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Does E-cigs or PG cause emphysema?

Discussion in 'Health, Safety and Vaping' started by mothakaf, Feb 14, 2009.

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  1. mothakaf

    mothakaf Full Member

    Dec 25, 2008
    Does E-cigs or PG cause emphysema? Is there is a scientific evidence on that?
  2. surbitonPete

    surbitonPete Ultra Member ECF Veteran

    Jan 25, 2009
    North Yorkshire UK
    If any of us thought that we wouldn't be doing it.
  3. Stylopora

    Stylopora Full Member ECF Veteran

    Jan 29, 2009
    Cambridgeshire UK
    Cellular and Connective Tissue Changes in Alveolar Septal Walls in Emphysema

    Duke University Medical Center, Durham, North Carolina; National Institute of Occupational Safety and Health, Morgantown, West Virginia; and National Jewish Medical and Research Center, Denver, Colorado


    Emphysema is commonly defined as enlargement of airspaces distal to terminal bronchioles accompanied by destruction of alveolar walls, but without obvious fibrosis. Morphometric techniques were used to correlate changes in components of the alveolar septa surrounding enlarged airspaces in human emphysema with the mean linear intercept (Lm) of those airspaces. Alveolar and capillary surface density decreased with increased Lm, but the ratio of these surface densities to each other remained close to normal for mild to moderate increases in Lm. This suggests that the decreased gas exchange observed in emphysema is initiated by a total loss of septa and not by selective pathological changes of the microvasculature. Increases in septal wall thickness directly correlated with increases in Lm. For the mild to moderate emphysema lesions included in this study, an increase of 100% in Lm correlated with a 130% increase in the relative volume of the alveolar septal interstitium. Significant increases occurred in both elastin (0.14 to 0.56 µm3/µm2 basement membrane [BM]) and collagen (0.49 to 1.63 µm3/µm2 BM). The increase in elastin and collagen raises the possibility of a remodeling process in the connective matrix in alveolar walls. Whether or not the new connective tissue represents a disordered, nonfunctional regional response needs to be determined. Vlahovic G, Russell ML, Mercer RR, Crapo JD. Cellular and connective tissue changes in alveolar septal walls in emphysema.

    Emphysema is characterized by abnormal enlargement of the respiratory regions of the lung distal to terminal bronchioles, accompanied by destruction of the walls, and with loss of tissue per unit volume (1). There are two major forms of emphysema: panacinar and centroacinar emphysema (1). Panacinar emphysema involves airspace enlargement throughout the acinus and is thought to commonly arise as a result of a deficiency in synthesis or secretion of 1-proteinase inhibitor (1-PI). The most frequently observed form of emphysema, centroacinar emphysema, develops in the central portions of the acinus in close proximity to respiratory bronchioles and is predominantly associated with prolonged exposure to cigarette smoke (5). The pathogenesis of emphysema is still unknown: the most accepted hypothesis is based on an imbalance in proteases and antiproteases. That hypothesis is that tissue injury results from the actions of excess proteolytic enzymes liberated from inflammatory cells such as neutrophils and monocytes (8).

    The role of cigarette smoking in the formation of emphysema is partly explained by recruitment of polymorphonuclear leukocytes and monocytes in the lower respiratory tract either as a consequence of epithelial injury caused by smoke or as a response to chemicals in smoke (5). The targets of proteolytic enzymes and free radicals liberated from polymorphonuclear leukocytes and monocytes are collagen, elastin, proteoglycans, and 1-PI, respectively. Damage to the proteolytic enzyme inhibitor accelerates and augments development of emphysema.

    Lung changes characterizing emphysema have been studied in both humans and animals via different methodologies (9, 11). Most of the findings in these studies suggest that connective tissue, especially elastin, is a major target of destruction in emphysema. The architectural rearrangement and loss of gas exchange surface caused by elastin degradation in emphysema is generally thought to be irreversible. Animal models of emphysema have been created by intratracheal administration of pancreatic elastase, and these models demonstrate synthesis of new elastin (12). The enhanced deposition of elastin in these models has been used as a basis to challenge the relevance of these animal models to human emphysema. It is not known how the development of emphysema in humans correlates with specific structural changes of the lung parenchyma, such as whether or not destruction of the vascular bed is an early event and whether or not early interstitial changes involve production or loss of either of the primary connective tissue elements, collagen and elastin.

    The goal of this study was to investigate structural changes of the walls of enlarged airspaces occurring in areas of mild and moderate human emphysema to determine if enhanced deposition or degradation of connective tissue occurs. Morphometric techniques combining light and electron microscopy were used to quantify changes in interstitial elastin and collagen, interstitial inflammatory cells, endothelial cells, and alveolar epithelial cells in areas of mild to moderate emphysema. This comparison of structural changes in lung tissue from areas of airspace enlargement to the structure of normal lung demonstrates that specific connective tissue changes are part of the early pathological events in emphysema.
  4. Stylopora

    Stylopora Full Member ECF Veteran

    Jan 29, 2009
    Cambridgeshire UK
    Many studies have demonstrated that degradation of elastin plays a key role in the initiation of emphysema (9, 25), although the loss of complete alveolar septal walls as a coordinated event raises questions as to whether or not elastin is the major target of destruction. The pathogenesis of emphysema involves a variety of events, including free radicals, activation of inflammation (polymorphonuclear and monocyte recruitment), and a variety of cellular derived mediators or cytokines all of which cumulatively lead to proteinase inhibitor inactivation, membrane lipid oxidation, and proteinase liberation (26). Focal lung injury, also a characteristic of emphysema, can be explained by the inhomogeneous distribution of cigarette smoke components (the major cause of acquired emphysema), antiproteinase inhibitors, antioxidants, and cellular derived oxidants in the lung (26).

    The progressive loss of complete portions of the alveolar septa during the formation of emphysema suggests that gas exchange in the early stages of emphysema primarily decreases due to the loss of entire segments of alveolar septa, and not to a selective loss of the alveolar microvasculature. The ratio of capillary to alveolar surface in the septal tissue of mild and moderate emphysematous lesions remains normal. The volume of endothelial cells per unit alveolar surface in these areas compared with nearby healthy areas of human lung also remained unchanged. Thickening of the interstitium could lead to a partial diffusion block for gas exchange; however, the magnitude of the interstitial changes is not sufficient for the diffusion block to be functionally significant in comparison to the effects of the loss of entire alveolar septal segments.

    In animal models of emphysema, repair has been shown to occur after acute injury to the lung (9, 11, 12). For instance, Mercer described gaps in elastin fibers of two hamster alveolar septal walls that occurred as a result of elastin destruction after exposure of the animals to a single dose of pancreatic elastase (12). He also illustrated enhanced deposition of elastin fibers during repair of the injured areas. This study supports the hypothesis that tissue repair and remodeling are a critical component of the process leading to emphysematous lesions. It is likely that following periods of intense elastolysis there are periods of repair in which elastin is remodeled perhaps in a disordered state and thus contributing to the loss of elastic recoil in the function of emphysematous lungs. Alternatively, phases of remission and repair, with fewer neutrophils present and macrophages predominating, could be the most common pathological expression of early phases of emphysema.

    The results of the current study show a significant correlation between degree of emphysema and the thickness of interstitium in the remaining alveolar septal walls. Substantially enhanced numbers of neutrophils were not found in the tissues studied. The lack of neutrophils could be due to the fact that the tissue was obtained from patients who underwent surgery, and presurgical therapy or abstention from smoking could have reduced the frequency of acute inflammation. Two primary connective tissue components, elastin and collagen, were found to be increased in relative volume in areas of emphysema. An increase in elastin- and collagen-producing cells is also an important indicator of tissue modeling or repair (12, 27). In the current study, interstitial fibroblasts were consistently found in close proximity to areas of elastin (Figure 6) and collagen in the alveolar interstitium of diseased areas. Quite often the long processes of interstitial fibroblasts enveloped adjacent connective tissue elements. In vitro studies have demonstrated potential mechanisms for a direct repair process. Cultured pulmonary fibroblasts derived from neonatal rats demonstrate an increase in tropoelastin messenger RNA (mRNA) and elastin synthesis after the cells are exposed to elastase and elastase-solubilized extracellular matrix peptides. In cultured fibroblasts incubated with matrix peptides but not treated with elastase, a significant reduction of tropoelastin mRNA and elastin synthesis occurred (28). This suggests that elastin synthesis occurs at the sites where both elastase and injured extracellular matrix elements are present. On the basis of these studies, elastin synthesis would be expected to occur in the very areas where elastolysis initiates an emphysematous-like lesion. The current report of a significant correlation between enhanced elastin and collagen deposition and the local degree of emphysema illustrates this concept of remodeling, although possibly disordered, as a possible step in the creation of the emphysematous lesion.

    The early stages of emphysema included in the present study were primarily characterized by the presence of macrophages rather than neutrophils. Mononuclear phagocytes usually accumulate in large numbers in the lung in response to cigarette smoking (1, 6). In this study they were found to be significantly increased in emphysematous lesions. It is believed that macrophages play a role in the pathogenesis of the alveolar septal injury that characterizes pulmonary emphysema, and that they may be important especially in the pathogenesis of chronic tissue destruction (10, 29). Their significance as a source of proteolytic enzymes and in the release of proteinase inhibitors is still questionable. It has been suggested that macrophages have elastolytic ability owing to liberation of the elastolytic enzymes metalloelastase and cathepsin L (28). Cathepsin L is significantly elevated and its mRNA highly expressed in alveolar marcrophages obtained from bronchalveolar lavage fluid from smokers compared with nonsmokers. This supports the concept that alveolar macrophages contribute to the proteolysis of elastin as part of the process of lung destruction associated with cigarette smoking.

    This study shows that the walls of emphysematous lesions contain increased amounts of elastin and collagen which is consistent with either loss of interalveolar septal walls normally low in connective tissue or enhanced synthesis of elastin and collagen in emphysematous areasor that both processes are occurring. An increase in synthesis of elastin and collagen would suggest a repair process but does not necessarily indicate functionality. Whether newly synthesized connective tissue in emphysema undergoes the full process of maturation to normal connective tissue that is able to perform its functional role or represents a disordered nonfunctional regional response needs to be determined.
  5. taz3cat

    taz3cat Ultra Member ECF Veteran

    Nov 2, 2008
    Port Arthur, Texas
    You can get emphysema from breathing desert sand during a sand storm. I know some older folks that never smoked in their lives and they have emphysema. You can't live forever, I don't care what people say. Take a chance enjoy life,
  6. Krakkan

    Krakkan Unregistered Supplier ECF Veteran

    Feb 22, 2009
    New Orleans, LA
    Bases on this article from 1942 PG can actually help kill harmful bacteria in the air wouldn't that be crazy to think our second hand vapors might actually be helpful? lol


    O. H. Robertson M.D.1, Edward Bigg M.D.1, Theodore T. Puck Ph.D.1, Benjamin F. Miller M.D.1, and With the Technical Assistance of Elizabeth A. Appell
    [SIZE=-1] 1 From the Department of Medicine, the Douglas Smith Foundation for Medical Research, the Bartlett Memorial Fund, and the Zoller Memorial Dental Clinic of the University of Chicago, Chicago

    It has been found that propylene glycol vapor dispersed into the air of an enclosed space produces a marked and rapid bactericidal effect on microorganisms introduced into such an atmosphere in droplet form. Concentrations of 1 gm. of propylene glycol vapor in two to four million cc. of air produced immediate and complete sterilization of air into which pneumococci, streptococci, staphylococci, H. influenzae, and other microorganisms as well as influenza virus had been sprayed. With lesser concentrations of propylene glycol, rapid and marked reduction in the number of air-borne bacteria occurred, but complete sterilization of the air required a certain interval of time. Pronounced effects on both pneumococci and hemolytic streptococci were observed when concentrations as low as 1 gm. of glycol to fifty million cc. of air were employed.
    Numerous control tests showed that failure of the glycol-treated microorganisms to grow on the agar plates was due to actual death of the bacteria. The means by which propylene glycol vapor produces its effect on droplet-borne bacteria is discussed and data relating the bactericidal properties of propylene glycol in vitro to the lethal action of its vapor is presented.
    Atmospheres containing propylene glycol vapor are invisible, odorless, and non-irritating. This glycol is essentially non-toxic when given orally and intravenously. Tests on possible deleterious effects of breathing propylene glycol containing atmospheres over long periods of time are being carried out.

