Could Sulfur Gases Prevent Respiratory Infections?

[mixin]

While going through PubMed archives, I found this letter written in 1919. The writer had seen a previous article about mine workers and below are some of his comments. I'm not sure what sulfo-cyanines are or how they differ from fumes.
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The reverberatory process of copper smelting was almost solely employed at Swansea, and the atmosphere seemed little else than sulphur fumes at times. I was constantly told that consumption was practically unknown amongst the copper smelters. I naturally at first attributed this, like everybody else then, to the SO2, etc., in the air.

At Dowlais, the old opentopped iron blast furnaces were still in use. Here I was told that the men charging the furnaces-at the top frequently got consumption, but not those at the bottom, engaged in tapping the furnaces. They worked in fumes. These were not sulphur fumes, but they contained sulpho-cyanides, and as these would have been present at the copper works also.

It occurred to me then-and still does-that possibly in the use of sulpho-cyanides there may be found at least a partial cure for plhthisis.-

http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=2341007&blobtype=pdf

 

[mixin]

Re: Could Sulfur Gases Prevent Respiratory Infections?

Here is the article the letter above was addressing:
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For many years it has been an accepted fact among
men working in gaseous fumes that they are practically
immune from nasal catarrah and respiratory diseases in
general.

Further, in some parts of the country it is the
custom to take children suffering from whooping-cough to
the nearest gasworks and expose them to the fumes
emnanating from the oxide of iron purifiers during the
process of cleansing, and the parents of these children
firmly believe that by doing so the attack is much
mitigated.

Table 1 incidence of flu between Navy (1350), Army(1050) and Gas workers (148):
July: Navy 23%, Army 9.5%, Gas workers 3.3%
Autumn: Navy 9.2%, Army 10.4%, Gas workers 3.3%

Table 2 Cordite workers verusu non-cordite workers
Not working in fumes: 30.1% got the flu
Working in fumes full time, part time and in acetone: 4.7%

Tin workers during the fall wave:
In the fumes: 11.1%
Underground workers: 60.8%

The burning--house of this mine lies in a valley, and
there are seven cottages, all situated within two hundred
yards of the stack from which the SO2 fumes are discharged.
Under certain atmospheric conditions the fumes
lie heavily on these houses. They have twenty-seven
inhabitants, and only one case of "influenza" occurred
among them, and he was one of the underground workers
in the mine.

A small village lies about a quarter of a
mile distant and quite outside the radius of the fumes.
Here the cases were numerous.
http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=2340878&blobtype=pdf

 

[gsgs]

Re: Could Sulfur Gases Prevent Respiratory Infections?

I searched a bit on pubmed:


http://www.ncbi.nlm.nih.gov/pubmed/...nel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum

Research findings indicated that residents had respiratory tract-related problems, suspected to be linked to the effects of air pollution caused by the emission of sulphur dioxide (SO2) from mining and smelting activities.

No clearly demarcating differences were noticed in the health status of residents living in the control site from those in the main study area. However, sites most affected were those close to where Ni-Cu is exploited. Environmental factors resulting from mining and smelting activities, among others, could be contributory to the negative health effects occurring at Selebi Phikwe.


http://www.ncbi.nlm.nih.gov/pubmed/...nel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
The results suggest an adverse effect of air pollution on consultations for upper respiratory symptoms, in particular in the case of PM(10) and SO(2). The effects are relatively small


http://www.ncbi.nlm.nih.gov/pubmed/...nel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
No effect was found [in Rome] for particulate matter and SO2

http://ije.oxfordjournals.org/cgi/content/full/29/2/271
The correlation coefficients are low

http://www.ncbi.nlm.nih.gov/pubmed/...nel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
Relative risk (RR) for admissions for respiratory disease for the four pollutants ranged from 1.013 (for SO2) to 1.022 (for O3),


INFLUENZA-INFECTED MICE EXPOSED TO SULFUR DIOXIDE DEVELOPED MORE PNEUMONIA THAN VIRUS CONTROLLED MICE.

chlorine:
http://www.inchem.org/documents/ehc/ehc/ehc21.htm
Vedder & Sawyer (1924)
reported that chlorine inhalations were used in 1915 in Germany, to
clear meningococcus and diphtheria carriers, and in 1918 in the
USA as a treatment for influenza. They conducted a series of
studies based on clinical observations that workers at a war gas
production plant did not suffer from influenza during the great
epidemic.

The therapeutic effects of chlorine were further discussed by
Gilchrist (1924). During World War I, medical officers assigned to
the front lines observed an apparent immunity to influenza in their
troops.

