Influences of Atmospheric Pressure and Temperature
on Intraocular Pressure
Sara Van de Veire,1 Peter Germonpre,2 Charlotte Renier,1 Ingeborg Stalmans,1 and
Thierry Zeyen1
PURPOSE. To determine whether the atmospheric pressure
(ATM) change experienced during diving can induce changes
in the intraocular pressure (IOP) of eyes in a normal popula-
tion.
METHODS. The IOP of 27 healthy volunteers (ages, 23.8 ⫾ 4.9
years; range, 18 – 44) was measured with a Perkins applanation
tonometer by two independent investigators who were
masked to the previous measurements. Measurements were
taken at baseline (normal ATM, 1 Bar and 24°C), at 28°C and
24°C after the ATM was increased to 2 Bar in a hyperbaric
chamber, at baseline again, and finally at the normal ATM of 1
Bar but a temperature of 28°C. Multivariate regression analysis
was used to evaluate the results.
RESULTS. The mean IOP decreased significantly from 11.8 mm
Hg in the right eye (RE) and 11.7 mm Hg in the left eye (LE) at
1 Bar to 10.7 mm Hg (RE) and 10.3 mm Hg (LE) at 2 Bar (P ⫽
0.024, RE; P ⫽ 0.0006, LE). The IOP decrease remained con-
stant during the ATM increase period (40 minutes) and was
independent of the temperature change. The temperature in-
crease alone did not significantly influence the IOP.
CONCLUSIONS. An increase of the ATM to 2 Bar (equal to condi-
tions experienced during underwater diving at 10 meters)
modestly but significantly decreased the IOP independently of
the temperature change. During the period of increased ATM
(60 minutes), the IOP decrease remained stable and was inde-
pendent of blood pressure change or corneal thickness. (Invest
Ophthalmol Vis Sci. 2008;49:5392–5396) DOI:10.1167/
iovs.07-1578
G laucoma is the second leading cause of irreversible blind-
ness worldwide and affects approximately 70 million peo-
ple, of whom 7 million are blind.1,2 Elevated intraocular pres-
sure (IOP) is widely regarded as the most important modifiable
risk factor associated with the development and progression of
glaucomatous optic neuropathy. Little is known about the
effects of external factors such as atmospheric pressure (ATM)
and surrounding temperature (T) on the IOP. Rather than
looking at changes in IOP, most published reports on the
effects of high altitude (low ATM) focus on high-altitude retinal
hemorrhage3–5 or on systemic side effects, such as increased
blood pressure,6,7 and on cardiac side effects,8 which lead to
mountain sickness. However, one study does mention that a
From the 1Department of Ophthalmology, Catholic Universities
Leuven, Leuven, Belgium; and 2Center for Hyperbaric Oxygen Ther-
apy, Military Hospital Queen Astrid, Brussels, Belgium.
Submitted for publication December 10, 2007; revised June 3 and
July 9, 2008; accepted October 10, 2008.
Disclosure: S. Van de Veire, None; P. Germonpre, None; C.
Renier, None; I. Stalmans, None; T. Zeyen, None
The publication costs of this article were defrayed in part by page
charge payment. This article must therefore be marked “advertise-
ment” in accordance with 18 U.S.C. §1734 solely to indicate this fact.
Corresponding author: Thierry Zeyen, Department of Ophthal-
mology, University Hospitals Leuven, Kapucijnenvoer 33, B-3000 Leu-
ven, Belgium; thierry.zeyen@uz.kuleuven.ac.be.