    [SIZE=+2] [/SIZE]
  7. Stylopora

    Stylopora Full Member ECF Veteran

    Jan 29, 2009
    Cambridgeshire UK
    (From the Department of Medicine, the Douglas Smith Foundation for Medical Research,
    the Bartlett Memorial Fund, and the Zoller Memorial Dental Clinic of the
    University of Chicago, Chicago)
    PLATES 18 Am) 19
    (Received for publication, February 27, 1942)
    The idea of employing bactericidal mists as a method for controlling airborne
    respiratory infection is not new, but until recently no one had succeeded
    in producing by such means a sterile or relatively bacteria-free atmosphere
    which could be tolerated by human beings. During the past few years new
    methods of chemical air sterilization have been devised. These consist in the
    dispersal of germicidal mists containing the effective chemical agents in such
    small amounts as to be non-detectable or at least unobjectionable to persons in
    the treated atmosphere. The compounds employed for this purpose are
    believed to be non-toxic in the minute amounts present in the inspired air.
    The initial report on this new approach to the control of air contamination was
    made by Douglas, Hill, and Smith (1) in 1928. By means of a very fine spray of
    electrolyzed sea water, containing NaOC1 with about 1 per cent available chlorine,
    these workers were able to effect a marked or complete killing of Bacillus coli dispersed
    in the air. The material appeared to be non-irritating in the concentration employedj
    which was approximately 1 gin. of the chemical solution in two million cc. of air.
    This paper apparently attracted little attention and it was not until 10 years later
    that active development of the subject began.
    In 1938 two publications appeared, one by Trillat (2) concerning the properties of
    germicidal aerosols, and the other by Masterman (3) on air sterilization by spraying
    or atomizing hypochlorite solutions. TriUat's earlier investigation, covering a period
    of many years, dealt with problems of droplet infection and the various properties of
    aerosols, and culminated in his discovery of the sterilizing properties of germicidal
    aerosols. 1 Trillat found that certain germicidal agents which killed bacteria in the
    test tube in dilutions not higher than 1:200, were capable of musing death of airborne
    bacteria when dispersed in aerosol form in concentrations of 1 gm. of the chemical
    substance in 5,000,000 cc. of air. He believed that this bactericidal activity was
    due to direct interaction between the aerosol droplets and the bacterial particles.
    Liquid aerosols consist of droplets 1 to 2~ in diameter, dispersed in air. An
    erroneous use of the term aerosol has been introduced by commercial concerns who
    have applied it as a trade name to certain wetting and detergent compounds.
    Downloaded from jem.rupress.org on February 23, 2009
    Published June 1, 1942
    Trillat tested a number of common bactericidal compounds and found that of these
    only resorcinol and sodium hypochlorite were satisfactory. The other compounds
    were either inactive as aerosols or too toxic, or proved to be irritating or unpleasant.
    He states that resorcinol is the agent of choice as the odor of hypochlorite becomes
    disagreeable after a time.
    Masterman presents evidence for the germicidal effect of fine mists of sodium
    hypochlorite. He found that 1 gin. of 1 per cent NaOC1 atomized in as large a volume
    as forty million cc. of air would produce sterilization. Masterman concludes that
    this marked bactericidal action is due to the HOC1 gas liberated from the mist and
    not to an aerosol effect (3, 4).
    During 1939 and 1940, two groups of workers in England, Pulvertaft and Walker
    (5), and Two,t, Baker, Finn, and Powell (6), confirmed and extended Trillat's and
    Masterman's observations. Pulvertaft and Walker tested various substances for
    activity as germicidal aerosols and recommended a solution of resorcinol in glycerol
    and water as satisfactory. These workers also found that NaOC1 was highly effective
    and killed air-borne bacteria in a dilution of 1 gin. of 2 per cent NaOCI in six million
    ce. of air. Their test microorganisms included pathogenic invaders of the respiratory
    tract as well as non-pathogens. Twort (6) and associates carried out an extensive
    investigation of the physical properties of aerosols, their droplet size and rate of
    evaporation, and the effects of various germicidal agents on a number of different
    microorganisms under a variety of conditions. Their most effective aerosol solution
    "S 2'' contained l0 per cent hexylresorcinol and 0.05 per cent alkyl sulfate, "lorol,"
    in alkaline propylene glycol. They reported bactericidal effects on certain nonpathogenic
    microorganisms with extraordinarily small amounts of this material, e.g.
    1 gin. to four billion cc. of air.
    Andrewes and coworkers (7) published a brief confirmatory report on the use of
    bactericidal mists for air sterilization, and in addition noted that a few viruses, including
    that of influenza, are susceptible to the mist action as judged by the reduction
    of their infectivity for mice.
    Twort and Baker (8) have proposed another and quite different type of agent for
    air sterilization, namely, certain kinds of smokes. Smokes from ignited cardboard
    soaked with potassium nitrate or from incense were found to be highly effective.
    They report that 1 gln. of the chemical substance dispersed in smoke form in 500
    million cc. of air causes destruction of 95 per cent of air-suspended bacteria within
    15 minutes.
    Our earlier work in this field consisted in an investigation of the air-sterilizing
    activity of certain bactericidal substances used as aerosols (9). We first employed
    certain of the synthetic detergents studied by Miller and Baker (10),
    since their activity in vitro gave promise of greater effectiveness as bactericidal,
    aerosols than the compounds used by the French and English workers. Preliminary
    experiments indicated only moderate effectiveness of aqueous solutions
    of these detergents. However, when the water was replaced by a hygroscopic
    vehicle such as propylene glycol, the aerosol activity was markedly
    Downloaded from jem.rupress.org on February 23, 2009
    Published June 1, 1942
    increased. We found subsequently that propylene glycol and certain related
    glycols themselves act as effective bactericidal aerosols. 2
    As the work progressed it was found that propylene glycol in vapor form was
    highly bactericidal, and that the marked and rapid germicidal action of propylene
    glycol aerosol was due to vapor liberated from the small glycol droplets.
    When pure vapor was employed, it was found to be more effective (12) than
    an equal quantity of propylene glycol dispersed as an aerosol. For the purpose
    of explicit exposition, the work will be presented in the sequence of its development.
    Methods and Materials
    Bacterial Suspensions.--Standardized bacterial suspensions were made by resuspending
    the centrifugated sediment of an actively growing culture in nutrient broth
    to a predetermined opacity corresponding to approximately one billion microorganisms
    per cc. Water and other diluents were employed occasionally. The suspensions
    were sprayed into the chamber with a Graeser atomizer (14). In some experiments
    other atomizers producing coarser droplets were used.
    Media for Recovering Bacteria from Air.--For Staphylococcus albus and most other
    non-pathogens nutrient agar with 0.5 per cent added dextrose was used. Rabbit
    blood agar was employed for recovering pneumococci and Streptococcus viridans;
    sheep blood agar for hemolytic streptococci and staphylococci and chocolate agar
    for ttemophilus influsnzae. It was found that chilling the agar plates before use
    resulted in maximum recovery of bacteria from the air samples.
    Test Chambers.--The chambers were made of glass and metal as shown and described
    in Text-fig. 1. Wooden chambers were found to be somewhat less sarisfactory.
    The air was gently agitated by means of a small fan rotating at a rate
    sufficient to produce detectable air movement in all parts of the chambers. A metal
    fan with 4 blades each 2½ inches long, run at 75 volts by means of a variable transformer
    which gave a speed of 500 R.P.M., proved satisfactory for this purpose. The
    fan was run for a period of only 5 minutes after the introduction of the bacterial spray.
    Method of Sampling Air.--The number of viable bacteria recoverable from the
    chamber air was determined by withdrawing a measured volume of air at a constant
    2 Although the English workers used glycols and glycerin as vehicles, they apparently
    ascribed little or no importance to these compounds beyond their usefulness as
    hygroscopic solvents for the germicidal substances, resorcinol and hexylresorcinol.
    The only reference to a possible independent action of propylene glycol is that made
    by Twort and coworkers (6), who reported a single experiment in which solutions of
    propylene glycol in alcohol exerted a very high degree of bactericidal activity when
    dispersed in mist form. It seems probable, however, that the germicidal action of
    this mixture was principally due to the alcohol, since alcohol vapor itself possesses
    marked germicidal properties. Furthermore, Baker and Twort state in a recent
    paper (13) that the presence of propylene glycol in their S 2 mixture contributes little
    or nothing to its bactericidal activity.
    Downloaded from jem.rupress.org on February 23, 2009
    Published June 1, 1942
    rate (2 liters in 2 minutes) through a glass funnel which was suspended directly abov(
    the surface of an agar plate within a sealed glass jar (Text-fig. 1). This is a modifica
    tion of the technique of air sampling described by Hollaender and DallaValle (15)
    The rubber and glass connections are made as short as possible. The air vent foJ
    equalizing internal and external pressure is covered with one or two layers of cantor
    Tower A
    to suction pump I~ atomizer.l
    ....... " Jl
    k- allar plate
    T•xT-Fm. 1. Apparatus employed for determining bactericidal activity of glycol
    vapors. A, 60 liter air-tight glass-walled chamber with one metal wall (opposite the
    side with vents) fitted with a door dosing on rubber gaskets. (All sides, 15 inches
    square.) The three upper orifices are actually on a horizontal line across the center
    of the wall. B, Graeser atomizer connected with inlet by rubber tube. C, sampling
    jar. G, air vent allowing water to return from bottle E to D.
    flannel. When pathogenic microorganisms were being studied, the orifices of the
    sampling jars were clamped and the jar containing the agar plate placed in the incubator.
    Before opening, a considerable volume of air was drawn through the jar
    and passed through a bead tower containing phenol (Text-fig. 1). Likewise, after
    each sampling the air from the measuring bottle was expelled through phenol in the
    bead tower. At the end of experiments with pathogens, the chambers were filled
    with propylene glycol aerosol or vapor and this air drown through the suction bottles.
    Canton flannel masks were worn as an added precaution.
    Downloaded from jem.rupress.org on February 23, 2009
    Published June 1, 1942
    Propylene GlycoL--The propylene glycol used in this study 3 was dear, colorless,
    and odorless, and when fractionated at a pressure of 25 ram., more than 80 per cent
    of the material was collected at a temperature of 99-101°C. (The boiling point
    given in the literature is 100-101.8°C. at 24 ram.) Propylene glycol is relatively
    non-volatile---its normal boiling point is 188°C., and at 200C. its vapor pressure is
    0.18 ram. Hg. Thus a concentration of 0.73 rag. per liter in the vapor state represents
    atmospheric saturation. No difference in behavior was detectable when the stock
    propylene glycol or the redistilled material was used in the experiments described in
    this paper.
    Production of Propylene Glycol A erosol.--An effective aerosol was produced by means
    of the Graeser atomizer which delivers a dry mist consisting of droplets averaging 2 to
    3/t in diameter. The DeVilbis atomizer No. 180 is also satisfactory. 4
    Production of Propylene Glycol Vapor.--The preparation of atmospheres containing
    various concentrations of propylene glycol in the vapor state was accomplished in a
    number of different ways. Placing the glycol in three Petri dishes on the floor of the
    chambers, and allowing it to evaporate overnight (for 14 to 16 hours) results in a
    vapor concentration of 0.35 rag. per liter, a quantity sufficient to produce almost
    immediate killing of the various organisms tested in this study. More rapid and
    complete saturation is effected by pouring propylene glycol, heated to 70--80°C.,
    into three Petri dishes placed in the chamber. The chamber is sealed, and allowed
    to cool to room temperature while a fan circulates the air inside. Still another
    method used consisted in filling the chamber with air bubbled through propylene
    glycol heated to 60°C. (in a thermostated water bath), which resulted in a glycol
    concentration of 0.66 rag. per liter in the vapor state.
    In order to achieve a more rapid and accurate means of filling the chambers with
    any desired concentrations of propylene glycol, the apparatus shown in Text-fig. 2
    was constructed. A 60 cycle synchronous motor of 1 R.1,.~r. speed drives forward a
    screw (c) of 20 threads per inch by means of a worm drive (a) and gear (b), (ratio
    7½ : 1) causing plate (d) to move forward and advance the plunger of a syringe. Propylene
    glycol contained in the syringe is forced out at a constant rate on to a heater
    which volatilizes the material. The heater consists of a 75 ohm, 10 watt "ohmite"
    resistor, across which 30 volts are applied. The needle of the syringe rests on a wick
    made up of a strip of cotton tape wound around the porcelain covering of the resistor.
    The wick serves to disperse the liquid over the hot surface. An air stream whose
    rate of flow is controlled by a pressure regulator and measured by a calibrated flow
    meter, impinges on the heater and carries the volatilized glycol into the chamber.
    The glass T tube (inner diameter 15 ram.) in which the heater is contained must be
    as short as possible to obviate the possibility of condensation of the glycol on the
    walls before it has been adequately mixed with the incoming air stream. Humidity
    is controlled by a humidifier placed in the path of the air stream, as shown in Text-
    We are indebted to the Carbon and Carbide Co. for supplying us with this highly
    purified material. It should be pointed out that there are preparations of propylene
    glycol on the market which contain impurities in toxic amounts.
    4 We wish to express our appreciation to the DeVilbis Co. for making a special
    experimental atomizer for us.
  8. Stylopora