Following these observations and the work of Vedder &
Sawyer, Gilchrist constructed an inhalation chamber and treated
some 900 patients with chlorine. Those with infectious diseases
tended to show improvement; those with asthma or hay fever did not.


While the results of these controlled therapeutic inhalations
appear dramatic, the studies of both Vedder & Sawyer and Gilchrist
were conducted without unexposed comparison groups. In Gilchrist's
study, no attempt was made to document disease at the onset or to
evaluate its evolution medically. The patients came with their own
diagnosis and reported the outcome.

Though these studies reflect an interesting and historical
hypothesis for the medical application of chlorine, experience has
not provided justification for its practical use in this context.


NO2:
http://www.erj.ersjournals.com/cgi/reprint/8/6/976.pdf

 

[mixin]

Re: Could Sulfur Gases Prevent Respiratory Infections?

It's possible in the 1919 observations, there weren't enough gas workers to get an accurate result.

I wonder how much the furnaces have changed over the years?

men charging the furnaces-at the top frequently got consumption, but not those at the bottom, engaged in tapping the furnaces.

From your first link, a 2005 study:

Residents were frequently in contact with SO2 and related gases and fumes, mineral and silica dust generated from the mining processes.

Silica dust is really bad:

What is silica dust?
Silica is the main component in sand and in rocks like sandstone and granite. Many workplaces are not aware that common building products such as clay bricks, concrete, tiles and fibro cement products contain silica. Silica dust is usually created when such building products, sandstone or rocks are cut, drilled or worked on in a way that creates fine particles of silica in the air. It is breathing in this crystalline form of silica that causes silicosis.
http://www.workershealth.com.au/facts060.html

Did this come from the Inchem link? INFLUENZA-INFECTED MICE EXPOSED TO SULFUR DIOXIDE DEVELOPED MORE PNEUMONIA THAN VIRUS CONTROLLED MICE. (I had a difficult time reading through all those awful animal experiments.)

Your last link is 20 pages .pdf

 

[gsgs]

Re: Could Sulfur Gases Prevent Respiratory Infections?

http://www.ncbi.nlm.nih.gov/pubmed/189703
Ozone inhalation caused pronounced inhibition of influenza virus growth in mousenoses
sulfur dioxide (6 ppm for 7 days) caused partial inhibition
Neither gas altered the propagation of influenza in the lungs
The inhibitory effect of ozone and sulfur dioxide on influenza virus growth in nasal epithelium
suggests a competitive interaction between the chemical inhalant, the virus, and host tissues,
http://aem.asm.org/cgi/reprint/44/3/723.pdf

http://www.sciencedirect.com/scienc...serid=10&md5=c6e66789d6c38c5ca698d3aaec498188
mice were exposed to influenza and sulfur dioxide,alone and in combination.
Temperature, relative humidity and length of exposure were all controlled.
Virus exposure produced pneumonia even at low dose.
Sulfur dioxide produced pneumonia at higher doses, but appeared to have an
inverse effect at lower doses
The two combined produced more pneumonia than either one did separately.
Sulfur dioxide produced more weight reduction than influenza virus,
and combination exposures produced more weight reduction than either
stimulus did separately.


http://www.netl.doe.gov/technologie...ty_research/health_effects/pdfs/AppendixB.pdf

virus shedding. It has been suggested
that mechanisms of asthmatic sensitivity
may be associated with a wild-type allele
of the TNF-alpha promoter
polymorphism or may involve mast cell
degranulation.

Non-Clinical Studies
Increased mortality and decreased
survival time was observed in a group of
female mice with respiratory infection
exposed to 10 ppm for up to 3 weeks
compared to non-exposed controls. Mice
exposed to 0.03 to 0.1 ppm and an
influenza virus developed antibodies to
the virus more rapidly than mice
exposed to the virus alone. The study
authors postulate from this that SO2
alters nasal mucus membranes thereby
decreasing a defensive barrier to disease
and resulting in increased severity of
influenza infection. However, another
study reported that exposure to 6 ppm
for 7 days resulted in partial inhibition of
influenza virus growth in the nasal
epithelium and no propagation in the
lungs. Studies on guinea pigs suggested
that exposure to low levels of SO2 (1
ppm) might enhance the development of
ovalbumin-induced asthmatic reactions
and reported a significant increase in
ovalbumin-specific antibodies in serum
and bronchoalveolar fluid with exposure
to 0.1 to 16.6 ppm for 8 hours/day for 5
days. A study on mice exposed to 250
ppm for 3 hours reported an increased
uptake of iron in airway epithelium. The
clinical significance of many of these
studies is unclear and not discussed in
the studies themselves.


