and vitamins that protect or sensitize has recently been
published (Jain, 2017). A few pharmacological agents are worth
mentioning here: scopolamine and cinnarizine (agents frequently
used to prevent and treat motion sickness) do not seem to either
attenuate or sensitize oxygen toxicity (Bitterman et al., 1991;
Arieli et al., 1999). Caffeine is effective in delaying convulsions in
rats, but its efficacy in humans has yet to be confirmed (Bitterman
and Schaal, 1995). Due to the unpredictability and operational
limitations, relying on pharmacological agents for extending SOF
diving is not currently relevant.
Prediction Model and Variability
The first prediction model (published by Harabin et al.) was based
on 661 CCR dives (Harabin et al., 1995). This was later refined by
Arieli et al. who based their model on 2,039 CCR dives and which
remains the most accurate model to date (Arieli et al., 2002). The
chance of oxygen toxicity (as Z-score in a normal distribution)
in any dive can be estimated by: Z=[ln(t)−9.63 +3.38 ×
ln(PO2)]/2.02. Note that this equation includes PO2(in kPa) and
time (in min) as variables. The recovery time (similar to “surface
interval” in air dives: the time for a diver to neutralize the oxygen
stress) is based on experiments in rats and estimated by: Kt=Ke
×e−0,079t, where Ktis regarded as a cumulative oxygen toxicity
index at time t(in min) and Kethe “toxicity dose” at the end of
exposure. However, to our knowledge, no studies have tested the
efficacy of these models in humans.
Although the methodology of the model is sound, a
considerable intra and interpersonal variability in oxygen toxicity
still remains. In an effort to identify the military divers at risk, the
“oxygen tolerance test” has long been advocated, where subjects
were exposed to breathing 100% oxygen at 2.8 ATA for 30 min
(Butler and Knafelc, 1986). However, after evaluation, this was
proven obsolete because it lacked predictive value and many
navies now refrain from using this test (Visser et al., 1996b;
Walters et al., 2000). A similar test for CO2, the Read test, has
also proven ineffective (Arieli et al., 2014). Although the ability
to detect CO2by divers can be trained, it is unknown whether
this reduces the incidence of oxygen toxicity (Eynan et al., 2003,
2005). To our knowledge no valid test is available to screen for
oxygen tolerance.
Operational Consequences
Even though the pathophysiological mechanisms and risk factors
are not yet clarified, there is a clear depth (PO2) and time
relationship. Oxygen toxicity of the CNS is a rare but potentially
life-threatening complication of exposure to high PO2, which
can occur without prodromal symptoms. If mild symptoms
do occur and can be timely recognized, convulsions may
be avoided by reducing depth. However, delayed progression
to convulsions after reducing oxygen exposure have been
described.
In sports diving, the PO2limit recommendations ranges
from 1.4 to 1.6 ATA (Lang, 2001). The limits for military
SOF diving are different, due to differences in the equipment
and the amount of “acceptable risk” (Table 1) (Vann, 1988;
United States Department of the Navy NSSC, 2008). The
model from Arieli et al. allows 24 min at a PO2of 2.5
ATA when accepting a risk of maximum 5% of CNS toxicity
(Arieli et al., 2002). The widely used US Navy Diving
Manual allows a single-depth exposure to a PO2of 2.5 ATA
for 10 min (United States Department of the Navy NSSC,
2008). However, these high risks are only taken with the
proper training, equipment and safety precautions, and only
when the operational demands leave no alternative options.
Incidence reports of oxygen toxicity using the Arieli model
are lacking, most likely due to the covert nature of SOF
diving.
PULMONARY OXYGEN TOXICITY
In 1899, the Scottish pathologist, James Lorrain Smith, published
the pathological effects of increased inspiratory oxygen tension
on several small animals (Lorrain Smith, 1899). In these classic
experiments, mice and larks were exposed to increasing pressures
of oxygen for long periods of time. Besides several episodes
of CNS toxicity, most of the animals perished because of
hypoxia as a result of insufficient ventilation due to acute or
chronic lung inflammation. Compared to CNS toxicity, a lower
partial pressure of oxygen is required to cause symptoms, but
the exposure time has to be much longer (hours to days).