    Stylopora Full Member ECF Veteran

    Jan 29, 2009
    Cambridgeshire UK
    fig. 2. The relative humidity can be varied either by changing the temperature or
    the amount of the water in the humidifier. Relative humidity inside the chamber
    was measured by means of wet and dry bulb thermometers, with the wet bulb placed
    opposite the fan.
    The concentration of propylene glycol vapor in the mixture issuing from the T tube
    is readily calculated, since both the rate of delivery of liquid propylene glycol and
    the rate of air flow through the vaporizer are known. Any desired concentration may
    be secured either by changing the rate of flow of air through the flow meter, or by
    inserting a syringe of a different diameter in the syringe holder. One cc. and 2 cc.
    syringes were found to be most suitable.
    The gas stream fed into the chamber is mixed completely with the air already present
    by means of a rapidly rotating electric fan and then passes out through an escape
    vent. A volume of gas four times that of the chamber is swept through for each
    filling. (Calculation shows that after four air changes under these conditions the
    propylene glycol content of the gas inside the chamber is 99.0 per cent of that in the
    entering air stream.) The chamber is then sealed off. Before beginning the experiment
    a sample of air is removed for analysis as an additional check on the glycol
    Method of Determining Concentration of Propylene Glycol Vapor in Air.--The determination
    of the concentration of propylene glycol vapor was accomplished by
    withdrawing a 2 liter sample of the air and bubbling it through 10 cc. of water with
    the aid of a fairly porous, fritted glass gas-disperser. Complete absorption of the
    propylene glycol is obtained at a sampling rate of 1/5 liter of air per minute.
    The propylene glycol content of the resulting solution can be analyzed by the
    method of Lehman and Newman (16), modified to accomodate the smaller concentrations
    involved (17). In this reaction the propylene glycol is quantitatively oxidized
    by a standard amount of periodic acid. The remainder of the oxidizing agent is
    determined by reduction with a known quantity of sodium arsenite, and the excess
    arsenite titrated with I2. The contents of the test tube are quantitatively washed into
    an Erlenmeyer flask. 1.0 cc. of M/10 periodic acid ~ is added, and the sample is placed
    in an ice box for 15 minutes. At the end of that time, 5 cc. of 7 per cent NaHCO3 is
    added, then 2.5 cc. of N/10 Na~AsOz, followed by 0.4 cc. of freshly prepared 20 per
    cent KI. The solution is allowed to stand for 15 minutes at room temperature,
    after which 1 cc. of 1 per cent starch is added. The solution is then titrated with
    0.01 N I2 to the end point marked by the appearance of the blue color of the starch
    iodine complex. A blank is run through the same procedure, and the number of
    milliliters of I~ solution used in the blank is subtracted from that required by the
    sample. One cc. of 0.01 N I2 solution is equivalent to 0.38 mg. of propylene glycol.
    Samples containing known amounts of propylene glycol varying from 0.3 to 1.0 mg.
    gave results accurate to within 0.04 mg., when analyzed by this method.
    5 The M/10 periodic acid is prepared by dissolving 5.35 gm. of sodium periodate
    (NaIO4) in 75 cc. of N/1 sulfuric acid, and diluting to 250 cc. in a volumetric flask.
    The resulting solution is stable indefinitely if stored in an ice box between runs.
    Directions for preparation of the standard sodium arsenate and iodine solutions are
    available in any standard textbook such as Pierce, W. C., and Haenisch, E. L., Quantitative
    analysis, New York, John Wiley & Sons, 1937.
    Downloaded from jem.rupress.org on February 23, 2009
    Published June 1, 1942
    Reproduceability of Bacterial Counts in Air Samples.--Agar plates exposed
    to the flow of bacteria-containing air by means of the technique outlined above
    yielded a remarkably

    Two different standard suspensions of staphylococcus were made up from the same
    culture on each of two occasions. The dilutions of the standard suspensions and the
    time of spraying are indicated in the first column of the table. The same atomizer
    filled to the same level and operated at 500 mm. air pressure was used in all the tests.
    Air samples (of 2 liters each) were withdrawn at exactly the same intervals following
    termination of the bacterial spray. The first sample (labeled immediately) was
    started 15 seconds afterwards and the second one at 5 minutes. Mter two samples
    had been taken, the chamber was cleaned out and the next test run under identical
    It will be noted in the table that suspensions 1 and 2 yielded approximately
    the same number of colonies on the plates while the difference in sampling
    yields between suspensions 3 and 4 indicates that we were less successful in
    making up suspensions of equal density.
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    Published June 1, 1942
    There is a progressive and quite constant diminution in the number of
    colonies recovered from successive air samples during the period of an hour, as
    illustrated in Plate 18, Figs. 1 to 4. This phenomenon may be ascribed to
    settling of the bacterial droplets, inelastic collisions with the chamber walls,
    and natural mortality of the bacteria. This necessitated the use of two identical
    chambers for each experiment, one for the test, the other as a control.
    Propylene Glycol Aerosol
    Tests on the bactericidal activity of propylene glycol aerosol were performed
    as follows: usually the bacteria were sprayed into the chamber first, and an
    air sample obtained, following which a weighed quantity of the aerosol was
    introduced. In order to control any possible effect of the germicidal aerosol
    other than its direct bactericidal action, distilled water was sprayed into the
    control chamber in each experiment. It was found that a concentration of
    Effect of Propylene Glycol Aerosol on Staphylococcus albus
    Time intervals of air samples
    Immediately after bacterial spray
    Immediately after H20 in control and aerosol
    in test
    15 min. later
    30 rain. later
    No. of colonies on plates from
    Test chamber
    1 gin. of propylene glycol aerosol in two million cc. of air effected complete
    sterilization of an atmosphere into which as many as 500,000 bacteria per liter
    of air had been sprayed. Furthermore, this action occurred with surprising
    rapidity. Air samples taken within a few seconds after the introduction of
    the aerosol yielded sterile plates while similar plates from the control chamber
    showed many hundreds or thousands of colonies depending on the amount of
    bacterial suspension used. A protocol of an experiment with Staphylococcus
    albus is recorded in Table II and photographs of another experiment are shown
    in Plate 18, Figs. 1 to 8.
    A number of other microorganisms were found to be similarly susceptible to
    the action of this aerosol. Among those tested were pathogenic invaders of
    the respiratory tract, i.e., pneumococcus Types I and III, hemolytic streptococci,
    and hemolytic staphylococci, as well as organisms of lesser or no pathogenicity,
    such as Streptococcus viridans, Bacillus coli, Micrococcus catarrhalis, and
    Bacillus subtilis (vegetative form).
    The order of introduction of the bacteria and the propylene glycol into the
    Downloaded from jem.rupress.org on February 23, 2009
    Published June 1, 1942
    chamber was found to have no effect on the result. Thus an equally rapid
    sterilization was obtained when bacteria were introduced into a test chamber
    already containing propylene glycol. Other glycols, such as ethylene and
    trimethylene, acted about as effectively as propylene glycol. Glycerin, on the
    other hand, exhibited only a slight killing effect.
    Propylene Glycol Vapor
    (a) Bactericidal Effect of Aerosol Not Explainable on Basis of Droplet I~eraction.--
    If the disappearance of bacteria in air treated with a propylene glycol
    mist represents a true bactericidal effect, and evidence presented later indicates
    that such is the case, how can this action be explained? The means by which
    bactericidal mists produce a lethal concentration of the active agent in the
    immediate environment of the bacteria would seem to be limited to two possibilities;
    (a) direct contact between germicidal aerosol droplets and bacterial
    particles; (b) production of sufficient vapor or gas by evaporation from the
    germicidal droplets to permit rapid and abundant collision of gas molecules
    with the bacterial particles. Trillat, Pulvertaft and Walker, and Twort and
    his associates, believe that germicidal mists exert their antibacterial action
    exclusively as aerosols. They state that the substances employed by them are
    ineffective in the gas phase. In fact, their investigations of different agents
    or mixtures for use as bactericidal aerosols have been directed toward developing
    a mist with a very slow rate of evaporation. Masterman, on the other
    hand, considers that the activity of the germicidal mist he employed, namely
    NaOC1, is due to the liberation of HOC1 gas.
    Calculations of the maximum number of contacts possible between aerosol
    and bacterial droplets (which Twort et al. have made (6) and which we have
    repeated) indicate that it would take between 2 and 200 hours for sterilization
    to occur if this were the mode of action of the germicidal aerosol. Since
    complete sterilization of a heavily contaminated atmosphere has been found
    to take place in as short a time as 5 minutes by the English workers, and within
    a matter of seconds by ourselves, the rate of interaction between the bactericidal
    agent and air-suspended bacteria must be of an entirely different order of
    magnitude. Such rapid interaction could occur only if the germicidal substance
    were present in the gas phase.
    (b) Postulation of Vapor-Droplet Effect.--Granted that rapid interaction
    between gas molecules and droplets does occur, would the resulting concentration
    of propylene glycol in the bacterial droplets be sufficient to produce the
    striking bactericidal effects observed? Experiments in vitro showed that
    propylene glycol in common with other closely related glycols exhibited relatively
    low germicidal action. Certain microorganisms grow well in broth
    containing as much as 5 to 15 per cent of the different glycols tested (propylene,
    ethylene, and trimethylene). The pneumococcus, for example, grows in
    Downloaded from jem.rupress.org on February 23, 2009
    Published June 1, 1942
    broth containing up to but not more than 5 per cent propylene glycol. Staphylococcus
    albus is not inhibited until a concentration of more than 10 per cent
    of this material is reached. However, when these bacteria are suspended in
    80 to 90 per cent propylene glycol, they are kiUed immediately. Since prowlene
    glycol possesses a marked affinity for water, rapid absorption of the vapor
    by aqueous droplets might be expected to occur. Indeed, calculations show
    that with vapor concentrations even considerably below the saturation value
    of propylene glycol, the number of collisions between gas molecules and droplets
    containing bacteria is sufficient to produce almost instantly, a lethal concentration
    (70 to 80 per cent) of propylene glycol in the droplets. Furthermore,
    the observed rate of evaporation of droplets of a propylene glycol mist
    is so rapid that a relatively high vapor concentration is liberated within a
    second or two. s
    Effect of Propylene Glycol Vapor on Streptococcus hemolyticus
    Time intervals of air samples
    Immediately after bacterial spray
    5 min. later
    15 min. later
    30 min. later
    60 man. later
    No. of colonies on plates from
    cChoanmtrboelr Test chamber
    370 36
    360 5
    312 0
    250 0
    96 0
    (c) Demonstration of the Bactericidal Activity of Propylene Glycol Vapor.-
    Tests carried out under conditions identical with those in which the aerosol
    was employed, showed that propylene glycol vapor was not only highly bactericidal
    but acted more effectively than did the aerosol of this substance. In
    carrying out such experiments the chamber was filled with glycol vapor of
    known concentrations by means of one of the several methods described, following
    which the bacterial suspension was introduced. Concentrations of not
    less than 1 gm. of propylene glycol in three or four million cc. of air resulted in
    immediate and complete sterilization of the chamber air. This effect was
    demonstrated with staphylococci, pneumococci, hemolytic streptococci, H.
    influemae, and H. pertussis. The results of an experiment in which pneumococcus
    Type I was employed as the test organism are exhibited in Plate
    6 The size and rate of evaporation of the droplets was determined by means of the
    Millikan oil-drop apparatus (18). These calculations together with a detailed discussion
    of th e physicochemical interactions of propylene glycol gas molecules and fine
    fluid droplets will be presented elsewhere.
    Downloaded from jem.rupress.org on February 23, 2009
    Published June 1, 1942
    19, Figs. 1 to 6. With diminishing concentrations of propylene glycol,
    immediate and marked bactericidal activity was still obtained, although complete
    sterilization of the air required increasing intervals of time. Table III
    shows the lethal action of a vapor concentration of 1:7,700,000 (0.13 mg. per
    liter) on Streptococcus hemolyticus. The effectiveness of low concentrations
    of propylene glycol vapor was found to depend also on other variable factors,
    such as numbers of microorganisms dispersed into the air, the number of bacterial
    droplets, humidity of the atmosphere, state of bacterial suspension, etc.
    A detailed presentation of this phase of the work will be given in a second
    paper. Suffice it to say here that under optimum conditions pronounced
    bactericidal action of propylene glycol vapor against certain of the respiratory
    pathogens could be demonstrated in concentrations as small as 1 gin. of the
    glycol in 50,000,000 cc. of air.
    Propylene glycol vapor was also found to exert a lethal or at least an inactivating
    effect on the virus of influenza. This was determined by tests in
    which the presence of the glycol vapor in concentration of 1:3,000,000 was
    shown to protect mice completely against infection with amounts of air-borne
    influenza virus that produced death regularly in the control animals (19).
    Tests with Other Glycols
    Experiments with other glycols in vapor form revealed variations in their
    bactericidal activity. Ethylene glycol, 2,3-butylene glycol, trimethylene
    glycol, and a number of compounds of related chemical composition were
    found to be highly effective. The relationship between chemical structure
    and bactericidal properties will be discussed in detail in a later communication
    dealing with the mechanism of the action of glycol vapors.
    Evidence for the Bactericidal Action of Propylene Glycol
    Other workers in this field have assumed that lack of growth on agar surfaces
    exposed to bacteria-laden atmospheres treated with germicidal mists
    represents actual death of the bacteria in the air. It seemed to us, however,
    that further experimental evidence was necessary to exclude the possibility
    that some factor or factors present in the air containing the germicidal mist or
    vapor might either inhibit growth or prevent adherence of the bacteria on the
    agar surface. In order to test for any growth-inhibiting effect due to condensation
    of the glycol itself on the collecting plates, the following control was
    performed: agar plates were exposed directly to air saturated with propylene
    glycol vapor or to the glycol spray from an atomizer, then used in taking
    samples from the control chamber. They yielded just as many colonies as
    plates not treated with glycol. The possibility that the reaction between the
    propylene glycol vapor and the bacterial droplets might somehow change the
    Downloaded from jem.rupress.org on February 23, 2009
  9. Stylopora