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Giddens and Fairchild (1972) exposed
mice to 10 ppm SO2 for 4 to 72 hours to
observe the effect of SO2 exposure on
the nasal and respiratory tracts. Lesions
consisting of edema, necrosis, and
desquamation of the olfactory and
respiratory epithelium were observed at
24-hour and longer exposures. More
injury was observed in the nasomaxillary
turbinates than in the rest of the
respiratory tract (Study ID .. 191).
Ukai (1977) investigated the effect of
SO2 exposure (0.03 to 0.1 ppm for 4
weeks) on upper respiratory infection
response in mice inoculated with
influenza virus. More rapid and more
severe inflammatory response, as well as
more rapid development and higher
levels of HI titer were observed in the
SO2-exposed mice (Study ID .. 207).
Fairchild (1977) observed an inhibition
in the growth of influenza virus in the
noses of mice exposed to 6 ppm of SO2
for 7 days. Virus propagation was not
altered (Study ID .. 238).
Hanacek (1987) investigated the effect
of SO2 on cough and expiratory reflexes
of 22 anaesthetized rabbits. Exposure to
200-300 ppm SO2 for 10-15 minutes
resulted in decreases in both
mechanically stimulated cough
excitability and cough reflex strength in
rabbits. Reporting of the experimental
methods and results lack detail (Study
ID ..300).

------------------------------------------------


Fairchild et al. (1972) investigated the
effect of exposure to SO2 on influenzal
pneumonia in mice. Mice were exposed
to concentrations ranging between 3.4
and 34.5 ppm continuously for up to 7
days. When SO2 was administered after
virus exposure, significantly increased
incidence of pneumonia was observed at
19 ppm and greater. When the virus was
administered after SO2 exposure, a
significant increase in pneumonia
incidence occurred only at 25 ppm after
4 to 7 days of exposure.
Histopathological effects were observed
at SO2 concentrations of 27 ppm and
greater after 7 days of continuous
exposure (Study ID .. 182).

------------------------------------------

Ukai (1977) investigated the effect of
exposure to low levels (0.03 to 0.1 ppm)
of SO2 on the pathogenesis of influenza
virus infection in mice. In mice exposed
to both SO2 and the virus, antibodies to
the virus developed more rapidly than in
those mice exposed to virus alone. In
addition, mice exposed to SO2 but not
the virus showed an increase in the
number of goblet cells in nasal epithelial
cells. These observations suggest that
SO2 alters the nasal mucus membranes,
eliminating a major defensive barrier
against disease and subsequently
resulting in increased severity of
influenza infection (Study ID .. 207).
Fairchild (1977) investigated the effects
of SO2 on the growth of influenza virus
in the nasal epithelia of mice. Exposure
to 6 ppm SO2 for 7 days caused partial
inhibition of influenza virus growth in
the nasal epithelium and no propagation
in the lungs (Study ID .. 238).

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Increased mortality and decreased
survival time was observed in a group of
female mice with respiratory infection
exposed to 10 ppm for up to 3 weeks
compared to non-exposed controls. Mice
exposed to 0.03 to 0.1 ppm and an
influenza virus developed antibodies to
the virus more rapidly than mice
exposed to the virus alone. The literature
suggests that SO2 alters nasal mucus
membranes thereby decreasing a
defensive barrier to disease and
resulting in increased severity of
influenza infection. However, another
study reported that exposure to 6 ppm
for 7 days caused partial inhibition of
influenza virus growth in the nasal
epithelium and no propagation in the
lungs. Studies on guinea pigs suggested

-----------------------------------------------

Fairchild,G., J.Roan, and J.McCarroll. 1972. Atmospheric pollutants and the
pathogenesis of viral respiratory infection: sulfur dioxide and influenza infection.
Archives of Environmental Health 25:174-182.
Ref ID: 182

Fairchild,G. 1977. Effects of ozone and sulfur dioxide on virus growth in mice. Archives
of Environmental Health 32:28-33.
Ref ID: 238

---------------------------------------
Table 3D ? ?Positive? Respiratory Effects Associated With Short-term Exposure to
SO2: Animal Toxicology Studies ? Greater Than 7 Day Exposures


Concentration
ppm
(mg/m3)
Effects Exposure
Duration
0.03 (0.08) ..More rapid and more severe inflammatory response to influenza infection (to 0.1
ppm; Mice)207
4 weeks
10 (26) ..Increased concentrations of cholesterol, total lipids, gangliosides and decreased
phospholipids (Guinea pigs)163
1 hr/d x 30d
100 (262) ..Decreased glutathione concentration and inflammation (Rats)251 5hr/d, 7 to 28d
150 (393) ..Increased lung resistance, decreased breathing frequency (Rabbits)239 12 x 3hr
600 (1573) ..Increase in solid material recovered by bronchial lavage (Rats)250 3 hr/d for 9,18,
or 30 d

