Advance Access Publication 17 May 2007 eCAM 2008;5(1)27–35
The Treatment of Pulmonary Diseases and Respiratory-Related
Conditions with Inhaled (Nebulized or Aerosolized) Glutathione
The Canadian College of Naturopathic Medicine, 1255 Sheppard Avenue East, Toronto, ON M2K 1E2, Canada
International Primary Health Care, The External Program, University of London, London, UK
Reduced glutathione or simply glutathione (g-glutamylcysteinylglycine; GSH) is found in
the cytosol of most cells of the body. GSH in the epithelial lining fluid (ELF) of the
lower respiratory tract is thought to be the first line of defense against oxidative stress.
Inhalation (nebulized or aerosolized) is the only known method that increases GSH’s levels in
the ELF. A review of the literature was conducted to examine the clinical effectiveness of
inhaled GSH as a treatment for various pulmonary diseases and respiratory-related conditions.
This report also discusses clinical and theoretical indications for GSH inhalation, potential
concerns with this treatment, its presumed mechanisms of action, optimal doses to be
administered and other important details. Reasons for inhaled GSH’s effectiveness include its
role as a potent antioxidant, and possibly improved oxygenation and host defenses. Theoretical
uses of this treatment include Farmer’s lung, pre- and postexercise, multiple chemical sensitivity
disorder and cigarette smoking. GSH inhalation should not be used as a treatment for primary
lung cancer. Testing for sulfites in the urine is recommended prior to GSH inhalation. Minor
side effects such as transient coughing and an unpleasant odor are common with this treatment.
Major side effects such as bronchoconstriction have only occurred among asthma patients
presumed to be sulfite-sensitive. The potential applications of inhaled GSH are numerous
when one considers just how many pulmonary diseases and respiratory-related conditions are
affected by deficient antioxidant status or an over production of oxidants, poor oxygenation
and/or impaired host defenses. More studies are clearly warranted.
Keywords: aerosolized glutathione (GSH) – antioxidant – inhaled GSH – nebulized GSH –
Reduced glutathione or simply glutathione
(g-glutamylcysteinylglycine; GSH) is found in the cytosol
of most cells of the body (1). It is a tripeptide consisting
of glycine, cysteine and glutamate. GSH functions in
several enzyme systems within the body that assist with
the quenching of free radicals and the detoxification of
fat-soluble compounds (Table 1) (2–5). It also plays a
significant metabolic role in supporting many different
biochemical processes (e.g. amino acid transport, deox-
yribonucleic acid synthesis and immune system augmen-
tation) considered to be important mediators of health
Glutathione in the epithelial lining fluid (ELF) of the
lower respiratory tract is thought to be the first line of
defense against oxidative stress (6). The ELF concentra-
tion of GSH is 140 times that of serum concentrations
with a redox ratio of 49 : 1 (7). In fact, alternations in
alveolar and lung GSH metabolism are widely recognized
as a central feature among many inflammatory lung
diseases (8–14). In healthy lungs, the oxidant burden is
balanced by local antioxidant defenses. However, in lung
For reprints and all correspondence: Jonathan Prousky, 1255 Sheppard
Avenue East, Toronto, Ontario, Canada MK2 1E2. Tel: 416-498-1255,
ext. 235; Fax: 416-498-1611; E-mail: email@example.com
ß2007 The Author(s).
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/
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diseases cellular damage and injury is mediated by an
increased oxidant burden and/or decreased antioxidant
In inflammatory lung diseases, supplementation with
exogenous sources of GSH would be necessary to reduce
the oxidant load and/or correct for antioxidant deficien-
cies within the lungs. A few published clinical studies
have shown the oral administration of GSH to be
ineffective at increasing plasma levels when given to
healthy subjects (15), or when used for the treatment of
hepatic cirrhosis (16). If the oral administration of GSH
cannot raise plasma levels in healthy and diseased
patients, it is doubtful that this method of delivery
would have any appreciable effects at increasing GSH
concentrations within the lungs.
Intravenous administration might be effective since it
bypasses the gastrointestinal tract, immediately enters the
blood stream, and presumably would saturate body
tissues such as the lungs. Unfortunately, the results of a
study did not show intravenous administration to be
effective at increasing GSH levels within the ELF (17).
When 600 mg of GSH was delivered intravenously to
sheep, the levels in the venous plasma, lung lymph and
ELF increased only for a very brief period of time.