    Stylopora Full Member ECF Veteran

    Jan 29, 2009
    Cambridgeshire UK
    Published June 1, 1942
    O. H. ROBERTSON~ v.. BIGG~ T. T. PUCK~ AND B. F. MTLI.ER 605
    TzxT-FIG. 3. Bead tower for collection of bacteria from chamber air. 20 to 25 cc.
    of broth diluted with equal parts of sterile water is placed in a 20 inch glass cylinder
    half filled with 3 ram. glass beads. This tower differs from that shown in Text-fig. 1
    in that there are two monel metal screens of 24 and 70 mesh inserted at A.
    TEx'r-Fic. 4. Device for collecting air-borne bacteria on a glass slide.
    Downloaded from jem.rupress.org on February 23, 2009
    Published June 1, 1942
    state of suspension of the latter and prevent their adherence to the agar surface
    was tested by employing another method of coUecting the vapor treated
    bacteria. Air from the chamber was drawn slowly through 25 to 50 cc. of
    diluted nutrient broth in a glass cylinder containing many small glass beads
    (Text-figs. 1 and 3). Hated samples of this fluid, through which air from the
    control chamber had been bubbled, yielded a large number of colonies, whereas
    samples of fluid through which the glycol-containing air had been drawn were
    Inoculation of Mice wlgh Pneumococcus Type I Exposed to Propylene Glycol Vapor
    introduced into
    glycol vapor.
    followed by
    Air Samples
    T/me taken
    Immediately after
    10 rain. later
    30 min. later
    Immediately after
    10 rain. later
    ]No. of pneumococcus
    Method ~ On
    of late culture P--I~
    Plate ¢
    Plate i12
    30 rain. later Plate 484
    In fluid from
    bead tower
    1 cc. -- 228
    Total --
    Mice inoculated
    with icc. of fluid
    from bead tower
    10 mice. All
    died of pneumococcus
    in 24 to 36
    The presence of kiUed bacteria in the glycol-treated air was demonstrated
    by condensing the moisture of the air drawn from the chamber on a chilled
    microscope slide, as shown in Text-fig. 4. When these preparations were
    stained, the bacteria appeared normal. Cultures of the condensed fluid on
    agar and in broth showed no growth.
    We have also eliminated the possibility that microorganisms, although
    rendered incapable of growth on artificial media, might retain their capacity
    to reproduce in a suitable host. Experiments were conducted in which highly
    virulent pneumococci Type I were sprayed into a chamber containing the
    propylene glycol vapor. The air was then drawn through sterile broth in a
    bead tower and 1 cc. quantities of this fluid were injected into mice. These
    10 mice. All
    remained well
    * The 2 liter air sample was drawn throu h 25 cc. of 50 per cent broth-water mixture.
    Downloaded from jem.rupress.org on February 23, 2009
    Published June 1, 1942
    animals survived. However, when the procedure was performed with air
    drawn from the control chamber, all the mice died of pneumococcic infection.
    The protocol of an experiment of this type is shown in Table IV.
    Further evidence of the bactericidal action of propylene glycol vapor was
    provided by cultures made from the floor and walls of the chamber at the end
    of the experiment. Whereas cultures from the control chambers always yielded
    large numbers of bacteria, those from the test or glycol-treated chamber were
    uniformly sterile.
    Additional Data and Comments
    The question as to how propylene glycol produces its rapid and marked
    bactericidal effect has not been elucidated. However, certain observed characteristics
    of the glycol-treated microorganisms indicate something of the
    general nature of the effect. Gram-positive bacteria killed by exposure to
    propylene glycol, either in vapor or liquid form, retain their Gram-positiveness
    as well as their morphological integrity. Glycol-killed pneumococci show
    typical capsular swelling in the presence of specific antipneumococci rabbit
    serum and retain their antigenic properties. Mice, vaccinated with pneumococci
    killed by propylene glycol, were found to be just as resistant to the
    injection of living microorganisms as were mice similarly immunized with
    heat-killed pneumococci. While pneumococci suspended in propylene glycol
    retain their Gram-positiveness for many weeks or months, removal from this
    medium results in their becoming Gram-negative. Such microorganisms freed
    from the glycol undergo gradual dissolution. Autolysis is hastened by the
    presence of bile salts. The change from the Gram-positive to the Gram-negative
    state can be brought about by simply adding an equal volume of water
    or physiological salt solution to the glycol suspension. These findings indicate
    that propylene glycol inhibits but does not destroy the autolytic enzyme system
    of the pneumococcus cell. Whether or not the other enzyme systems of
    the pneumococcus are affected remains to be determined.
    We have not made comparative studies of the effectiveness of propylene
    glycol and the several compounds and mixtures previously employed by other
    workers, except in the case of Twort's "S ~''. Our observations with "S ~''
    (10 per cent hexylresorcinol in alkaline propylene glycol) have been confined
    to tests on Staphylococcus albus. These experiments showed that the addition
    of hexylresorcinol to propylene glycol increased markedly the bactericidal
    activity of the latter substance. The difference between the two agents both
    in aerosol and vapor forms was slight as judged by the immediate sterilizing
    effect, but became apparent after 5 to 15 minutes. An increased lethal action
    might have been anticipated from the presence of hexylresorcinol since, in
    vitro, this substance has been shown to be bactericidal in dilutions of between
    1:2,000 and 1:20,000 (depending on the manner of testing) in contrast to
    Downloaded from jem.rupress.org on February 23, 2009
    Published June 1, 1942
    propylene glycol which requires a concentration of 1:1, i.e., equal parts of
    bacterial suspension and glycol to produce a similar effect. Even higher
    concentrations of propylene glycol were needed to kill certain non-pathogenic
    microorganisms. Since rapidity of action of the air sterilizing agent would
    seem to be of great importance in the application of such a method to the control
    of air-borne droplet infection, and since the addition of hexylresorcinol
    appears to contribute little to the immediate bactericidal effect of propylene
    glycol, we feel that for this and other reasons the use of the latter substance
    alone is to be preferred. However, it may be desirable to employ, for certain
    purposes, highly bactericidal agents such as hexylresorcinol even though they
    possess much greater potential toxicity than does propylene glycol.
    Atmospheres containing propylene glycol vapor in concentrations up to the
    saturation point (0.7 mg. of glycol per liter of air or 1:1,400,000) are invisible,
    odorless, non-irritating, and tasteless, except in the highest concentrations
    when a faintly sweetish taste is detectable. Tests on the toxicity of propylene
    glycol administered by the usual routes, i.e., oral and intravenous, have shown
    this substance to he essentially non-toxic (20). While it would seem probable
    that propylene glycol taken into the body by way of the respiratory tract would
    be equally innocuous, such an assumption is not justifiable in the absence of
    direct experimental evidence. We have carried out tests on the effect of
    maintaining rats in atmospheres of propylene glycol vapor for a year or more.
    The results of these experiments will be presented in the second paper.
    It has been found that propylene glycol vapor dispersed into the air of an
    enclosed space produces a marked and rapid bactericidal effect on microorganisms
    introduced into such an atmosphere in droplet form. Concentrations
    of 1 gm. of propylene glycol vapor in two to four million cc. of air produced
    immediate and complete sterilization of air into which pneumococci, streptococci,
    staphylococci, H. influemae, and other microorganisms as well as influenza
    virus had been sprayed. With lesser concentrations of propylene
    glycol, rapid and marked reduction in the number of air-borne bacteria occurred,
    but complete sterilization of the air required a certain interval of time.
    Pronounced effects on both pneumococci and hemolytic streptococci were
    observed when concentrations as low as 1 gm. of glycol to fifty million cc. of
    air were employed.
    Numerous control tests showed that failure of the glycol-treated microorganisms
    to grow on the agar plates was due to actual death of the bacteria.
    The means by which propylene glycol vapor produces its effect on droplet-borne
    bacteria is discussed and data relating the bactericidal properties of propylene
    glycol in vitro to the lethal action of its vapor is presented.
    Atmospheres containing propylene glycol vapor are invisible, odorless,
    Downloaded from jem.rupress.org on February 23, 2009
    Published June 1, 1942
    and non-irritating. This glycol is essentially non-toxic when given orally and
    intravenously. Tests on possible deleterious effects of breathing propylene
    glycol containing atmospheres over long periods of time are being carried out.
    1. Douglas, S. R., Hill, L., and Smith, W., J. Ind. Hyg., 1928, 10, 219.
    2. Trillat, M. A., Bull. Acad. m~d., 1938, series 3, 119, 64.
    3. Masterman, A. T., J. Ind. Hyg., 1938, 20~ 278.
    4. Masterman, A. T., J. Hyg., Cambridge, Eng., 1941, 41, 1, 44.
    5. Pulvertaft, R. J. V., and Walker, J. W., J. Ityg., Cambridge, Eng., 1939, 39~ 696.
    6. Twort, C. C., Baker, A. H., Finn, S. R., and Powell, E. 0., J. IIyg;, Cambridge,
    Eng., 1940, 40, 253.
    7. Andrewes, C. H., Lancet, 1940, 2, 770.
    8. Twort, C. C., and Baker, A. H., Lancet, 1940, 2, 587.
    9. Robertson, O. H., Bigg, E., Miller, B. F., and Baker, Z., Science, 1941, 93, 213.
    I0. Miller, B. F., and Baker, Z., Science, 1940, 91, 624.
    11. Robertson, O. H., Bigg, E., Miller, B. F., Baker, Z., Puck, T. T., Tr. Assn. Am.
    Physn., 1941.
    12. Robertson, O. H., Bigg, E., Miller, B. F., Puck, T. T., and Baker, Z., in Moulton,
    F. R., Aerobiology symposium, The American Association for the Advancement
    of Science, 1942, No. 17, in press.
    13. Baker, A. H., and Twort, C. C., J. Hyg., Cambridge, Eng., 1941, 41~ 117.
    14. Graeser, J. B., and Rowe, A. H., Am. J. Dis. Child., 1936, 52, 92.
    15. Hollaender, A., and DallaValle, J. M., Pub. Health Rep., U. S. P. H. S., 1939,
    54, 1,574.
    16. Lehman, A. J., and Newman, H. W., J. Pharmacol. and Exp. Therap., 1937,
    60, 312.
    17. Puck, T. T., Science, 1942, 95, 178.
    18. Millikan, R. A., The electron, Chicago, The University of Chicago Press, 1924, 90.
    19. Robertson, O. H., Loosli, C. G., Puck, T. T., Bigg, E., and Miller, B. F., Science,
    1941, 94, 612.
    20. Hanzlik, P. S., Newman, H. W., Van Winlke, W., Lehman, A. J., and Kennedy
    N. K., Y. Pharmacol. and Exp. Therap., 1939, 67, 101.
  10. DaveyRoots

    DaveyRoots Senior Member ECF Veteran

    Feb 13, 2009
    San Diego
    whoa! this is bigtime info! thanks alot guys, really helpfull.
  11. Hector

    Hector Full Member

    Jun 23, 2008
    If I was worried about emphysema I certainly wouldn't be living in Cairo that's for sure !
  12. Stylopora

    Stylopora Full Member ECF Veteran

    Jan 29, 2009
    Cambridgeshire UK
  13. booboo

    booboo Super Member ECF Veteran

    Feb 11, 2009
    San Diego, CA
    Lol, we KNEW cigarettes caused birth defects, lung cancer, emphysema, copd, death and everything else and still did that! (At least I did for 20 years). I was one of those smokers who said I didn't care if it killed me, I was going to die happy doing what I loved, at least. Until it hurt to move and I was sick every damn day for 4 years. As long as I feel better now and can walk more than 5 feet without having a cough-til-I-puke attack, I don't care! I feel so much better on e-cigs, I can't even believe it. If you are that worried about emphysema, don't inhale anything!
  14. Stylopora

    Stylopora Full Member ECF Veteran

    Jan 29, 2009
    Cambridgeshire UK
    Super Member
    Join Date: Jan 2008
    Location: Port Charlotte, FL USA
    Posts: 3,236

    A germ-killing vapor
    Far from posing a threat to our health, the propylene glycol in e-smoking liquids might help keep us healthy. It would accomplish that by its germicidal action. It kills many of the major bacteria that threaten lung entry into our bodies.