---------------------------------------------

Table 6. Respiratory Health Effects Associated with Short-term Exposure to SO2
Summary of ?Positive? Findings: Clinical and Non-clinical studies


Concentration
(ppm)
Effects
0.03 ..More rapid and more severe inflammatory response to influenza infection (to 0.1 ppm; Mice)207


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0.1 ..Increased respiratory pause (Guinea pigs)259
..Slight reduction in FEV1, Vmax 50 (AC)277
..Bronchoconstriction at lower concentrations in dry air than humidified air (HA)057
..Slight reduction in lung clearance (Rats)235
..Increased antigen-specific antibodies in serum and bronchoalveolar fluid (Guinea pigs)133
0.15 ..Decreased specific a

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..Increased frequencies of polychromatic erythrocyte formation (Mice)380
6 ..Inhibition of influenza virus growth in mice exposed for 7 days238

-----------------------------------------------

Study ID Reference SO2
Concentration
Time Species/Population
Group
Effect
..207 Ukai, 1977 0.03 to 0.1 ppm 4 wk Mice More rapid and more severe
inflammatory response to influenza
infection
..238 Fairchild, 1977 6 ppm 7 d Mice Inhibition of virus growth
..300 Hanacek, 1987 200-300 ppm 10-15 min Rabb

----------------------------------------------------

..238 Fairchild, 1977 6 ppm 7 d Mice Inhibition of influenza virus growth
..134 Trimpe et al., 1986 27 ppm Not clear Hamsters No difference in bacterial clearance
rates
..259 Park et al., 2001 0.1 ppm 5 hr/d, 5 d Guinea pigs Enhanced ovalbumin-induced
asthmatic reactions
..133 Riedel et al., 1988 0.1 to 16.6 ppm 8 hr/d, 5 d Guinea pigs Increased ovalbumin-specific
antibodies and bronchoalveolar fluid
..201 Gause and
Rowlands, 1975
Unclear Not reported Human lymphocyte
membranes

-------------------------------------------------------------

More rapid and more severe
inflammatory response to influenza
infection (to 0.1 ppm; Mice)207
(4 weeks)

 

[mixin]

Re: Could Sulfur Gases Prevent Respiratory Infections?

That was a lot of studies; thanks.

I thought this one you posted was a good one:
Exposure to Ozone Reduces Influenza Disease Severity and Alters Distribution of Influenza Viral Antigens in Murine Lungs

There were 4 groups of 100 mice each
Groups A and B were exposed to 0.5 ppm ozone and
groups C and D were exposed to filtered air for a 2-week period.
All mice were then infected with influenza virus by aerosol.
Half of the ozone-adapted animals remained in an ozone environment for a 2-week period
half were moved to filtered air for 2 weeks.
Half of the filtered-air-adapted animals were moved into ozone.
half continued in a filtered-air environment for a 2-week period to serve as the infected control group.

Mortality
* Exposure to ozone after infection significantly reduced influenza virus mortality
* Animals moved from ozone into filtered air after infection showed variable mortality in two experiments.
* Exposure to ozone after infection also resulted in a significant increase in mean survival time when compared with survival time in the infected control group D.
* There was no effect on mean survival time in ozone-adapted animals movedinto filtered air after infection in either of two experiments.

Discussion:
* Reduction of disease severity appeared to be dependent on the continuedpresence of ozone during the infectious process rather than on the atmosphere before infection.
* mice exposed to ozone showed a significant alteration in the distribution of viral antigens within the pulmonary tissues, resulting in a less widespread infection of the lung.
* The striking difference early in infection in animals continuously exposed to ozone was a virtual absence of viral antigens from the respiratory epithelium.
* The removal of ozone from the airways by transfer of ozone-adapted animals to filtered air resulted in the appearance of viral antigens within the epithelium as early as 2 days postinfection
* no increase in infection of airways occured when animals were newly exposed to ozone after infection.
* These observations suggest that the presence of ozone within the airway
results in inactivation of virus infectivity in vivo.

Our recent in vitro studies have shown that enveloped viruses such as influenza can be readily inactivated within a short period by exposure to levels of ozone comparable to that employed in this experiment.

These pulmonary changes may result in airway lining which is more resistant to infection by influenza virus.

 

[gsgs]

Re: Could Sulfur Gases Prevent Respiratory Infections?

OK, so test it in ferrets,humans.

is ozone toxic in that concentration ?

would it be easy and cheap to use it ?

is there fewer influenza in countries/towns with high ozone level
during flu-season ?


test also also ClO2