However, when the same amount of GSH was delivered
through inhalation (nebulized or aerosolized), the base-
line GSH level in the ELF (45.7 10 mM) increased 7-fold
at 30-min (337 64 mM), remained above the baseline
level 1 h later (P50.001) and returned toward baseline
levels by 2 h. Despite this short-term increase in GSH
concentrations within the ELF, the inhalation method
did not significantly increase the amount of GSH in the
lung lymph, venous plasma and urine during the 2 h
study period. The authors of this report concluded that
inhalation specifically increased GSH levels at the lung
Given that inhalation is the only known method that
increases GSH levels in the ELF for a significant
duration, a review of the literature was conducted to
examine the clinical effectiveness of inhaled GSH
as a treatment for various pulmonary diseases and
respiratory-related conditions. Only reports involving
human subjects were included in the analysis. The clinical
and theoretical indications for GSH inhalation were
summarized and potential concerns with this treatment
reported. Other pertinent details such as its presumed
mechanisms of action and optimal doses to be adminis-
tered were compiled and evaluated.
Computer searches were conducted of English and non-
English language articles in the Biomedical Reference
Collection (1984 to August 2006), CINAHL (1982 to
August 2006), MEDLINE (1965 to August 2006) and
Nursing and Allied Health Collection (1985 to August
2006) databases. Articles were searched with the key
search terms ‘Nebulized Glutathione,’ and ‘Glutathione’
in combination with ‘Aerosol’ OR ‘Inhalation.’ These
keywords were also searched with words related to
pulmonary and/or respiratory disease. To supplement
the search, references of the articles found from the initial
search were reviewed. Hand searching of relevant
journals was also completed as part of the search.
Selection of Articles
To be included in the final review, articles had to report
on the use and administration of inhaled GSH for
pulmonary diseases and respiratory-related conditions in
human subjects. Only peer-reviewed articles were
An evidence grade was determined for each article. These
evidence grades were adapted from the hierarchy of
evidence developed by the Oxford Centre of Evidence
Based Medicine (Table 2) (18).
Table 1. Enzyme systems involving glutathione
Enzyme system Function
Glutathione synthetase Gamma-glutamyl cycle.
Riboflavin-containing glutathione reductase Catalyzes the conversion of oxidized glutathione
(glutathione disulfide; GSSG) to its reduced form.
GSH transferase isoenzymes Conjugation of GSH with fat-soluble substances for
liver detoxification and the detoxification of
environmental carcinogens, such as those found in tobacco smoke.
Protects cells from hydrogen peroxides and lipid hydroperoxides.
If not neutralized, these peroxides will damage cellular membranes
and other vital cellular components.
synthase Conjugation of leukotriene A
with GSH, resulting in the generation
of leukotrienes C
. Gamma-glutamyl transpeptidase then metabolizes
to leukotrienes D
28 GSH in pulmonary diseases and respiratory-related conditions
A total of 12 reports were screened (9,10,17,19–27). Only
one report was excluded because it involved the use of
inhaled GSH in sheep (17). In total, 11 articles were
found to meet the inclusion criteria and were included in
this review (9,10,19–27). Table 3 displays the character-
istics of the studies included in this review.
Based exclusively on the published evidence included in
this review, inhaled GSH is potentially indicated for the
following clinical conditions: cystic fibrosis (CF), chronic
otitis media with effusion (OME), HIV seropositive
individuals, idiopathic pulmonary fibrosis (IPF) and
chronic rhinitis. These conditions were chosen since the
published studies were of good quality, received A and B
evidence grades, and their respective results demonstrated
benefits from the use of GSH inhalation.
Inhaled GSH cannot be recommended as a potential
treatment for emphysema since the quality of evidence is
lacking at the present time. The emphysema case report
had notable limitations since serial spirometry was not
documented, and the placebo effect could not be
ruled-out (22). However, this does not necessarily
indicate that GSH inhalation would be of no benefit
for emphysema patients. There is experimental and
human data demonstrating a link between GSH, oxidant-
derived damage and possible protection against the
development of emphysema. An in vitro study demon-
strated that GSH could retard the oxidant-mediated
down-regulation of a-1-proteinase inhibitor activity in
smokers’ emphysema (28). This finding is important since
one of the principal pathophysiological mechanisms of
emphysema is the down-regulation of this enzyme by
means of oxidative damage (29). Moreover, in a recent
review of lung GSH and cigarette smoke-induced airway
disease, increased GSH in the ELF of chronic smokers
was presumed to be a protective adaptive mechanism
against the development of chronic obstructive pulmon-
ary disease (COPD) (30). Considering that not all chronic
smokers go on to develop COPD, the authors in that
review pointed out that genetic variations in the
molecular mechanisms that regulate GSH metabolism
might explain why some individuals are better protected
against the development of COPD. It thus appears that
emphysema patients are subjected to progressive tissue
damage due, in part, to the consequences of GSH
deficiency and/or genetic variations in GSH metabolism.