5392
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higher baseline IOP is a significant risk factor for altitude
retinopathy.9
IOP at high altitude has been the subject of controversy for
many years. Ninety years ago, Wilmer and Berens10 measured
the IOP of 14 aviators in a hypobaric chamber, but no signifi-
cant changes were found. More recently, the effect of de-
creased ATM on IOP has been studied by several groups;
however, their results are conflicting. Some groups have ob-
served a decrease in IOP,11 some have found either an increase
in IOP12,13 or no change in IOP,14,15 and some have observed
a reduction in IOP that occurs within hours of ascent and
subsequently recovers to baseline levels during acclimatiza-
tion.16,17 The mechanisms of these changes remain unknown,
but many different explanations have been suggested. Some
investigators speculate that increases in IOP could result from
altered intracranial pressure18,19 or corneal thickness.20 Other
studies support the idea that lowered IOP may occur with
hypobaric hypoxia acclimatization11,16,17 or may be an effect
of retinal vasodilatation.21
This controversy may be partially attributable to the differ-
ent methodologies used in each of these studies. Some inves-
tigators examined subjects only several days before departure
to and after descent from high altitude; in these cases, the IOP
always returned to baseline levels but could have been even
lower with prolonged exposure to altitude.22 Furthermore,
most studies used a portable device (Perkins or Tonopen) to
measure IOP,14,21 but in a few experiments this measurement
was taken at low altitude using the weight-dependent and,
hence, altitude-dependent Schiotz tonometer.18
Reports on the effect of increased ATM on IOP are rare.
Ersanli et al.23 observed that exposure to hyperbaric oxygen
therapy at 2.5 Bar significantly reduced IOP, which was indi-
rectly attributed to hyperoxic vasoconstriction. Although a
matter of controversy, increased IOP has been observed with
decreased ATM,13 but it remains to be established whether this
same effect occurs during ATM increase without pure oxygen
breathing.
The aim of this prospective study was to investigate the
effect of ATM and temperature increase on the IOP of healthy
eyes. This study was inspired primarily by frequent inquiries
from glaucoma patients about the potential deleterious effects
of underwater diving, airplane travel, and mountaineering on
IOP.
MATERIALS AND METHODS
Our sample population, consisting of 27 healthy, nonsmoking subjects
(54 eyes; subject ages, 23.8 ⫾ 4.9 [range, 18 – 44] years; male/female
ratio, 1.25) was randomly divided into two groups. None of the sub-
jects had any ophthalmologic disorder apart from a refractive correc-
tion of less than ⫾4 D with glasses or contact lenses. Physical pre-
examination consisted of standard intake examination for hyperbaric
treatments, including plain chest x-ray, tonal audiometry, and resting
electrocardiography. Ophthalmologic examination consisted of biomi-
croscopy, nondilated funduscopy, and central corneal thickness (CCT)
measurement. All subjects were treated in accordance with the Dec-
laration of Helsinki. They were asked to fill out a general health
Investigative Ophthalmology & Visual Science, December 2008, Vol. 49, No. 12
Copyright © Association for Research in Vision and Ophthalmology
 IOVS, December 2008, Vol. 49, No. 12
questionnaire and to sign an informed consent form. Ethics committee
approval was obtained.
The aim of our experiment was to determine whether there is a
correlation between ATM and temperature on IOP in a healthy popu-
lation. To accomplish a reproducible increase in experimental ATM,
we used a hyperbaric chamber and stabilized all other parameters,
including temperature. We also looked for a correlation between
fluctuations of the surrounding temperature and the IOP. For this, we
stabilized the ATM and increased the temperature.
We noninvasively measured the IOP in both eyes with applanation
tonometry (portable Perkins tonometer; Clement-Clarke International,
Harlow, Essex, UK) under topical anesthesia (Unicaine; Bournonville
Pharma, Braine-l’Alleud, Belgium) and with locally applied fluorescent
strips.19 The Perkins tonometer evaluates IOP (using a small applana-
tion pin) with a minimal weight mass and has the ability to measure the
IOP of a subject in an upright position inside the hyperbaric chamber.
IOP was measured in five different settings by two independent inves-
tigators. Measurements were alternated for each investigator (investi-
gators A and B each alternately monitored groups A and B). A third
independent observer registered all the measurements so that the
investigators were masked to the previous measurements.