    Until yesterday, I was unfamiliar with this potentially beneficial consequence of propylene glycol vapor.

    Back in the late '30s, researchers at the University of Chicago stumbled onto its effectiveness as a germ-killer, as related in this Time magazine story from Nov. 16, 1942:

    "A powerful preventive against pneumonia, influenza and other respiratory diseases may be promised by a brilliant series of experiments conducted during the last three years at the University of Chicago's Billings Hospital. Dr. Oswald Hope Robertson last week was making final tests with a new germicidal vapor — propylene glycol — to sterilize air. If the results so far obtained are confirmed, one of the age-old searches of man will finally achieve its goal...

    the researchers found that the propylene glycol itself was a potent germicide. One part of glycol in 2,000,000 parts of air would — within a few seconds — kill concentrations of air-suspended pneumococci, streptococci and other bacteria numbering millions to the cubic foot.

    "How did it work? Respiratory disease bacteria float about in tiny droplets of water breathed, sneezed and coughed from human beings. The germicidal glycol also floats in infinitesimally small particles. Calculations showed that if droplet had to hit droplet, it would take two to 200 hours for sterilization of sprayed air to take place. Since sterilization took place in seconds, Dr. Robertson concluded that the glycol droplets must give off gas molecules which dissolve in the water droplets and kill the germs within them.

    "Dr. Robertson placed groups of mice in a chamber and sprayed its air first with propylene glycol, then with influenza virus. All the mice lived. Then he sprayed the chamber with virus alone. All the mice died."

    The complete Time story can be read here:

    In a scientific summary of the discovery, it was noted that "Tests on possible deleterious effects of breathing propylene glycol containing atmospheres over long periods of time are being carried out."

    Those tests were done and a second summary report on propylene glycol vapor was released:

    "Propylene glycol is harmless to man when swallowed or injected into the veins. It is also harmless to mice who have breathed it for long periods. But medical science is cautious — there was still a remote chance that glycol might accumulate harmfully in the erect human lungs which, unlike those of mice, do not drain themselves. So last June Dr. Robertson began studying the effect of glycol vapor on monkeys imported from the University of Puerto Rico's School of Tropical Medicine. So far, after many months' exposure to the vapor, the monkeys are happy and fatter than ever. Dr. Robertson does not expect mankind to live, like his monkeys, continuously in an atmosphere of glycol vapor; but it should be most valuable in such crowded places as schools and theaters, where most respiratory diseases are picked up."

    The monkeys lived in enclosures filled with propylene glycol vapor. No deleterious effect was ever reported. And the concentrations of PG we inhale on a regular basis surely must equal the amount inhaled by the monkeys for this test. Obviously, no scientist saw a time when a device would atomize a PG mist that would then be inhaled for fun. But time and technology has given us the electronic cigarette. With each inhalation, we are washing our lungs with a germicidal agent used today in some "air sanitizers".

    Glycerine, by the way, has some germicidal impact, but not, apparently, to the degree provided by inhaling propylene glycol vapor. Glycerine is now used by dairy farmers to help prevent bacteria entering a cow's teats after milking. Glycerine both softens the teats and kills bacteria.

    One more quote on PG: "The vapour from as little as 0.5 mg of propylene glycol can kill nearly all the microorganisms in a liter of heavily contaminated air within 15 seconds."

    The initial experiments with PG vapor were part of a search to find ways to create clean rooms, so the 1918 Spanish Flu pandemic that killed so many millions would never be repeated. Today, researchers have wondered online if propylene glycol vapor might not offer protection against a widely feared coming pandemic of bird flu, tagged H5N1.

    Imagine e-smokers being healthier than non-smokers in such a scenario.
  15. surbitonPete

    surbitonPete Ultra Member ECF Veteran

    Jan 25, 2009
    North Yorkshire UK
    Yes I could see the stupid Irony of my own comment almost as soon as I posted it...but I couldn't be bothered to change it.........lol....my bad.
  16. Stylopora

    Stylopora Full Member ECF Veteran

    Jan 29, 2009
    Cambridgeshire UK
    this helps us to understand a little about some effects of inhaling propylene glycol vapor.
    However the really big unknown is the effect of the flavours we use mixed into the propylene glycol.
  17. Stylopora

    Stylopora Full Member ECF Veteran

    Jan 29, 2009
    Cambridgeshire UK
    As this thread is related to emphysema I thought it would be worth adding more info on What it is how it works hows and whys of getting it and symptoms etc etc.
    As many that have or think they may have emphysema may search for info on this site for emphysema and Electronic Cigarettes.
    I have been diagnosed with Mild Emphysema I smoked for 35 years and I am 50 years old in May.
    I did stop smoking for 2 years 5 years ago when diagnosed with a blood clot on the lung and with Mild Emphysema, However I then started smoking again for the last 3 years when my wife was diagnosed with Breast cancer (She is in remission now) and stopped smoking on Christmas Day 2008 when I went down with a bad lung infection.
    Found Electronic Cigarettes on the 31st dec and started using 6th Jan 09.
    Just recently found this site and it is full of very helpful and useful information
    As I don't have 15 posts yet I can't add full links so add parts of the link to info added below


    Emphysema is called an obstructive lung disease because the destruction of lung tissue around smaller airways, called bronchioles, makes these airways unable to hold their shape properly when you exhale.
    Normally, the lungs are very spongy and elastic.
    When a breath is taken, the chest wall expands, expanding the sponge.
    Similar to the way a squeezed sponge will draw water into it when released, suction draws air into the lungs when the chest wall expands.
    Air is brought though the trachea (windpipe) and bronchi (the main air tubes going to right and left lungs).
    These tubes divide into smaller and smaller tubes, finally ending in alveoli.
    Alveoli, the tiniest structures in the lung, are very small air sacs that are arranged like a bunch of grapes.
    The alveoli are at the ends of the smallest tubes called bronchioles.
    The alveoli and the bronchioles are very important structures for the lungs to function properly.
    It is these structures that are destroyed by emphysema.

    A sponge works to pick up water because all of the tiny little holes expand all at once after being squeezed.
    If the holes were larger, the sponge would not pick up as much water.
    This is because a larger hole cannot expand enough by itself to equal the action of multiple smaller ones.
    Thinking of the lungs as a sponge in this way, it becomes easier to see how emphysema acts to cause impaired lung function.
    Lungs require an elastic quality, so that they can expand and contract well.
    Additionally similar to the holes of the sponge, lungs need many alveoli (hundreds of millions, in fact) to draw enough air into them.
    The fewer and the bigger the alveoli, the less effectively they perform.

    Cigarette smoking is by far the most dangerous reason that people develop emphysema, and it is also the most preventable cause.
    Other risk factors include a deficiency of an enzyme called alpha-1-antitrypsin, air pollution, airway reactivity, heredity, male sex, and age.

    The importance of cigarette smoking as a risk factor for developing emphysema cannot be overemphasized.
    Cigarette smoke contributes to this disease process in 2 ways.
    It destroys lung tissue, which is the cause of the obstruction, and it causes inflammation and irritation of airways that can cause the disease to get worse.

    Destruction of lung tissue occurs in several ways.
    First, cigarette smoke directly affects the cells in the airway responsible for clearing mucus and other secretions.
    Occasional smoking temporarily disrupts the sweeping action of tiny hairs called cilia that line the airways.
    Continued smoking leads to longer dysfunction of the cilia.
    Long-term exposure to cigarette smoke causes the cilia to disappear from the cells lining the air passages.
    Without the constant sweeping motion of the cilia, mucous secretions cannot be cleared from the lower respiratory tract.
    Furthermore, smoke causes mucous secretion to be increased at the same time that the ability to clear the secretions is decreased.
    The resulting mucous buildup can provide bacteria with a rich source of food and lead to infection.

    The immune cells in the lung, whose job it is to prevent and fight infection, are also affected by cigarette smoke.
    They cannot fight bacteria as effectively or clear the lungs of the many particles (such as tar) that cigarette smoke contains.
    In these ways cigarette smoke sets the stage for frequent lung infections.
    Although these infections may not even be serious enough to require medical care, the inflammation caused by the immune system constantly attacking bacteria or tar leads to the release of destructive enzymes from the immune cells.

    Over time, enzymes released during this persistent inflammation lead to the loss of proteins responsible for keeping the lungs elastic.
    In addition, the tissue separating the air cells (alveoli) from one another also is destroyed. Over years of chronic exposure to cigarette smoke, the decreased elasticity and destruction of alveoli leads to the slow destruction of lung function.

    Air pollution acts in a similar manner to cigarette smoke.
    The pollutants cause inflammation in the airways, leading to lung tissue destruction.
    Abnormal airway reactivity, such as bronchial asthma, has been shown to be a risk factor for the development of emphysema.

    Men are more likely to develop emphysema than women.
    The exact reason for this is unknown, but differences between male and female hormones are suspected.

    Older age is a risk factor for emphysema.
    Lung function normally declines with age.
    Therefore, it stands to reason that the older the person, the more likely they will have enough lung tissue destruction to produce emphysema.

    Close relatives of people with emphysema are more likely to develop the disease themselves. This is probably because the condition may be inherited.
    The role of genetics in the development of emphysema, however, remains unclear.

    Alpha-1-antitrypsin is a substance that fights a destructive enzyme in the lungs called trypsin.
    Trypsin is a digestive enzyme, most often found in the digestive tract, where it is used to help the body digest food.
    It is also released by immune cells in their attempt to destroy bacteria and other material. People with alpha-1-antitrypsin deficiency cannot fight the destructive effects of trypsin once it is released in the lung.

    The destruction of tissue by trypsin produces similar effects to those seen with cigarette smoking.
    The lung tissue is slowly destroyed, thus decreasing the ability of the lungs to perform appropriately.

    Shortness of breath is the most common symptom of emphysema.
    Cough, sometimes caused by the production of mucus, and wheezing may also be symptoms of emphysema.
    You may notice that your tolerance for exercise decreases over time.
    Emphysema usually develops slowly.
    You may not have any acute episodes of shortness of breath.
    Slow deterioration is the rule, and it may go unnoticed.
    This is especially the case if you are a smoker or have other medical problems that limit your ability to exercise.

    One of the hallmark signs of emphysema is "purse-lipped breathing."
    The person with emphysema is struggling to exhale completely, with airways that close when the chest wall collapses during expiration.
    They purse the lips, leaving only a small opening.
    Then, when they exhale, the lips block the flow of air, increasing pressure in the collapsed airways, and opening them, allowing the person to fully exhale.

    People with emphysema may develop a "barrel chest," where the distance from the chest to the back, which is normally less than the distance side to side, becomes more pronounced. This is a direct result of air becoming trapped behind obstructed airways.

    If you have new or worsening shortness of breath, seek medical attention from your doctor. Shortness of breath can occur with other diseases, particularly heart disease and other lung diseases, so it is important not to overlook or minimize this symptom.
    A gradual decrease in the ability to exercise or perform daily activities, a persistent cough, and wheezing also suggest a visit to the doctor.

    Because cigarette smoking is such a dangerous risk factor for emphysema, you may also wish to contact your doctor for help with making a plan to quit smoking, even in the absence of shortness of breath or other symptoms.
    Doctors can offer you many options to help you stop smoking.
    The support from a doctor may make the process easier than doing it alone.
    Shortness of breath should always be taken seriously, especially if it comes on suddenly or if it gets worse over a relatively short period of time.
    If you know you have emphysema, go to the hospital's emergency department with any new, severe, or worsening shortness of breath.
    The inability to speak in full sentences may be a sign of shortness of breath.
    Any hint of the lips, tongue, fingernails, or skin turning a shade of blue should prompt a visit to the hospital's emergency department.
    This sign, called cyanosis, can indicate severe worsening of your lung condition.

    The failure of shortness of breath to improve or worsening shortness of breath in spite of home medications can indicate the need for emergency department care.
    A new or worsening cough can be a sign of an infection, such as pneumonia, and should prompt a visit to the hospital's emergency department for evaluation.
    Increased sputum production may also be a sign of infection.
    Infections make emphysema worse and can lead to long-term problems.

    Medical Treatment
    Treatment for emphysema can take many forms.
    Different approaches to treatment are available.
    Generally, a doctor will prescribe these treatments in a step-wise approach, depending on the severity of your condition.