Since GSH inhalation would presumably offer both
antioxidant protection and GSH replenishment, this
method of treatment would potentially benefit emphy-
Asthma is another condition where inhaled GSH
cannot be recommended since this treatment caused
notable side effects (e.g. breathlessness, bronchoconstric-
tion and cough) in the cited study (21). These side effects
were linked primarily to the production of sulfites that
occurred when GSH was in solution. GSH inhalation
should continue to be explored as a potential treatment
for asthma. None of the asthma patients in the study had
their urine tested for sulfites. A positive test for sulfites
would have eliminated these patients from entering the
study. Accordingly, the results might have been much
more favorable if patients without sulfite sensitivities
This issue of asthma and sulfite sensitivities is an
important one for clinicians to be mindful of. Sulfites are
found in beer, wine, restaurant salad bars, seafood,
potatoes, processed foods and many pharmaceuticals
(31). Many asthma patients report being sensitive to
sulfites. In an Australian study, 30% of asthmatic
patients reported being sensitive to sulfites in wine (32).
A more recent and rigorous scientific study, however,
demonstrated that asthma patients can tolerate varying
amounts of sulfites in wines ranging from 20, 75 or 150
parts per million (ppm) (33). Only a small minority of
patients in this study (4 of 24 self-reported wine-sensitive
asthmatics) exhibited reactions when challenged with
300 ppm of sulfites. One report indicated that 4–8% of
asthmatics are sensitive to sulfites (34). Other reports
have estimated the incidence of sulfite sensitivity to be
around 5–11% (35,36). Even though the exact percentage
of sulfite-sensitive asthmatics is difficult to ascertain,
sulfite sensitivity is an important factor to assess when
using or evaluating research done on inhaled GSH.
Future Research Directions
There are additional clinical conditions that might benefit
from this type of treatment, but further studies are
necessary. One such condition is Farmer’s lung (FL),
which is a hypersensitivity pneumonitis caused by the
inhalation of thermophilic actinomycetes and spores of
Aspergillus specie (11). A study was undertaken to
investigate the effect of pulmonary GSH levels after
hay exposure in patients with FL and in asymptomatic
farmers (AF) (11). Fifteen symptomatic patients with FL
Table 2. Grades of evidence
A Systematic reviews of randomized controlled trials
and/or randomized controlled trials with or without
double-blind placebo control.
B Systematic reviews of observational studies and/or
high-quality observational studies including
cohort and case-control studies and/or cohort
‘outcomes’ research and/or nonrandomized
C Case-series, case-reports, and/or poor-quality
cohort and case-control studies.
D Expert opinion without explicit critical appraisal
or based on physiology, bench research or
eCAM 2008;5(1) 29
Table 3. Summary of articles demonstrating the effectiveness of inhaled glutathione for the treatment of pulmonary diseases and respiratory-related
Reference Condition NDosages of inhaled
Outcome Evidence grade
(21) Asthma Eight asthma patients
[mean age, 29 7
600 mg once weekly for
A subset of patients
with clinically stable
effect when treated with
(23) Chronic otitis media
30 patients (3–12 years of
age; mean age, 5.8 years)
and 30 controls (3–12 years
of age; mean age, 6.1 years)
600mg of GSH in 4 ml
of saline subdivided
into five 2-min sessions
by nasal aerosol every
3–4 waking h for
GSH should be
considered for the
(24) Cystic fibrosis (CF) Nine patients [mean age,
16.1 1.44 (SD) years]
11 patients [mean age,
19.9 3.45 (SD) years]
received the phosphate-
buffered saline (PBS)
0.05 ml/kg of 10 mM
The treatment group
showed a modest
oxygenation that was
thought to be
independent of the
physiological effects of
(27) CF 19 patients (6–19 years of
age) were randomized to
treatment [mean age,
13.3 4.1 (SD) years] or
placebo groups [mean age,
12.9 4.9 (SD) years]
Total daily dose
administered to the
patients in the
treatment group was
66 mg/kg of body
GSH can improve
clinical parameters in
CF patients, and that
should include the
correction of GSH
10 patients with IPF [mean
age, 46 3 (SD) years] and
19 normal nonsmokers
[mean age, 36 3
600 mg twice daily for
Inhaled GSH might be
beneficial among IPF
patients by reversing the
B: Nonrandomized con-
14 HIV seropositive
age, 32 2 (SD) years]
600 mg twice daily for
It is a reasonable
therapeutic strategy to
augment the deficient
GSH levels of the lower
respiratory tracts of
B: Cohort ‘outcomes’
(20) Chronic rhinitis 13 patients with chronic
rhinitis and 13 healthy
subjects (4–15 years of age
for all subjects; mean age,
600 mg daily for 14 days Statistically significant
improvement in nasal
and ear fullness.