We started measuring IOP at baseline with a normal ATM of 1 Bar
and an ambient temperature of 24°C. Pressure exposure was accom-
plished by placing our volunteers in a clinical multiplace hyperbaric
chamber (Starmed 2800; Haux, Karlsbad, Germany) with microproces-
sor-controlled pressure and temperature levels. During compression,
adiabatic phenomena led to a temperature increase, which, when
combined with the air-conditioning system of the chamber, resulted in
a surrounding temperature of 28°C once the 2 Bar level was reached.
During the pressure “plateau,” the temperature could be modified
independently of the pressure. After the first measurements, the cham-
ber was gradually cooled to the baseline temperature of 24°C. Oxygen
and humidity levels were kept constant throughout at 21% and 40%,
respectively, during exposure, and the noise level never exceeded 85
dB. During the experiment, all subjects remained seated, and no
physical exercise was performed.
During compression, some subjects had to perform repeated Val-
salva maneuvers to equalize their middle ear pressure to the surround-
ing pressure. The rate of pressure increase was low (0.1 Bar/min),
allowing for easy equalization in all but one subject. All subjects
succeeded in equalizing their middle ears using only very light and
brief (nonstrenuous) Valsalva maneuvers.
On the day of the experiment, the outside climatologic conditions
were sunny, 16°C, and 1016 mBar of pressure. However, the hyper-
baric chamber complex was housed in an air-conditioned room with a
fixed temperature of 24°C and humidity set at 40%. All the volunteers
stayed in these controlled conditions for at least 1 hour before the start
of the measurements. A small adjacent room was heated to 28°C with
electric heaters.
Two hyperbaric chamber sessions were performed on the same day
in the afternoon, and the subjects were randomly assigned to either
session. Settings of the hyperbaric chamber at the time of the IOP
measurements were as follows:
1. Baseline (normal ATM ⫹ normal temperature [T]): measure-
ment of the IOP inside the hyperbaric chamber with a normal
ATM of 1 Bar (sea level) and a T of 24°C.
2. 1ATM ⫹ 1T: measurements of the IOP inside the hyperbaric
chamber after increasing the ATM to 2 Bar and the T to 28°C
(also called “the dive”). It took approximately 10 minutes for
these conditions to be reached. Five minutes later, the IOP was
measured.
3. 1ATM (1ATM ⫹ normal T): measurements of the IOP inside
in the hyperbaric chamber with a stable ATM of 2 Bar after the
T had been lowered to 24°C. It took approximately 20 minutes
for the T to be lowered by 4°C. Five minutes later, the IOP was
measured.
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Role of Atmospheric Pressure on IOP 5393
4. Baseline (normal ATM ⫹ normal T): measurements of the IOP
inside the hyperbaric chamber after the ATM was decreased
again to 1 Bar with a stable T of 24°C. It took 10 minutes for the
ATM to be lowered back to baseline. Five minutes later, the IOP
was measured.
5. 1T (normal ATM ⫹ 1T): measurements of the IOP took place
outside the hyperbaric chamber. Subjects were taken to a small
room heated to 28°C with a normal ATM of 1 Bar. After 5
minutes of acclimatization, the IOP was measured.
Overall, the cycle inside the hyperbaric chamber took approximately
60 minutes.
All subjects underwent the same procedure in the same order.
During the experiment, the investigators were also inside the hyper-
baric chamber to measure the IOP. Before every measurement, we
waited 5 minutes to allow for acclimatization.
In addition to IOP, we measured CCT with a handheld device
(Pachmate DGH55; DGH Technology, Exton, UK), and we measured
systemic blood pressure before and after the dive at the baseline
settings 1 and 4. Five subjects routinely wore soft contact lenses for
myopia, but these were removed the evening before the examination.