Exposure above 0.5 ATA is regarded as potentially damaging
for the pulmonary system. In humans, early symptoms include
tracheobronchial irritation with retrosternal pain and coughing
(Klein, 1990). Longer exposures damage the tracheal mucosa
with impaired mucus clearance (Sackner et al., 1975). These
complaints precede changes in lung function tests, such as, a
decrease in vital capacity (VC), but have a low predictive value
due to high variability (Klein, 1990). The incidence in divers is
unknown, since no studies have investigated the epidemiology.
TABLE 1 | Single-depth oxygen exposures.
Depth
(fsw/msw)
Limit US Navy
(United States Department
of the Navy NSSC, 2008)
(min)
Risk of CNS
toxicity (Arieli
et al., 2002)(%)
Limit Arieli
et al. <5%
(min)
25/7.7 240 13.1 83
30/9.2 80 6.3 63
35/10.7 25 2.4 48
40/12.3 15 1.7 38
50/15.3 10 1.8 24
Depth in feet of sea water (fsw) and meters of sea water (msw). The limits are printed as in
the US Navy Diving Manual with (in the third column) their associated risk for CNS toxicity
based on the model of Arieli et al. (2002). The last column shows the bottom time when
accepting a maximum risk of CNS toxicity of 5%.
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Wingelaar et al. Special Operating Forces Oxygen Diving
Pathophysiology and Risk Factors
Pulmonary oxygen toxicity (POT) can be divided into two phases.
The first exsudative phase (Figure 2, left side) is marked by local
inflammation with capillary and endothelial edema, a decrease of
type I alveolar cells, and an influx of inflammatory cells (Miller
and Winter, 1981; Bryan and Jenkinson, 1988; Demchenko et al.,
2007). These changes are reversible and the lung returns to
its normal state (Figure 1) if the inspired oxygen pressure is
reduced below 0.5 ATA. In the following proliferative phase
(Figure 2, right side) fibroblasts and type II alveolar cells infiltrate
the inflamed endothelia. With continuing inflammation, this
ultimately leads to alveolar fibrosis and a four- to fivefold increase
of thickness of the air-blood membrane and, as a consequence,
loss of diffusion capacity (Kapanci et al., 1972; Robinson et al.,
1974). These changes are irreversible. The rate at which these
changes occur is directly related to the inspired PO2and can
occur as early as 3 h at a PO2of 3 ATA during a dry dive (Winter
and Smith, 1972; Klein, 1990).
When divers are immersed, many physiologic processes
are altered. Circulating volume is redistributed due to the
hydrostatic pressure on the body and peripheral vasoconstriction
when immersed in cold water, both resulting in volume shift
and intrathoracic pooling (Norsk et al., 1985; Choukroun
et al., 1989; Pendergast and Lundgren, 2009). Even though
the mammalian diving reflex lowers the heart rate, the net
result of both processes is pulmonary hypertension, because the
cardiac output is increased as a result of the Frank-Starling
mechanism (Dahlback et al., 1978). The increased blood flow
in the lung recruits apical fields (compared to exercise), but
also stiffens the lung (Choukroun et al., 1983; Pendergast and
FIGURE 1 | Schematic representation of the normal alveolocapillary region. 1,
alveolar type 1 cell; 2, alveolar type 2 cell; 3, basement membrane; 4,
interstitium; 5, capillary endothelial cell; 6, fibroblast; 7, alveolar macrophage;
8, surfactant layer; 9, red blood cell; 10, capillary base membrane. Adapted
with permission from van Ooij et al. (2013).
Lundgren, 2009). Beside these effects on lung circulation, the
intrathoracic pooling and pulmonary hypertension triggers the
baroreceptors in the right atrium, which increases diuresis
through an increased vasopressin release (Norsk et al., 1986;
Boussuges et al., 2007, 2009). Lastly, the position of the diver
in the water (horizontal or vertical) and the position of the
breathing apparatus compared to the body (deeper or lower than
the diver) also influences perfusion of the lung and breathing
dynamics (Badeer, 1982; Taylor and Morrison, 1991). As a result
of all of the above processes, gas exchange in the lung during
immersion is substantially different from that during dry dives
(Prefaut et al., 1978; Taylor and Morrison, 1990; van Ooij et al.,
2011).