(10) CF Seven CF patients [mean
age, 25 1 (SD) years]
600 mg of GSH for
Inhalation therapy with
GSH does normalize
balance in CF patients.
B: Cohort ‘outcomes’
(25) CF 21 patients with CF (16–37
years of age for all
300 or 450 mg three
times daily for 14 days
can permeate the lower
airways of the lungs
and improve important
parameters of lung
function in CF patients
despite not having any
effect upon markers of
B: Cohort ‘outcomes’
30 GSH in pulmonary diseases and respiratory-related conditions
[mean age, 42 1 (SD) year] were compared with 10 AF
[mean age, 43 1 (SD) year] serving as the control group.
All patients had baseline lung function testing and testing
at various time intervals following hay exposures. The
authors of this study concluded that FL and AF patients
have characteristically different intrapulmonary levels of
GSH, and that the pathogenesis of FL is likely related to
GSH regulatory mechanisms. They also speculated that
AF patients have a better ability to upregulate their
pulmonary GSH levels, which would protect them
against active disease. Clinical testing of inhaled GSH
in patients with FL is warranted.
The administration of GSH inhalation before and/or
immediately following exercise is another potential
application of this novel treatment. Exercise is a known
inducer of oxidative stress leading to free radical
production, which can encourage lipid peroxidation and
tissue damage among individuals with deficient and/or
impaired antioxidant systems. As stated in the beginning
of this report, selenium is a cofactor in the GPX enzyme
that protects cells from hydrogen peroxides and lipid
hydroperoxides. When under situations of oxidative
stress, the GPX enzyme will markedly increase in
the lungs as an antioxidant adaptive response (37).
By supplying more GSH to the lung tissues, more of
this enzyme might be available to help reduce the
production of free radicals associated with exercise.
Although these assumptions are very speculative, it does
seem possible and even logical that GSH inhalation
would benefit those who regularly exercise by increasing
exercise tolerance, and by maintaining and/or replenish-
ing the antioxidant systems within the lungs.
Multiple chemical sensitivity disorder (MCSD) is
another condition that might be clinically responsive to
this treatment. Patients with this disorder are known to
have bronchial hyperreactivity and even exhibit asthma-
like symptoms (38). Unlike asthma, MCSD is not
associated with atopy and immunoglobulin E (IgE)-
mediated allergic mechanisms (39). The prevailing theory
explaining the cause of MCSD is a fusion between two
separate theories—the neural sensitization and nitric
oxide/peroxynitrite theories (40). This fusion theory,
proposed by Pall, links long term potentiation of N-
methyl-d-aspartate (NMDA) receptors at the synapses of
nerve cells by glutamate and aspartate to an increased
production of nitric oxide and its oxidant product,
peroxynitrite (40,41). Treatment with antioxidants may
improve symptoms of MCSD by reducing the peroxy-
nitrite elevations and other biochemical dysfunctions that
are associated with such elevations (40,41). Glutathione
inhalation may be ideal since the primary route by which
patients with MCSD get triggered is through smelling
and breathing. Sulfite sensitivity would have to be
considered since inhaled GSH could provoke adverse
events. This treatment might be capable of providing
antioxidant protection to both the upper and lower
respiratory airways, which would theoretically help to
reduce the symptoms of MCSD and the production of
peroxynitrite. More research studies are necessary.