    Stop smoking: Although not strictly a treatment, most doctors make this recommendation for people with emphysema (and everyone).
    Quitting smoking may halt the progression of the disease and should improve the function of the lungs to some extent.
    A doctor may be able to prescribe medications to help in breaking the addiction and can also recommend behavioral therapies, such as support groups.
    You and your doctor should work to find an approach that results in the successful end to cigarette smoking and, in the process, the beginning of improved lung function and quality of life.

    Bronchodilating medications: These medications, which cause the air passages to open more fully and allow better air exchange, are usually the first medications that a doctor will prescribe for emphysema.
    In very mild cases, bronchodilators may be used only as needed, for episodes of shortness of breath.

    The most common bronchodilator for mild cases of emphysema is albuterol (Proventil or Ventolin).
    It acts quickly, and 1 dose usually provides relief for 4-6 hours.
    Albuterol is most commonly available as a metered-dose inhaler or MDI, and this is the form that will be used most often for mild emphysema, with intermittent shortness of breath.
    When used for this purpose, some people refer to their albuterol inhaler as a "rescue" medication.
    It acts to rescue them from a more serious attack of shortness of breath.

    If you have some degree of shortness of breath at rest, a doctor may prescribe the albuterol to be given at regularly scheduled intervals, either through the MDI, or by nebulization. Nebulization involves breathing in liquid medication that has been vaporized by a continuous flow of air (in much the same way a whole-room vaporizer causes liquid droplets to enter the air by the flow of air through water).
    Nebulized albuterol may be prescribed once scheduled doses via inhaler are no longer adequate.

    Ipratropium bromide (Atrovent) is another bronchodilating medication that is used for relatively mild emphysema.
    Similar to albuterol, it is available in both an inhaler and as a liquid for nebulization.
    Unlike albuterol, however, ipratropium bromide is usually given in scheduled intervals. Therefore, it is not usually prescribed for "rescue" purposes. Atrovent lasts longer than albuterol, however, and often provides greater relief.

    Methylxanthines (Theophylline) and other bronchodilating medications are available that have varying properties that may make them useful in certain cases.
    Another fairly common medication is available in a tablet form.
    Theophylline (Theo-Dur, Uniphyl) is a medication given orally.
    It can have a sustained effect on keeping air passageways open.
    Theophylline levels must be monitored by blood tests.
    Too much theophylline can produce an overdose; too little, and there will not be enough relief of shortness of breath.
    In addition, other drugs can interact with theophylline, altering the blood level without warning.
    For this reason, doctors now prescribe theophylline very carefully.
    If you take theophylline, take the medication as prescribed and check with your doctor before starting any new medication.

    Steroid medications: They decrease inflammation in the body.
    They are used for this effect in the lung and elsewhere and have been shown to be of some benefit in emphysema.
    However, not all people will respond to steroid therapy.
    Steroids may either be given orally or inhaled through an MDI or another form of inhaler.

    Antibiotics: These medications are often prescribed for people with emphysema who have increased shortness of breath.
    Even when the chest x-ray does not show pneumonia or evidence of infection, people treated with antibiotics tend to have shorter episodes of shortness of breath.
    It is suspected that infection may play a role in an acute bout of emphysema, even before the infection worsens into a pneumonia or acute bronchitis.

    Oxygen: If you have shortness of breath and go to a hospital's emergency department, you often are given oxygen.
    It may even be necessary to give oxygen by placing a tube in your windpipe and allowing a machine to assist your breathing. In some cases, it may be necessary for you to receive oxygen at home as well.
    There are home-based oxygen tanks available and portable units that enable you to be mobile and engage in normal day-to-day activities.
    Oxygen Therapy/Ozone Therapy a different thing altogether something I would like add about at a later stage.
    I Have been using Home Salt Therapy via a Salt pipe I ll add a little info on this now.


    The benefits of salt therapy (also called Halotherapy) or speleotherapy are well known and documented in Europe.
    Halotherapy uses dry aerosol micro particles of salt and minerals to treat respiratory diseases and seeks to replicate the conditions of speleotherapy (from Greek speleos=cave), a treatment that has been practiced in old salt mines of Eastern Europe since the early 19th century.

    In the mid 18th Century a Polish health official Felix Botchkowski, noticed that the workers of salt mines did not get ill with lung diseases.
    He wrote a book about the effects of salt dust in 1843.
    His successor M. Poljakowski founded a Salt Spa in Velicko near Krakow, which is still in operation.
    During the Second World War salt mines were often used as bombproof shelters.
    After spending time there many people who suffered from asthma felt that their health had gotten better!
    Today there are many salt sanatoriums in Europe ( Austria , Hungary , Poland , Romania , Russia …).

    The Halotherapy belongs to the category of the physical therapies non-drug and non invasive treatments of diseases.
    In the former Soviet Union, medical researchers engaged in a concerted effort to develop physical therapies in order to avoid the costs and side effects of drug therapy as well as microbial and tumour resistance.
    Russia has become the world leader in developing and testing new and increasingly effective physical therapies.
    Many of the clinical trials have focused on Halotherapy as a treatment of asthma and chronic bronchitis and also very effective as a main or adjuvant therapy across the entire range of upper and lower respiratory tract diseases.

    Respiratory diseases are a major cause of morbidity and mortality worldwide.
    Most drug therapies of respiratory diseases have only palliative effects, and many have significant side effects, especially those with corticoids or steroids.
    So, a physical therapy like Halotherapy is greatly needed.

    Speleotherapy also makes a great demand on patients' time.
    The mines are not conveniently located for most people and the total cost is fairly significant.

    The effectiveness of speleotherapy is not acknowledged in all countries of the world, but in countries like Romania (Praid, Tg.Ocna, Seiged, Sovata, Slanic, Ocna ), Poland ( Wieliczka), Germany ( Teufelshöhle), Austria (Hallen, Solzbad-Salzeman ), Armenia, Belarus, Bulgaria, Hungary, Russia, Slovenia, Ukraine, Nakhichevan mines in Azerbaijan, the salt aerosol plays an important role in the treatment of chronic respiratory diseases, working well with or without medical treatment and without any known side effects.
    Because of these, pregnant women with asthma or other respiratory diseases could use this therapy without any harm to the child.
    Very well known and appreciated in these middle-eastern European countries, this therapy is covered by the public health care system.
    In Romania there are also many salt lakes - Sovata with 7 salt lakes, Ocna Sibiului with 52 salt lakes in S-W of Transilvania, very well known in the treatment of infertility, metabolic diseases, skin diseases.
    These salt lakes were usually formed by collapsing of salt caves ceilings.
    All these salt lakes have different salinity, increasing with deepness – from 9g/l to 320g/l.

    This salt therapy being very well known for its beneficial effects, a Romanian inventor put his mind at work and developed a device that is able to reproduce a speleotherapy micro environment in your home in an affordable and convenient way.
    Internationally recognized, with Gold and Silver medal at “Salon International des Inventions", Geneva and “World Exhibition of Innovation, Research and New Technology", Brussels , this Romanian invention brings new hopes in the natural treatment of chronic respiratory diseases.
    The inventor thought this device as an air salinizer that uses forced ionization of the indoor air by salt sublimation creating a micro climate of dry aerosol salt therapy in your living space. He used a natural process of salt crystallization to obtain salt micro crystals under 5µm in diameter, invisible to human eyes, being able to penetrate deep into the lung. The device uses only natural salt from within the mountain of salt, untreated or touched by the human processing technology.
    Based on clinical studies, the inhaled saline has bactericide, mucokinetic, hydrophilic, anti inflammatory properties, reducing inflammation in the whole respiratory tract, absorbing edema from the mucosa lining the airway passages leading to widening of the airway passages, restoring the normal transport of mucus and unclog blockages in the bronchi and bronchioles leading to rapid elimination of the residual tar and foreign allergens, all of these in a natural process.
    Edema of the nasal mucosa and the oropharynx and soft palate, causing nasal obstruction and snoring is diminished, leading to widening of the airway passage in the nose and the tubes of the sinuses and improving the sinuses drainage and reducing snoring.
    In the auditory tube, edema of the Eustachian tube causing ear infection, is also diminished, leading to widening of the airway passages, better drainage and better aeration behind the tympanic membrane.
    The salt therapy was found to have beneficial effects in the treatment of:

    Asthma and Chronic Bronchitis
    COPD (Chronic Obstructive Pulmonary Disease)
    Allergic Rhinopathy or Hay Fever
    Cystic Fibrosis
    Ear Infections
    Smoking Cough
    Various acute or chronic respiratory disease
    Reduce snoring and activates better sleep by clearing the airway passages in oropharyngeal region
    Increased resistance to Cold & Flu by opening and clearing the nasal airway and improving the drainage of the sinuses
    Humidifies the bronchial secretions reducing broncho-spasm and facilitating elimination of the smoke residual tar, phlegm expel and other allergens
    Improves the quality of the indoor air by eliminating the dust, cigarette smoke, bad odours, mould and mites, having bactericide reduction properties.

    The salt therapy is a natural method of therapy and does not involve any risk and is finally adapted to the living space.
    However, this is NOT a substitute for medical treatment and should only be used as an adjuvant helping to improve the quality of patients’ life, reducing the antibiotics and corticoids or steroids intake, reducing the rate of annual hospitalizations and decrease the frequency of respiratory diseases attacks.
    For more information, clinical studies and testimonials you can visit the web site.
    LTiba .

    Daily use of a Salt Pipe for at lest several minutes will produce beneficial effects in the following illnesses:

    - pollen allergy and other allergies of the respiratory tract
    - asthma, bronchitis;
    - whooping-cough, nasal catarrh, hay-fever, cold
    - infectious respiratory diseases
    - last but not least, the respiratory problems caused by smoking

    Dr. Hegyi Gabriella MD.PhD., Division leader doctor:

    Yamamoto Institute for Rehabilitation, Training institue of Semmelweis University (Complementive Medical Attendance) Budapest, 1196 Petofi u. 79. Hungary,
    Tel/ fax: +36 1 2813035 E-mail: drhegyi@elender.hu
    Medical inspection of the inhaler set called the Saltpipe

    The inspection of the instrument requested by: B.B. System Kereskedelmi és Szolgáltató Kft.
    (B.B. System Ltd. For Commerce and Services )
    1146 Budapest, Francia út 57/c. (repr.: Békefi Imre)
    The date of arrival of the instrument to our institute: 01. 09. 2002.

    Description of the instrument: A ceramic container, filled with a mixture of special salt crystals and minerals

    Application of the instrument: Setting it in the way of the inhaled air it helps the easier penetrability of the upper respiratory tructs with a special inhaling opportunity

    The basics of the functioning of the instrument:

    Inhalation is a special method for the local treatment of respiratory illnesses. The advantages of the inhalational method are:
    - Local effect
    - Higher salt concentration in the upper tructs
    - Fast results
    - The systematic effect is lower than in case of medication implied orally or injected
    - The instrument employs only fully natural resources

    The obtainable physiological effects are:

    - Mucolysis
    - Secretolysis
    - Eventually: bronchospasmolysis
    - In case of special material (minerals) antiphlogisticus effect

    Indications of the application:
    For the chronic illnesses of respiratory tructs (asthma, bronchiale), and for different forms of allergic rhinitis

    In case of long term application of the set the vital capacity intensifies and subjectively, it provides an improved general state of health

    Our Experiences:

    For the proper way of application the user must be trained and the process must be controlled, monitored later on.
    With the remission of the patien's condition an individual dose must be defined with other expression: the duration of application must be determined.
    The hypocamnia, caused by the forced - too hard - inhalation must be avoided so the aquirement of the proper technique is essential.
    In order to avoid contamination, and in order to keep the instrument clean, only one patient should use one set.
    During the application of the instrument we did not change the dosage of the patients.
    The voluntarily involved patients we randomly divided into the "treatment" and the "control" groups.
    The "treatment" patients used the instument several times a day for a determined period of time. Weekly and after two months we examined the patients - with attention to iron-, and vitalcapacity.
    Observations:The application of the Saltpipe is effective even in case of chronic upper respiratory illnesses, but in these cases there was a need for medicinary supplementation also.
    In case of the chronic illnesses, the patients reported about a subjectively easier breathing and inspirational experiences, which was officially confirmed by objective vitalcapacity measurements.
    Based on the above mentioned statements, the outcome of the adjuvant application of the instrument has proven to be EFFECTIVE in many of the cases.
    During the test period no side effects have been observed.


    I suggest the application of the "Saltpipe" instrument as a complementive, supportive method with the following completion:
    It must be distributed with a suitably informative and ethic description for users, which does not deceive the user and does not make him or her abandon the previously used traditional medicaments and treatment.

    Budapest, 08. 10. 2002.