Very few studies have reported risk factors for developing
POT in divers, let alone in SOF divers. Most of the results are
derived from dry dive experiments. Many of these studies use a
decrease in VC as a marker to determine the amount of POT;
however, the validity of this measurement is questioned (see
below). Shykoff reported that exercise in an immersed setting
and repeated exposure increases POT (Shykoff, 2008a,b). To our
knowledge, no other risk factors have been identified. In animal
studies, scavengers (such as, SOD and catalase) were shown
to protect lung tissue against the overload of oxygen radicals;
however, this effect has not been confirmed in humans (Kimball
et al., 1976; Frank et al., 1978; Potter et al., 1999).
Prediction Model and Variability
In military and commercial diving, the current standard for
determining the maximum pulmonary oxygen exposure in
FIGURE 2 | Exsudative stage (left) and proliferative stage (right) in pulmonary
oxygen toxicity. 1, type 1 alveolar cell; 2, type 2 alveolar cell; 3, alveolar
edema; 4, neutrophil; 5, hyaline membrane; 6, edematous interstitium; 7,
fibroblast; 8, fibrin thrombus; 9, swollen capillary endothelial cell; 10, denuded
basement membrane; 11, alveolar fibrin formation; 12, collagen fibers
deposition; 13, incorporation of hyaline membrane; 14, fibroblastic
proliferation; 15, interstitial fibrin.
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Wingelaar et al. Special Operating Forces Oxygen Diving
diving is “units of pulmonary toxicity dose” (UPTD). One UTPD
equals the amount of damage caused by breathing 1 min of
100% oxygen at 1 ATA (Bardin and Lambertsen, 1970). The
basic concept of UPTD is that a certain threshold (amount of
oxygen molecules) is required to cause local damage, which can
be measured by a decrease in VC. For instance, an exposure of
615 UPTD causes the VC to decrease 2% in 50% of the divers,
while 1425 UPTD lowers the VC by 10% in 50% of the divers
(Clark and Lambertsen, 1970; Wright, 1972). Since the 1970s,
many studies have further refined the basic model (Clark et al.,
1999). To calculate the amount of UPTD, the following equation
must be solved: UPTD =t×[0.5/(PO2−0.5)]−5/6, with PO2in
ATA and time in minutes. Arieli et al. published an improved
equation to more accurately determine the decrease in VC in
a dry setting, based on data from several studies that included
exposures with humans: 1VC =0.0082 ×t2(PO2/101.3)4.57;
please note that, here, PO2is in kPa and time is in hours
(Eckenhoff et al., 1987; Clark et al., 1991; Arieli et al., 2002).
The “cumulative units of pulmonary toxicity dose” (CPTD), the
“oxygen toxicity unit” (OTU) and derived equation for repetitive
exposure (REPEX) were introduced to include recovery and
facilitate multi-day exposures, but was never validated in divers
(Hamilton, 1989). Arieli et al. also published an updated equation
to estimate the recovery of lung volume, which was extrapolated
from data derived from animal experiments performed in a dry
setting (Arieli et al., 2002). There is no consensus which model is
the most valid to plan SOF operations.
The main flaw in the UPTD concept and the derived equations
is the change in VC as the sole indicator to determine oxygen
stress. VC has a circadian rhythm and there is a strong intra and
interpersonal variability when measuring lung volumes (Hruby
and Butler, 1975; Harabin et al., 1987). Ventilation during
anaesthesiology with a high PO2is known to influence VC,
possibly due to absorption atelectasis (O’Brien, 2013). Whether
this also occurs in SOF divers, or how long this endures after
diving, is unknown. Recent findings have proven that immersion
itself alters VC regardless of oxygen stress (Shykoff, 2005; van
Ooij et al., 2011, 2012). Since the UPTD model was derived
from dry dives, the above-mentioned factors are not taken into
account. Although the original authors recognized the limitations
of the UPTD model, more advanced diagnostic measurements
were either too difficult to perform or were unavailable in the
1960s/1970s (Bardin and Lambertsen, 1970).