Two final conditions, cigarette smoking and lung
cancer, are worth mentioning since they are intimately
related to each other and are affected by GSH and its
related enzymes. These conditions are influenced by the
glutathione S-transferase (GST) group of enzymes that
are found in significant quantities in the bronchioles and
alveoli of the lungs (42), and in very high concentrations
in the bronchial epithelium (43). Among smokers, a lack
of the GST mu enzyme was thought to be associated with
a greater risk of lung cancer, especially if there was a
cancer and/or lung cancer history among the relatives of
the patients in this study (44). Since the GST mu enzyme
detoxify carcinogens in tobacco, any deficiency of this
enzyme was presumed to be associated with an increased
risk of lung cancer. However, a more recent study
pertaining to the GST group of enzymes found no such
association (45). In this meta-analysis, polymorphisms in
the GST genes had no associations or weakly positive
associations with risk factors for lung cancer. Despite the
Table 3. Continued
Reference Condition NDosages of inhaled
Outcome Evidence grade
(26) CF 17 patients with CF (18–29
years of age for all subjects;
mean age, 24 years)
450 mg three times daily
for 14 days
Inhaled GSH did not
affect the oxidative
status of the patients
who were tested, but it
did favorably modulate
their immune responses.
B: Cohort ‘outcomes’
(22) Emphysema One (95 year-old male) 120 mg of GSH in
office, then 120 mg
twice daily for 3 days,
of treatment (dose
unknown) for 2 years
When the patient
returned for a follow-up
visit, he no longer
required the use of his
wheelchair and oxygen.
The striking results
were unexpected and
unlikely to be due to
C: Case report
eCAM 2008;5(1) 31
need for more research, GSH inhalation might be
beneficial for smokers to augment their GST enzymes,
which would help facilitate the detoxification of carcino-
gens. Even though the best intervention for these patients
would be smoking cessation, many patients lack the
necessary willpower to quit. For these patients, regular
GSH inhalation might reduce oxidants generated from
cigarette smoke (10
free radicals/puff) (46), and the
epithelial lung injury associated with smoking (47).
For lung cancer patients, the use of GSH inhalation is
not recommended. Cancer cells use multiple mechanisms
(e.g. altered transport of a drug, inhibition of drug-
induced apoptosis and elevation of cellular GSH) to
circumvent the cytotoxic effects of chemotherapeutic
agents (48). Early research studies showed that GSH
was able to reduce cytotoxicity to chemotherapeutic
compounds by boosting the metabolism of drugs to less
active compounds, or by the detoxification of free
radicals (49,50). More recently, research has revealed
that the levels of a specific GST enzyme increases among
cancer cells with higher differentiation grades, and that
these drug-resistant gene products are found in lung
carcinomas at the time of surgical resection (51). There is
also speculation that GSH might be capable of repairing
drug-induced injury at the DNA level (48). A recent
review article has described the involvement of glu-
tathione in the detoxification or inactivation of platinum
drugs—the most commonly employed drugs for the
treatment of advanced stage lung cancer patients (52).
Based on this information, it would be unwise and
illogical to use GSH inhalation while lung cancer patients
are undergoing active chemotherapy treatment.
Mechanism of Action
Inhalation of GSH results in a mechanism of action
confined to the upper airways and lungs (Fig. 1), and will
not influence plasma levels to a significant degree. In the
studies that measured both lung and plasma levels of
GSH, the plasma levels remained essentially unchanged
following GSH inhalation. Seven of the studies included
in this review demonstrated that GSH inhalation
exerts its effects upon the lower respiratory tract
(9,10,19,24–27). The upper respiratory tract also appears
to benefit from GSH augmentation. Two studies invol-
ving patients with upper respiratory tract diseases showed
clinical benefits from GSH inhalation treatment (20,23).
The predominant mechanism responsible for GSH’s
therapeutic effects are probably related to its antioxidant
properties that offer protection against oxidative injury,
and/or assist with the normalization of the oxidant–
antioxidant balance within the upper and lower respira-
tory tract. Even though the majority of these studies
suggested that antioxidant protection was the principal
reason for the favorable treatment responses, some of the
studies were unable to demonstrate a change in markers
of oxidation from this treatment. More data is necessary
to confirm the precise nature of GSH’s antioxidant
properties within the upper and lower respiratory tract.
Additional explanations for GSH’s therapeutic effects
might include an improvement in host defenses (e.g.
increased cytotoxic lymphocytes), and better oxygenation
(e.g. an increase in oxygen saturation). GSH inhalation
produced clinically meaningful results in the majority of
diseases that were studied. Specifically, GSH inhalation
was shown to improve clinical markers of respiratory
function that inevitably impact upon quality of life and
disease progression. These improvements were the most
important outcomes and features of this novel treatment.