    Dr. Hegyi Gabriella MD.PhD.
    Division leader specialist
    Dr. Ferenc Pátz

    Groups of patients consisting of 7 boys and 3 girls which :
    6 Asthma bronchiale
    2 Sinusitis maxillaris
    2 Laryngitis subglottica

    The youngest child: 3 years old
    The eldest: 16 years old
    Average: 9 years

    Average: 6 weeks. The longest: 2 months period. The shortest: 4 weeks period

    The product is catching the attention of both the children and the parents with its nice looks, especially with the latest elephant design, which does not give the impresson of a medicament.
    The description should be attached in the form of a little brochure, the method of application should be described in a more detailed, pointed, highlighted way /introduction, "what to do-s", and the importance of the daily, regular usage/.

    Because of the relatively short testing period, we could draw only a few conclusions.

    We received indisputably positive feedbacks from both of the patients suffering from recitive sinusitis.
    As a result of the application of the set, in the first 2-3 weeks the nasal discharge intensified, later the intensity of the mornig and evening coughings decreased.

    In case of one of our two patients suffering from the illness of pseudo-croup, we did not experience any significant changes, the "barking-like" coughing did not emerge less frequently, its progress was similar to the previous way.
    There wasn't much of a chance for the good outcome anyway, because of the conditions created by the possibility of virus infection.
    In the other case, the patient did not have coughing seizures in the testing period, but it might be a coincidence, because of the short period (again) we cannot give a "clear-cut", certain explanation.

    In case of our asthmatic patients (who were represented in a greater number) we would have also needed longer time for drawing more reliable conclusions.
    Since at wintertime the chance of infection is greater and the existance of allergens is not significant, these circumstances also influenced the effects of the instument.

    In two cases, the parents experienced that the relief from the asthmatic seizures come sooner and the torturing coughing ended faster.

    In two cases the frequency of seizures decreased and it the last two cases we did not observe any significant changes.
    Dr. Valéria Burzuk

    Notices about the experiences in connection with the Saltpipe used in the case of 10 patients suffering from Chronic Bronchitis, COPD and Asthma Brochiales:

    10 patients were using the Saltpipe in the period starting in October 2002, finishing in February 2003, for 2-3 months of duration.
    These patients were suffering from respiratory illnesses; 3 of them suffered from chronic bronchitis, 7 of them from asthma bronchiales: 2 of this 7 people had severe bronchitis and COPD.
    4 patients out of the 10 were females and 6 of them were males.
    2 patient between the age of 50 & 55, 3 between the age 55 & 60, 2 of them were between 60 & 65, and only one of the patients was above 70.
    Out of these 10 patients 6 suffers from heart diseases, which aggrevated the applicability of antispasmiodic sprays - for the bronchial tubes - because of the side effects which exert the functioning of the heart.
    I was trying to choose patients whose illness was severe (chronic bronchitis, COPD, and/or ashtma bronchiale).
    The experiences of the patients show that the Saltpipe helps to dissolve sediments, helps in the process of discharge and doing so, easens their breathing.
    As a doctor, I found the Saltpipe a very effective complementary tool in the therapy of patients with respiratory illnesses.
    We can almost equalize the effects of the mineral-filled air inhaled through the Saltpipe with the effects of the salt caverns (apart from the fact that the temperature of air inhaled through the Saltpipe is identical with body temperature), further more, it is more moderate from a financial point of view than the expenses of salt cavern therapies. As a summery I would like to conclude the followings:
    The secretion-discharge is easier and so, the breathing of the patient becomes more relief. I also observed that the speed of the air-stream in the small bronchial tubes accelerated which results in an easier breathing.
    I find the application fo the Saltpipe indisputably beneficial.
    I owe you my gratitude - also in the name of my patients - for the Saltpipe.
    Aerosol Salt Treatment of Respiratory Diseases

    Halotherapy (HT, from Greek halos=salt) uses dry aerosol microparticles of salt and, in one version, minerals to treat respiratory diseases.
    HT seeks to replicate the conditions of speleotherapy (from Greek speleos=cave), a treatment that has been practiced in old salt mines of Eastern Europe since the early 19th Century.

    Halotherapy belongs to the category of the physical therapies--non-drug treatments of diseases, many associated with the spa treatments of Eastern Europe.
    In the former Soviet Union, medical researchers engaged in a concerted effort to develop physical therapies in order to avoid the costs and side effects of drug therapy as well as microbial and tumor resistance.
    Russia has become the world leader in developing and testing new and increasingly effective physical therapies.

    Most of the dozens of clinical trials thus far, mainly reported in Russian-language journals, have focussed on HT as a treatment of asthma and chronic bronchitis.
    But HT may also be effective as a main or adjuvant therapy across the entire range of upper and lower respiratory tract diseases and potentially against systemic diseases as well.

    Respiratory diseases are a major cause of morbidity and mortality worldwide.
    Asthma has become ever more prevalent in industrialized societies, with special impact on children.

    Meanwhile, cigarette smoking has spread chronic bronchitis and emphysema everywhere; in developing countries biomass cooking smoke has a similar devastating impact on women and children.
    The situation in especially bad in China, with its 350 million smokers and terrible air pollution.

    Most drug therapies of respiratory diseases have only palliative effects, and many have significant side effects.
    So a physical therapy like HT is much needed. HT's excellent action and modest cost make it a very attractive kind of medicine.


    It is likely that miners and others knew about the beneficial health effects of the microclimate of salt mines for centuries before they were first described in a book published by a Polish physician in 1843.
    Since then, the practice of bringing patients with respiratory diseases down into salt mines for cures gradually spread throughout Eastern Europe, and it has become a standard feature of spa treatment there.

    By its very nature, speleotherapy resists scientific norms.
    The reported healing and invigorating effects of the microclimate of salt mines are variously ascribed to the microparticles of salt floating in the air, the temperature, the relative humidity, the near or total absence of pathogens and allergens, the effects of radiation from minerals, and the tranquillity of the setting.
    But it is difficult to determine the relative influence of these factors, and presumably some synergy exists.
    In addition, each chamber in each mine has a distinct microclimate. Conducting clinical trials in such conditions is not easy.
    Often speleotherapy has been combined with other modalities.
    And many of the early clinical trial reports lacked scientific rigor.

    Speleotherapy also makes a great demand on patients' time.
    The mines are not conveniently located for most people.
    The total cost is fairly significant.
    Determining a specific dose and tracking long-term effects of speleotherapy have proven very elusive goals.

    Nonetheless, various clinical trial reports and the favorable outcomes for many individual patients have led to growing scientific attention and a devoted following for speleotherapy (for a sample report, see Horvath, 1986).
    They also gave the Soviet (now Russian) space agency the idea of developing microclimate optimization devices for cosmonauts that would replicate the microclimates of salt mines. Most of this work has been done in St. Petersburg, which is now the location of the leading Russian HT company, Aeromed Ltd, and of the Arsenal Design Bureau, which works on the salt + mineral approach.

    HT Devices

    In the 1980s the Russians began to build halochambers that recreated in clinics the microclimate of salt mines.
    These halochambers have floors and walls lined with rock salt (halite).
    Patients sit in the halochamber for an hour per session while music and pleasant videos are played to create a relaxed mood.
    Halochambers are certified as medical devices in Russia, are in use in Eastern Europe, and are starting to spread to North America.

    Another approach has been the desktop HT device, which has tubes for breathing in the aerosol salt or simply fills the air with microparticles of salt.
    Thus far no multimineral aerosol appears to have been supplied this way, though halochambers have been lined with silvinite, the rock from potash mines that contains about 60 percent sodium chloride, 35 percent potassium chloride, and 5 percent of other minerals. Pure halite is the precipitate from the shores of ancient seas, while silvinite results from the evaporation of a dead sea.
    Often a desktop HT device is used in combination with a halochamber.

    A ceramic salt pipe from Hungary represents a third approach.
    The patient breathes in gently through the mouth, then exhales through the nose.

    A fourth, popular device is the rock crystal lamp (Pakistan) or salt lamp (Poland), which is comprised of a largish piece of rock salt with an attached light bulb that glows through the salt and whose heat causes microparticles to become airborne.

    Serious clinical studies have been done of the first two methods, where the number of microparticles per cubic meter is monitored, permitting accurate dose measurement.
    The ability to deliver a specified dose represents a major advantage of halotherapy over speleotherapy.
    Still, speleotherapy retains importance as a source of scientific evidence regarding the as-yet not well-characterized, multiple factors that deliver the therapeutic effect.
    Depending on the conditions of a certain salt mine or cave, speleotherapy might also prove more effective than halotherapy in a given case.


    Aerosolized microparticles larger than 10 microns in diameter are caught in the upper airways and transported up and out of the respiratory tract by the mucociliary system.
    In the range of 5-10 microns, they penetrate into the trachea and central bronchial area, but no farther.
    Only below 5 microns do the microparticles penerate deep into the lungs, though the larger microparticles have useful effects in the upper respiratory tract.
    In the range of 0.1-2.5 microns--the same size as the most damaging microparticles from auto and industrial pollution, and invisible to the human eye--the microparticles of salt penetrate into every corner of the bronchi, bronchioles, and alveoli and deposit upon the surface.
    Even though the salt microparticles spread over an area in the alveoli roughly the size of a tennis court, only a few milligrams of salt are needed.
    So there need be no concern about the possibility of excessive salt intake from halotherapy in the case of hypertensive patients.

    The extremely small size, relatively low amount, and slow dosing of the microparticles also make them much less likely to provoke a hyperreactive response in asthma patients than moist hypertonic saline.
    The hygroscopic characteristics of moist particles make them grow significantly during transit and therefore to deposit mainly in the upper respiratory tract and in the central area of the trachea and bronchi.
    Still, studies have shown that moist particles of salt from hypertonic saline have beneficial effects in cystic fibrosis, for instance, at least in the short term (Wark and McDonald, 2004).

    A significant parameter for HT devices, therefore, is the fraction of the microparticles produced that is below 2.5 microns.

    According to many authors, maintaining a room temperature in the vicinity of 18-24° C and a relative humidity around 50% can conduce to better treatment outcomes.
    Devices can be set to emit different amounts of salt microparticles-e.g., four levels from 1 to 16 mg/m³, monitored by a microparticle counting device.

    Another parameter of note is the negative electrical charge on the particles, which has been measured at 6-10 nK/m³ (Chervinskaya, 2002).

    One last bit too add I also have changed from Refined salt to Unrefined Salt in my eating habits.
    Added below in a 2nd post
  18. Stylopora

    Stylopora Full Member ECF Veteran

    Jan 29, 2009
    Cambridgeshire UK
    A Pillar of Salt
    Jon Barron
    A couple of issues ago, I made a passing comment about the AMA's recent public statement concerning salt, questioning both the validity of their pronouncement and their qualifications to make such a statement in the first place. What a furor it created!
    Since then, I have been interviewed by several newspapers, magazines, and appeared on radio talk shows -- all to talk about salt. Who knew it was such a big deal? But since it is, it seems worthwhile to revisit the subject again in more detail.

    The primary issue that got lost by the AMA is that not all sources of sodium and salt are the same.
    As far as the body is concerned, there is no connection between the chemically-cleansed sodium chloride table salt you buy in the supermarket (which is also added to virtually every processed food you buy) and the mineral rich organic unrefined sea salt available in health food stores. One can kill you; the other heals you. In fact, it's essential for life.

    Of course, everyone can agree that just like anything else, salt or sodium should not be consumed in excess. (But then again, that's true of water and oxygen as well.) Which brings us back to why the AMA came out with a warning at all:
    Americans are consuming ever higher amounts of sodium, up to 6,000 milligrams a day, instead of the recommended 500 to 2,000 milligrams per day.
    These high amounts, in a form that is unfriendly to the human body and with no ancillary trace mineral benefits, are what lead to serious health problems.

    However, this is not necessarily the heart of the debate.
    The issue is that the AMA is against all forms of salt, a broad-brush condemnation designed more for media sound bites than to truly advance the cause of health.
    This is a point echoed in a U.S. Food and Drug Administration article A Pinch of Controversy

    Shakes Up Dietary Salt:
    "Now modern technology has made salt readily available and at a price almost anyone can afford.
    As a result, many of us take salt and its merits for granted. But scientists keep salt in the news by debating its role in a healthful diet.
    At times, discussion and controversy threaten to obscure salt's importance and to confuse thoughtful consumers."
    So let's examine the true nature of salt to gain an understanding of how different types of salt act in our bodies.
    And let's also examine some real health issues connected with salt; and finally, let's talk about how to choose and balance salt in your diet.