Operational Consequences
POT is more insidious than CNS toxicity; it affects the
oxygen divers in long shallow-water dives or when recurrently
exposed. The current prediction model (UPTD) was developed
in dry setting during a time when capabilities to measure
lung parameters were limited. Newer parameters, such as, the
ratio between diffusion capacity of carbon monoxide and nitric
oxide (DLNO/CO), fraction of exhaled nitric oxide (FENO ) or
volatile organic compounds (VOCs), might be more accurate
in determining POT, but these tests have yet to be validated
(Shykoff, 2008a,b; Caspersen et al., 2011; van Ooij et al., 2014b,a,
2016; Vermeulen et al., 2016). Especially the VOCs are of interest
because, in the field of pulmonology, this noninvasive diagnostic
modality is increasingly utilized for diagnosing asthma, acute
respiratory distress syndrome and lung cancer (Bos et al., 2014,
2016; Boots et al., 2015). However, until a new valid parameter to
determine POT has been established, the UPTD model remains
the gold standard, despite its limitations.
As equipment improves and dive times are extended, SOF
divers might be increasingly exposed to a level at which
irreversible damage may occur. The Royal Netherlands Navy
currently dives with the LAR 5010 by Dräger and within the
limits given by NATO (Allied Diving Publication), which are
highly similar to the US Navy Diving Manual (United States
Department of the Navy NSSC, 2008). Oxygen exposure is
limited to 450 UPTD per day and 2250 UPTD per week. A
single exposure up to 1425 UPTD is regarded the absolute
maximum and only to be used in exceptional circumstances
with sufficient medical support available (i.e., recompression
facilities and medical capacity within the operational theater).
The Royal Netherlands Navy Diving Medical Center performs
yearly dive medicals on all Dutch SOF divers according to and
surpassing the standard of the European Diving Technology
Committee (Wendling and Nome, 2004). In a recent 20-year
longitudinal cohort study, we found no significant changes
in pulmonary function and diffusion capacity of SOF divers
compared to other Navy divers or non-divers (Voortman et al.,
2016). Tetzlaff et al. published similar results (Tetzlaff et al.,
2005). Yearly exercise tolerance testing shows VO2 max values
regularly surpassing 50 ml/kg/min and all divers remain fit for
diving duties during their career. This may be due to either
sufficient “recovery” time between extreme dives, or because
exposures are not severe enough to cause irreversible damage.
Although current monitoring does not show any deleterious
effects, it remains necessary to continue this monitoring of long
term health effects as the level of exposure in recent years has
increased.
OTHER PATHOPHYSIOLOGIC CHANGES
While CNS toxicity and pulmonary toxicity have been described
as separate entities in this review, their occurrence may be
more closely related. In addition to cold, stress and physical
activity, CNS toxicity activates the sympathetic nervous system,
which in animal experiments leads to pulmonary edema though
the pulmonary venule adrenergic hypersensitivity response
(Winklewski et al., 2013). Hyperoxia, even at normobaric
conditions, induces many physiological changes which are often
not fully understood. In addition, the clinical relevance of these
changes and impact on SOF diving remains to be elucidated.
Although this paper does not aim to give a full review of all
known pathophysiological effects of oxygen in divers, the effects
on sight and exercise tolerance are important in the context of
SOF diving. For further reading of the effects of hyperoxia on
other parts of the body we suggest the work of Bennett and Elliott
(Brubakk and Neuman, 2003).
Ocular Toxicity
Visual acuity is of crucial importance to SOF divers. Visual
complaints are a frequent side-effect of daily clinical treatments
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Wingelaar et al. Special Operating Forces Oxygen Diving
in recompression chambers (hyperbaric oxygen therapy: HBOT).
Transient myopia with up to 0.25 dioptres loss for each week
exposed to high oxygen pressures can occur, but generally
resolves after a few weeks (Butler et al., 2008). Apart from
one case report, hyperopic myopia has not been reported in
oxygen divers (Butler et al., 1999). Although extreme HBOT
exposures can cause irreversible cataract or keratoconus, this has
not been described in divers (Palmquist et al., 1984; Butler, 1995;
McMonnies, 2015). These effects of oxygen on the ocular system
are probably irrelevant for SOF divers, as oxygen pressures are
generally much lower and exposure is less frequent compared
with daily HBOT in patients for several weeks.