Considerations Prior to Initiating GSH Inhalation
The urine should be tested for sulfite sensitivity. A special
test strip can be dipped in the urine, and is known as the
‘EM-Quant 10013 Sulfite Test.’ It can be easily located
through any search engine on the Internet (53). Even
though instructions for sulfite testing have been published
elsewhere (54), a brief description of the procedure is
A random (fresh) urine sample is suitable, but a
first morning void may be preferable due to its
higher concentration. Once the test strip is
dipped in the urine (for 1 s), the reaction zone
changes color to indicate the concentration of
sulfites present. After 30 s, the color on the test
strip is compared to a color scale on the bottle
indicating the concentrations of sulfites in the
urine (can detect 10, 40, 80, 180 and 400 ppm of
sulfites). The resultant concentration should be
multiplied by a factor of 1.5 to provide the
amount of free sulfites in mg/l (ppm). The strip
will not detect below 10 ppm. The urine samples
should be preservative free, and the urinary pH
should also be tested with pH paper. If the urine
pH is below 6, then the amount of sulfites might
be underestimated by the test. In such cases,
consider adding sodium acetate or sodium
hydroxide to raise the pH to at least 7–10
(should not exceed a pH of 12), and then repeat
with a new test strip.
If the urine test were positive for sulfites (normally they
are absent), the use of inhaled GSH would be strictly
Method of Delivery, Recommended Daily Dosages
and Side Effects
With a nebulizer, a solution of GSH is made into an
aerosol and is delivered to the upper respiratory tract
and the lungs through a mask that covers the nose
and mouth, or is delivered directly into the lungs via
a mouthpiece. Any compounding pharmacist would be
32 GSH in pulmonary diseases and respiratory-related conditions
able to prepare the solution of GSH at the desired
concentrations. The typical dosages used in the
studies cited in Table 3 were 600 mg once daily, 600 mg
twice daily, 900 mg daily, 1350 mg daily or a daily dose of
66 mg/kg of body weight. Better results are more likely to
be achieved with doses of at least 600 mg or more each
day. One of the studies used much larger doses (66 mg/kg
of body weight) since the authors speculated that these
would be necessary to replace half of the amount of GSH
that is produced each day (e.g. a 150 lb male synthesizes
10 g daily and would need 5 g as a replacement dose) (27).
When patients are unresponsive to doses in the range of
600–1350 mg per day, it might be suitable to try doses
that would replace half the estimated amount of GSH
that is synthesized each day. These gram doses might
yield better clinical results.
In terms of side effects, GSH inhalation is very safe.
Minor side effects such as mild coughing and an
unpleasant odor were reported in some of the studies
included in this review. These minor side effects, better
described as mild nuisance problems, were not severe
enough to cause any of the study participants to
discontinue treatment with inhaled GSH. The only
worrisome or potentially life-threatening side effect to
note is bronchoconstriction, which would be more likely
to occur among sulfite-sensitive asthma and MCSD
patients. However, if proper precautions such as sulfite
testing are done prior to treatment, this serious side effect
should be avoidable.
Monitoring the Clinical Response to Inhaled GSH
For pulmonary diseases or respiratory-related conditions,
baseline pulmonary function testing with a spirometer or
a simple peak flow meter is recommended prior to the
Increases GSH concentrations
Increases antioxidant production
Decreases oxidant-induced damage
Increases host immune responses
(i.e. increases cytotoxic lymphocytes)
Increases oxygen saturation
Reduces ear fullness, nasal
obstruction and rhinorrhea
Improves pulmonary function
(i.e. increases FEV1 and FVC)
Figure 1. Inhaled GSH’s mechanism of action. GSH, reduced glutathione; FEV
, forced expiratory volume in 1 s; FVC, forced vital capacity.
eCAM 2008;5(1) 33
first treatment. After a prescribed period of treatment
time, pulmonary function tests should be repeated. This
will help to establish if there are any clinical improve-
ments from regular GSH inhalation.
GSH inhalation is an effective treatment for a variety of
pulmonary diseases and respiratory-related conditions.
Even very serious and difficult-to-treat diseases (e.g., CF,
IPF) yielded benefits from this novel treatment. GSH
inhalation is very safe, and rarely causes major or life-
threatening side effects. The potential applications are
numerous when one considers just how many pulmonary
diseases and respiratory-related conditions are affected by
deficient antioxidant status, poor oxygenation and/or
impaired host defenses. More studies are clearly
The author would like to thank Mr Glen Carr and Mr
Andrew Dick for their wonderful illustration of GSH’s
mechanism of action.
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Received December 22, 2006; accepted February 13, 2007
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