Statistical analysis was performed to determine the statistical sig-
nificance of the observed changes in IOP in response to the change in
pressure, temperature, or both. A multivariate normal model with the
covariance matrix modeled by the Kronecker product of a 2 ⫻ 2
covariance matrix for side and a 5 ⫻ 5 covariance matrix for repetition
(five settings) was used to model the 10 repeated IOP measurements
per subject. Based on this model, the interaction between repetition
and side was significant (P ⫽ 0.026). Therefore, the analysis was
performed separately for each side (using a multivariate normal model
with an unstructured 5 ⫻ 5 covariance matrix for the five repeated
measures of IOP per eye). Analyses were performed using statistical
software (PROC MIXED procedure, SAS version 9.1; SAS Institute Inc.,
Cary, NC). The confidence interval was set at 95%.
RESULTS
Increased ATM in the hyperbaric chamber lowered the IOP
significantly, regardless of the temperature. The IOP-lowering
effect was more pronounced in the left eyes than in the right
eyes, probably because of random fluctuation (Figs. 1, 2). For
FIGURE 1. The influence of ATM and temperature (T) on the IOP of
the left eyes.
 5394 Van de Veire et al. IOVS, December 2008, Vol. 49, No. 12

FIGURE 3. The influence of ATM increase on the IOP.

a small, but not significant, IOP-lowering effect in both eyes,

FIGURE 2. The influence of ATM and temperature (T) on the IOP of
the right eyes.
one subject, no measurements were available at the third and
fourth settings because of ear clearance problems; as a result,
the subject was prematurely removed from the hyperbaric
chamber. One subject was substantially (20 or more years)
older than the others; his results were 4 mm Hg higher than
observed in the other subjects’ IOP measurements, but the
measurements followed the same pattern during the five set-
tings. One subject had outlying data points for the third and
fourth settings; IOP increases of 3 mm Hg for the right eye (RE)
and 2 mm Hg for the left eye (LE) were observed.
Under normal temperature conditions, we found that in-
creased ATM significantly lowered IOP (RE, 11.74 –10.72 mm
Hg [P ⫽ 0.026]; LE, 11.69 –10.32 mm Hg [P ⫽ 0.003]).
Regardless of temperature, when we took into account the
overall effect size of the ATM increase on the IOP, the IOP-
lowering effect was still significant (RE, P ⫽ 0.024; LE, P ⫽
0.0006; Table 1 and Fig. 3). However, the correlation between
IOP and temperature was not significant in both eyes (RE, P ⫽
0.18; LE, P ⫽ 0.24). Therefore, we can conclude that the effect
of ATM was independent of temperature.
To determine whether temperature influences IOP, we al-
tered the temperature under both ATM settings. We observed
where RE IOP measurements ranged from 11.74 mm Hg to
10.93 mm Hg (P ⫽ 0.22) and LE IOP measurements ranged
from 11.69 mm Hg to 11.2 mm Hg (P ⫽ 0.52; Table 1).
We found that the IOP was still reduced after the complete
hyperbaric cycle (60 minutes), where the average RE IOP
measurement was 11 mm Hg after cycle compared with 11.74
mm Hg before cycle (P ⫽ 0.13), and the average LE IOP
measurement was 11.2 mm Hg after cycle compared with
11.69 mm Hg before cycle (P ⫽ 0.18); however, these differ-
ences were not significant. Corneal thickness was measured as
an independent variable before and after the hyperbaric cycle
examination, and we found that it did not have a significant
influence on IOP values (P ⫽ 0.997). CCT values for contact
lens users were also not significantly increased compared with
values for those who did not wear contact lenses (P ⫽ 0.37).
Systemic blood pressure was measured before and after
hyperbaric exposure; there was no significant difference be-
tween the two readings. It has been previously shown that
systemic blood pressure is not modified during mild hyperbaric
exposure24; however, systemic blood pressure measurements
during the entire experimental protocol were not performed.