Exercise Tolerance
There are several reports on fatigue and reduced exercise
tolerance after high oxygen exposures (Comroe et al., 1945;
Lambertsen, 1978; Shykoff, 2005). Divers complained about
retrosternal pain or the inability to “give their full” for several
days. To what extent this is a subjective complaint, or limits
(diving) performance, is unknown. Although the mechanism
behind these complaints is not fully understood, generalized
oxidative stress depletes the scavenger system and leads to
lipid peroxidation of the cell membranes causing cell damage
(Ferrer et al., 2007; Perovic et al., 2014). After diving, because
there is an upregulation of glutathione peroxidase (GPx) and
catalase activity in lymphocytes, the inflammatory system may
also be involved (Ferrer et al., 2007). Damage and dysfunction
of erythrocytes has been described after hyperbaric hyperoxic
exposure and in saturation divers, its effect on exercise tolerance
is unknown (Dise et al., 1987; Hofsø et al., 2005). To what
extend performance is impaired in SOF divers after oxygen diving
remains to be confirmed.
SUMMARY
In diving and hyperbaric environments, oxygen toxicity has been
a topic of interest for over a century. Although many human
experiments are not reflecting current equipment or procedures
anymore, the results do illustrate the damaging potential of
oxygen. Diving with high partial pressures of oxygen can result
in acute life-threatening neurologic complications or irreversible
pulmonary structural changes. However, the extent to which
these problems occur in oxygen diving remains unknown, due
to the lack of studies on humans during immersion, and/or
epidemiologic studies.
In SOF diving, where 100% oxygen rebreathing diving systems
are frequently used, operational demands and health risks are
taken into account when planning dives. All current limits
or diving tables with high PO2possess a certain quantity of
“acceptable” risk. The question arises as to whether civilian or
commercial divers should use the same limits as SOF divers.
To develop more accurate prediction models, we need to
identify the pathophysiological mechanism of oxygen toxicity
and the factors that, subsequently, increase or decrease the
risk to various parts of the body. This is complicated by
the covert nature of SOF diving, limiting publication of
data. Also, in view of the considerable inter- and intra-
personal variability, perhaps the future of oxygen diving
requires real-time individual monitoring of early symptoms
of oxygen toxicity, such as, CBF or exhaled VOCs, to
protect humans from the harmful effects of oxygen when
diving.
Current Limits on Oxygen Exposure in the
Royal Netherlands Navy
Central Nervous System Oxygen Toxicity
Divers exposed to a PO2above 1.3 ATA should be considered
to be at risk for developing CNS toxicity. An estimation of
the chance of CNS toxicity in diving, as Z-value in a normal
distribution with tin minutes and PO2in kPa, can be made
(Arieli et al., 2002). There is no consensus regarding a “maximum
acceptable risk.”
Z=ln (t)−9.63 +3.38 ×ln(PO2)
2.02 (1)
Pulmonary Oxygen Toxicity
Any PO2above 0.5 ATA is regarded as toxic for the
pulmonary system. The amount of “units of pulmonary
toxicity dose” (UPTD), with tin minutes and PO2in ATA,
can be calculated with the function below (Bardin and
Lambertsen, 1970). Many authorities regard an exposure of
615 UPTD as the “maximum safe exposure for a single
dive”.
UPTD =t−1.2s0.5
PO2−0.5 (2)
AUTHOR CONTRIBUTIONS
TW student of RvH: Acquisition and review of literature,
drafting, and revising manuscript. PJvO co-promotor of TW:
Review of literature, help with theoretical framework, writing,
and reviewing concept manuscripts. RvH promotor of TW:
Review of literature, help with theoretical framework, writing,
and reviewing concept manuscripts.
FUNDING
This research received no specific grant from any funding
agency in the public, commercial, or not-for-profit
sectors.
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Conflict of Interest Statement: The authors declare that the research was
conducted in the absence of any commercial or financial relationships that could
be construed as a potential conflict of interest.
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Frontiers in Psychology | www.frontiersin.org 9July 2017 | Volume 8 | Article 1263