    Brief History of Humans and Salt
    "Worth its weight in gold" is an expression that served well for salt in ancient times.
    The history of salt is sprinkled with piracy, war, economics, religion, and health.
    In fact, the next time you contemplate your current salary, consider that the very word "salary" is derived from the Latin word sal because Romans often received their pay in salt.
    If this is hard to accept, consider that during the Age of Discovery, Africans and European explorers traded an ounce of salt for an ounce of gold -- even-steven.
    Around 110 BC, salt trade was so valued that salt piracy was punishable by death.
    And Mahatma Gandhi even used salt as major leverage against the British Empire in 1930 when he led thousands of people to the sea to collect their own salt in order to avoid the salt tax imposed by the British.

    The Importance of Salt
    One point everyone can agree on is that the body needs sodium chloride to function.
    If we look at the big picture for a moment, we can recognize that:
    A human embryo develops in salty amniotic fluid.
    Our developed human bodies possess three distinct fluid systems - blood plasma, lymphatic fluid, and extracellular fluid -- all salty fluids.
    As a main component of the body's extra-cellular fluids, salt helps carry nutrients into the cells.
    It also helps regulate other body functions, such as blood pressure and fluid volume, and works on the lining of blood vessels to keep the pressure balance normal.
    The concentration of sodium ions in the blood is directly related to the regulation of safe body-fluid levels.
    0.9% sodium chloride in water is isotonic with blood plasma.
    It is known medically as normal saline.
    It is the mainstay of fluid replacement therapy that is widely used in medicine in prevention or treatment of dehydration, or as an intravenous therapy to prevent hypovolemic shock due to blood loss.
    The propagation of nerve impulses by signal transduction is regulated by sodium ions. (Potassium, another metal closely related to sodium, is also a major component in the same body systems).

    Sodium is an energy carrier.
    It is also responsible for sending messages from the brain to muscles through the nervous system so that muscles move on command.
    When you want to move your arm or any muscle in the body, the brain sends a message to a sodium molecule that passes it to a potassium molecule and then back to a sodium molecule etc., etc., until it gets to its final destination and the muscle moves.
    This is known as the sodium-potassium ion exchange.
    Therefore, without sodium, you would never be able to move one muscle of your body.

    Salt VS Sodium
    Although the words salt and sodium are often used interchangeably when it comes to nutrition, they are not the same.
    Salt is sodium chloride (NaCl) and Sodium (Na) is, well, just sodium -- a soft metal occurring in isolation only on the periodic table of elements or in a lab.
    While it is correct to say that our bodies need sodium, nature has not designed sodium as a solo player but offers it in a complex consisting of natural salt and essential trace minerals, as well as providing it in a variety of foods.
    Some foods naturally high in sodium/salt are fish, eggs, nuts, prawns, crabs, lobsters and seaweed (Note: all of these natural sources of salt are also natural sources of iodine.)
    Other naturally occurring sources of sodium (although not quite as high) are celery, carrots, cauliflower, pineapples, jackfruits, and even fresh cow's milk. And then, of course, there is pure, natural unrefined salt -- the salt once worth it's weight in gold and the focus of this newsletter.
    So, with all these great natural sources of sodium, why do we have refined table salt?
    Good question.

    A Modern Misconception
    Much like the story of refined flour it seems to come down to aesthetics and economics.
    Unrefined salt tends to be off-white or gray in color, whereas refined table salt is bright white. It's prettier.
    Unrefined table salt tends to clump in the presence of moisture and be unusable in shakers. As for table salt, what's the slogan for Morton® Salt? "When it rains, it pours."

    Since unrefined table salt tends to clump in the presence of moisture, grocers and suppliers have to eat the cost of salt that has to be pulled from shelves when it becomes unsellable. Not so with refined salt that doesn't clump.
    In other words, refined salt is more profitable.
    Refined table salt has added iodine to make up for the nutrients lost in refining.
    As a point of comparison, here's the story of white flour.
    White flour is "prettier" than brown flour, aesthetically more appealing.
    White flour bakes lighter in texture because it has no bran.
    White flour doesn't spoil because all the beneficial oils have been removed, which means it lasts far longer on the grocer's shelf than whole wheat flour.
    Again, economically more profitable.
    White flour is "enriched" to put back a small amount of the nutrients lost in refining.
    And white flour products are now getting added fiber (sawdust in some cases) and essential fatty acids to improve their nutritional profile.
    Salt and flour have suffered the same fate.
    The process of turning naturally occurring non-white salt into the white-powdery-easily poured table salt involves a distinct trade-off between health and aesthetics/profitability.

    And there's one other financial reason for the dominance of refined salt in the market.
    Only 7% of salt goes for food; the other 93% goes to industry.
    Industry requires chemically pure sodium chloride for manufacture of explosives, chlorine gas, soda, fertilizers and plastics.
    In effect, table salt represents a "cheap" production overrun.

    Two Salts
    In today's market, we now have two distinct choices when it comes to salt: unrefined and refined. Unrefined salt (sea salt) is 84% sodium chloride and 16% other minerals.
    Refined salt is 97.5% sodium chloride and approximately 2.5% chemical additives.
    Unrefined salt is at heart sea salt, but can come from two sources: either freshly dried from the sea, as in Celtic Sea Salt, or mined from ancient inland ocean beds as in Himalayan Salt.

    In either case, the salt is a naturally occurring complex of sodium chloride, major minerals such as calcium and magnesium, and a complete complement of essential trace minerals.
    This is the form of salt the body recognizes and is designed to use.
    Note: much of the salt labeled "sea salt" is actually refined table salt unless the package is clearly labeled "unrefined." (This is also true for Kosher salt!)

    Refined salt, on the other hand, is a manmade creation of the last century that contains anti-caking chemicals (with very important health consequences as we shall see in a minute) and added iodine.
    Iodine was added for people who lived inland and at one time did not benefit from natural iodine found in seafood.
    Truth be told, all refined table salt is actually sea salt at heart, either refined from the sea (brine sourced) or found in salt mines created by ancient seabed deposits known as halite. Refined salt is processed at high temperatures altering the molecular structure of the salt (not good) and removing the beneficial trace minerals.
    The human body doesn't like it.

    Refined and unrefined salt act and react differently in our bodies.
    Fundamental differences

    Unrefined sea salt
    Natural salt is a prime condiment that stimulates salivation and helps to balance and replenish all of the body's electrolytes.
    The natural iodine in these salts protects against radiation, atomic fallout, and many other pollutants.
    Unrefined sea salt supplies all 92 vital trace minerals, thereby promoting optimum biological function and cellular maintenance:

    Here is a partial list of the minerals found in unrefined salt and their function in human metabolism:

    Sodium: Essential to digestion and metabolism, regulates body fluids, nerve and muscular functions.

    Chlorine: Essential component of human body fluids.

    Calcium: Needed for bone mineralization.

    Magnesium: Dissipates sodium excess, forms and hardens bones, ensures mental development and sharpens intelligence, promotes assimilation of carbohydrates, assures metabolism of vitamin C and calcium, retards the aging process and dissolves kidney stones.

    Sulfur: Controls energy transfer in tissue, bone and cartilage cells, essential for protein compounds.

    Silicon: Needed in carbon metabolism and for skin and hair balance.

    Iodine: Vital for energy production and mental development, ensures production of thyroid hormones, needed for strong auto-defense mechanism (lymphatic system).

    Bromine: In magnesium bromide form, a nervous system regulator and restorer, vital for pituitary hormonal function.

    Phosphorus: Essential for biochemical synthesis and nerve cell functions related to the brain, constituent of phosphoproteins, nucleoproteins and phospholipids.

    Vanadium: Of greater value for tooth bone calcification than fluoride, tones cardiac and nervous systems, reduces cholesterol, regulates phospholipids in blood, and a catalyst for the oxidation of many biological substances.

    Refined table salt
    Inorganic sodium chloride upsets your fluid balance and constantly overburdens your elimination systems, which can impair your health.
    When your body tries to isolate the overdose of refined salt you typically expose it to, water molecules must surround the sodium chloride molecules to break them up into sodium and chloride ions in order to help your body neutralize them.
    To accomplish this, water is taken from your cells, and you have to sacrifice the water stored in your cells in order to neutralize the unnatural sodium chloride.
    This results in dehydrated cells that die prematurely.
    Refined table salt contains added iodine, which may indeed have helped eliminate the incidence of endemic goiter, but has conversely increased the incidence of hypothyroidism.
    Refined table salt lacks all trace minerals.
    Refined salt contains anticaking agents such as ferrocyanide, yellow prussiate of soda, tricalcium phosphate, alumine-calcium silicate, sodium aluminosilicate.
    All work by preventing the salt from mixing with water, both inside the box and inside the human body.
    This prevents the salt from doing one of its important functions in the organism: regulating hydration.
    The problem of excess salt in the diet

    Salt and Water
    Fish survive by ex......g large amounts of salt through their gills.
    Humans excrete salt through their kidneys.
    But there is only so much salt that can be urinated away, and salt-sensitive individuals excrete less sodium than normal.
    If the body can't reduce the salt, the next best way to hit the right level is to increase the amount of water.
    This causes the body's extremities to swell up.
    If you're not drinking enough water, the body finds the extra water it needs by robbing its own cells.
    In extreme cases, neurons shrink and begin to stretch; brain and spinal membranes may begin hemorrhaging.
    The brain shrinks.
    Too high a concentration of salt in the body can lead to irritability, muscle twitching, seizures, brain damage, coma, and sometimes death. Usually, though, the results aren't quite so drastic.
    Dr. Myron Weinberger, an Indiana University medical school professor who authored the salt sensitivity study, says that given the "horrendous excess of salt that we end up with every day," some individuals can't get rid of it all, especially those born with subtle kidney problems that may go undiagnosed.
    Part of the problem is the chemical attraction between sodium and water.

    High levels of sodium in the diet combined with low water consumption leads to hypertension. "Every grain of salt that is retained in the body carries with it 20 times its weight in water which increases the (amount of) fluid in circulation," Weinberger said. "If you think of the blood vessels as piping, as you push more fluid in them, then the pressure goes up."

    Choosing and balancing salt in your diet.
    Unfortunately, you can't rely on fruits and vegetables any more for your trace minerals: they just don't contain them.
    Even organic fruits and vegetables are largely deficient, unless the grower goes to the extra expense of remineralizing the soil.
    In the end, you have to supplement either with unrefined sea salt or with a trace mineral supplement.
    Of course, we can all agree on one thing: a healthy diet is a diet in moderation.
    Unfortunately, refined salt addiction is perhaps as prevalent and subtly dangerous in modern society as drug addiction, poor diet, and a sedentary lifestyle.
    Excess refined salt increases appetite and decreases bone density. Hmmm!
    The bottom line is unrefined natural sea salt is as essential to life as oxygen, water, vitamins, proteins and essential fats -- in conscious moderation of course.
    The health benefits of unrefined salt must not be overlooked based on an overgeneralization in salt guidelines.
    In that light, I recommend:
    Use unrefined sea salt (Celtic, Himalayan, etc.) instead of refined table salt.
    Use it in moderation.
    Read labels and back way down on sodium in packaged foods.
    Minimize fast food consumption since most fast food is off the charts when it comes to sodium.
    Avoid salt-based household soft-water systems.
    They can significantly increase the sodium levels in your body.
    Hydrate sufficiently (but not to excess).
    Keep your kidneys functioning properly. Twice a year (more often if you have kidney problems) use a bottle of chanca piedra or a kidney flush formula.

    Index of archived newsletters and reports
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    Baseline of Health Foundation
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  19. Stylopora

    Stylopora Full Member ECF Veteran

    Jan 29, 2009
    Cambridgeshire UK
    The salt you buy at the store is only sodium chloride; all of the other beneficial elements have been removed.
    They then refine this salt.
    This is where things go wrong, at least in terms of your health.
    The salt is refined to remove impurities, to make it attractive and uniform in appearance, and to extract most of the mineral elements.
    When they have finished refining your salt, it looks great, and flows easily out of your salt shaker, but 82 of the 84 mineral elements have been extracted.
    They have added chemical additives which bleach the salt whiter, prevent water absorption while the salt is in the box, make the salt flow freely in your salt shaker, and add iodine and iodine stabilizers.
    The chemical additives which prevent the refined salt from absorbing water while it is in the box also prevent the refined salt from being properly absorbed in your body.
    This is why we are constantly being told that it is harmful to our health to consume too much salt.
    Natural salt, which has not been refined, can be consumed in any amount.
    As a matter of fact, it is impossible to consume too much natural unrefined salt! Why? Because the body, with its natural affinity for unrefined salt, will simply pass the excess unrefined salt out of our bodies.
    Not all sources of sodium and salt are the same.
    As far as the body is concerned, there is no connection between the chemically-cleansed sodium chloride table salt you buy in the supermarket (which is also added to virtually every processed food you buy) and the mineral rich organic unrefined sea salt available in health food stores.
    One can kill you; the other heals you. In fact, it's essential for life.
  20. Stylopora

    Stylopora Full Member ECF Veteran

    Jan 29, 2009
    Cambridgeshire UK
    Still can't find how to delete any of my posts
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