DISCUSSION
In the present study, an increase in ATM resulted in a signifi-
cant and sustained decrease in IOP, both at increased and at
baseline temperature. A second experiment was performed
consecutively in which the temperature was increased while
the ATM was kept constant. This condition did not lead to a
significant change in IOP. Therefore, the observed decrease in

TABLE 1. Effect of ATM and T on the IOP in Healthy Persons

Right Eye Left Eye

Estimate Estimate
(mm Hg) SE P (mm Hg) SE P

Effect ATM at nl T ⫺1.02 0.43 0.026 ⫺1.36 0.42 0.003

Effect ATM at 1T ⫺0.22 0.34 0.53 ⫺0.65 0.36 0.080
Overall effect ATM ⫺0.62 0.26 0.024 ⫺1.01 0.26 0.0006
Effect T at nl ATM ⫺0.74 0.48 0.13 ⫺0.50 0.44 0.27
Effect T at 1ATM 0.06 0.30 0.84 0.21 0.28 0.46
Overall effect T ⫺0.34 0.27 0.22 ⫺0.14 0.22 0.52
Interaction T and ATM ⫺0.80 0.59 0.18 ⫺0.71 0.59 0.24
Difference settings 1 vs. 4 ⫺0.69 0.43 0.13 ⫺0.52 0.38 0.18

The overall effect sizes of the ATM and T on the IOP are stated in italic. Significant values are stated in bold; significant intervals were set at
P ⬍ 0.05.

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 IOVS, December 2008, Vol. 49, No. 12
IOP was presumably caused by the elevated ATM rather than
by the concurrent change in temperature in the hyperbaric
chamber.
To the best of our knowledge, this is the first report docu-
menting the effect of elevated ATM on IOP in a healthy pop-
ulation without supplemental oxygen breathing. Ersanli et al.23
also studied the effect of hyperbaric oxygen on the IOP, but
their study required patients to breathe hyperbaric oxygen
(100% O2 at 2.5 Bar) while in the hyperbaric chamber.
In our study, the ATM increase led to a significant and
sustained IOP decrease. After the complete hyperbaric cycle
(60 minutes), the IOP was still reduced, so there was no sign
that the eyes had adapted to the ATM. This might have been
because of the prolonged effect of the ATM; it is not known
how long external pressure changes can influence IOP. It
should be noted that although the differences in IOP were
small, they remained significant during the entire investigation.
It is likely that longer recovery time after hyperbaric exposure
would have normalized the IOP back to a baseline level. This is
a shortcoming of our methodology that may be addressed in
future studies with the introduction of an additional time-
course of IOP measurements into the cycle. Additionally, it is
possible that IOP differences may be larger in elderly persons,
as suggested by the increased IOP measurements observed in
the older subject in our sample population.25
The mechanisms underlying the IOP decrease after the ATM
increase are unclear. We hypothesize that different mecha-
nisms could produce the IOP-lowering effect after ATM in-
crease.
One possible cause is that the subjects were breathing
higher oxygen levels at 2 Bar than at sea level. The percentage
of oxygen in the breathing air was kept constant at 21% during
the experiment; therefore, at increased ATM, all subjects
breathed a gas with partial oxygen pressure of 0.42 Bar (ac-
cording to Dalton’s law, 0.21 ⫻ Bar), corresponding to 42%
oxygen breathing at sea level. It has been shown that 75%,26
but not 25%,27 oxygen breathing causes moderate hyperventi-
lation and consequent respiratory alkalosis. Although we did
not measure PaCO2 in our subjects, this minimal hyperventila-
tion might have contributed to the observed IOP decrease.13,28
To address issues of oxygen and CO2 partial pressure, fol-
low-up studies should adjust the concentration of the breath-
ing gases to keep the partial pressure constant.
Additionally, it has been reported that hyperoxygenation
induced by breathing 100% oxygen induces retinal vasocon-
striction, which may be responsible for a slight decrease of
IOP, independently of changes in arterial CO2 tension.29 –31
This has been confirmed by measurements of IOP in patients
undergoing hyperbaric oxygenation (FiO2 ⫽ 2.5).23 However,
the effect of moderate (FiO2 ⫽ 0.42) hyperoxygenation on
ocular pressure has not been studied. From the literature we
know that breathing air at 2 ATM causes only minimal arterial
PCO2 changes and cerebral vasoconstriction, or approximately
one-third the effect of 100% oxygen breathing at 1 Bar.32 It is
possible that a similar effect contributed to the observed de-
crease in IOP in our study33 because the degree of IOP de-
crease was proportionally less than what was observed by
Luksch.29
Another possibility is that, at higher ATM, the increased
density of the breathing gas may modify respiratory dynamics
by increasing the breathing resistance; this might, in theory,
increase blood pressure by increasing the workload of the
inspiratory and expiratory muscles. However, this effect is
absent in resting conditions at 2 Bar. All subjects remained
seated, and no physical exercise was performed because exer-
cise is known to provoke a decrease in episcleral pressure.34
Nonstrenuous Valsalva maneuvers were performed to equalize
middle ear pressure during the pressure increase (compression
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Role of Atmospheric Pressure on IOP 5395
phase). All subjects avoided strenuous Valsalva because this
could have been a confounding factor and could have led to an
increase in IOP instead of a decrease.35,36 It is possible that
these Valsalva maneuvers could have increased IOP in a small
and transient way, but then the consequent IOP decrease
would have even been lower.
Because of practical reasons, we only measured arterial
blood pressure before and immediately after exposure and
found no significant difference, consistent with the findings of
Thomson et al.24 Although it is possible that some psycholog-
ical stress could have caused a temporary increase in blood
pressure, this seems unlikely in the hyperbaric chamber used
for the experiments because it was spacious, comfortable, and
confidence-inspiring. In fact, this hyperbaric chamber is spe-
cifically designed for treatments of a wide variety of patients,
and all stress-provoking aspects of hyperbaric technology are
concealed.
Although it is unlikely, an external tonographic effect by the
ATM (e.g., massage after trabeculectomy) could have caused
the IOP-lowering effect in our study. Pascal’s law states that
external pressure is transmitted integrally to any fluid-filled
space, such as the eyeball. Similarly, we do not think this effect
was caused by external pressures on the eyeball (e.g., Schiotz
tonometry) because the tonometer we used was not influ-
enced by external pressure.
We found that IOP decreases as ATM increases to condi-
tions similar to those experienced when diving underwater to
approximately 10 meters. Theoretically, the observed IOP de-
crease in our healthy sample population should be helpful to
glaucomatous eyes; however, real underwater diving requires
not only the physical exercise and pressure increase itself but
also the use of goggles or a diving mask. Because our study did
not account for all these variables, we could not immediately
conclude that this activity is safe for such patients. Indeed,
another recent report indicates that wearing swimming gog-
gles significantly increases IOP at sea level conditions.37,38 This
is probably related to an external pressure on the orbit that
should not be present when wearing a real scuba diving mask
because the rubber or silicon skirt of this type of mask rests on
the facial bones around the orbit and not on the eyeball itself.
CONCLUSION
ATM was inversely correlated to IOP in our healthy sample
population. Our results show a small, but significant and sus-
tained, decrease of IOP in a hyperbaric chamber at 2 Bar
(equivalent to the pressure at 10 meters under water). The IOP
decrease remained present throughout the entire experiment
(60 minutes) of increased ATM. This decrease was of minor
physiological significance in these subjects, whose IOP values
were within the normal range. We can presume that hyper-
baric exposure is not harmful for glaucoma patients. If there is
any effect, induced by either a slight hyperventilation, hyper-
oxygenation or any other mechanism, it results in an IOP
decrease.
This study was designed to observe the effect of ATM
changes in a healthy population. We plan to determine
whether the IOP changes observed in a healthy population
after increased ATM carry over to glaucomatous eyes by con-
ducting a prospective follow-up study with a higher ATM
change (up to 4 Bar) on healthy persons and on glaucoma
patients. Furthermore, to verify as precisely as possible the
mechanisms responsible for any observed change in IOP, sub-
groups will be studied in whom the partial pressures of oxygen
will be kept constant during exposure; longer periods of equil-
ibration between the experimental steps will be included.
 5396 Van de Veire et al.
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