Smoke Gets In Your Baby

H/T Harley, I’ve been musing over this all day, on and off :

Atherosclerosis in children can begin in the womb as passive tobacco smoke crosses the placenta, leading to low birth-weight and impaired lung development. The condition can lead to blood clots and strokes later on in life. (my emphasis)

Smoke crosses the placenta?

I wouldn’t mind if they’d said “some of the constituents of tobacco smoke”. But they didn’t. They said “smoke”. And that meant that there’s billowing smoke inside pregnant women, and their babies are inhaling it. Well, how else does it lead to “impaired lung development”?

Not being a woman, I’m not much of an expert on gynaecology, mostly because I don’t expect to get pregnant any time soon. But I always had the impression that babies don’t actually start breathing until they are born, very often with a smack on the back to help them get started, as shown in countless movies. And the reason the little critters don’t breathe is because there isn’t any air in there, and they float in amniotic fluid. Perhaps an experienced mother reading this can help out here.

But then, if tobacco smoke can get in, I suppose that air must be able to as well. So maybe a womb is a big airy place like Victoria station. In fact, if tobacco smoke can get to a developing baby, then it must be able to get absolutely anywhere. So it’s not just that a womb is like Victoria station, but that the whole interior of the human body is like Victoria station.

We must all be hollow, and when we smoke a cigarette, it must fill up every nook and cranny inside us, from the tips of our toes to the insides of our empty heads. And here was me thinking we just breathed it into our lungs, and the rest of our bodies were full up with hearts and kidneys and intestines and brains and bones and blood vessels, and it was next to impossible for smoke to get anywhere, particularly down arms and legs.

And then I thought, well, if we’re all hollow inside, like inflatable plastic dolls, then it ought to be possible for us to be squeezed down into a really small bundle of skin for the purposes of air flights, and re-inflated when we got to the other end. I wondered if Easyjet did this yet, for a small extra charge? Perhaps that’s how they managed to fit so many people onto their cheap flights, and didn’t offer any meals? Because when you’ve been rolled up into a bundle, it’s a bit hard to eat anything?

Anyway, the more I thought about it, the idea that tobacco smoke could get into developing babies’ lungs began to do extreme violence to my understanding of human physiology, and replace it with a notion of the interior milieu of human beings as a pretty airy place, like Victoria station, in which tobacco smoke could easily blow from one end to the other, and where there might even be No Smoking signs everywhere. And it also began to do damage to my idea of air travel. In fact, it began to completely dismantle everything I thought I knew about absolutely everything.

I think I’m going to write to Dr Julia Dratva, of the Swiss Tropical and Public Health Institute, and ask her how tobacco smoke manages to get to the placenta. Perhaps she’ll write back and say that it just blows in there, because a woman’s womb is much like Victoria station, and smoke easily blows around inside it, and that we’re all hollow inside, a bit like inflatable dolls, and we could have the air inside us squeezed out, and be rolled up into little bundles, for easy transportation by Easyjet.

But if she replies and says, “Oh no, smoke doesn’t get in there. It’s only some of the constituents of smoke that get there – via the blood stream from the lungs,” I’ll ask her to request that the Washington Post correct their article, by adding “the constituents of”, and to apologise to any readers who gained the misapprehension that people were hollow inside like Victoria station, and could have the air squeezed out of them, and be rolled up into little bundles for easy transportation.

Like Frank Davis in England, for example.

Anyway, here’s Bryan Ferry singing Smoke Gets In Your Eyes…

And once it’s got in there, it gets into your baby’s eyes, and shrivels them up into little black prunes. And it causes cataracts too. Not just in your own eyes, but also in the eyes of anyone you make eye contact with, and thus pass the smoke from one eye to another eye. In fact it causes cataracts in anything you look at, including washing machines. It’s true! I read it somewhere, while I was on an Easyjet flight, rolled up in a little bundle, and squinting at a travel magazine, with one eye inflated with tobacco smoke.

About Frank Davis

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18 Responses to Smoke Gets In Your Baby

  1. jaxthefirst says:

    Right at the beginning of the article it says “Aug. 25 (Bloomberg)” The very inclusion of that name anywhere on any article about anything health-related indicates that some degree of histrionic lunacy is bound to follow.

    But what does it mean, exactly? That Nanny B funded the study (wouldn’t surprise me)? Or that his press office submitted the Press Release (wouldn’t surprise me, either)?

    • Frank Davis says:

      I noticed the Bloomberg thing too. But, despite the proprietor being a nutter, Bloomberg reporting generally seems pretty straight. Or am I mistaken?

      • mikef317 says:

        As opposed to the man, Bloomberg the business is a large and legitimate news organization (and would be as biased about smoking as any other news organization like the Washington Post). While they cover a variety of subjects, mostly Bloomberg specializes in business / financial news and do it quite well as far as I know.

        Typical of science “reporting,” someone takes a press release, rewords it a bit, adds some boilerplate about how many people smoking kills, and publishes it as news.

        The link below is to the Bloomberg internet site. They also have print publications and a cable TV station (where I can watch the opening of the London stock market if I stay up late enough).

  2. Frank, you’ll notice that the part of the article about fetuses and lung development does not come FROM THE STUDY… but just from bubbly antismoking statements that are being tied to the story about the study. Slick, eh? And I bet you (and 99% of the article readers) thought they’d actually done a study finding evidence of such.

    Let me fill you in on what this statement is probably based on. Here’s a passage from my eventually forthcoming “TobakkoNacht” section that analyzes this sort of deceptive nonsense as it applies to news stories about a “thirdhand smoke” study and which was probably the basis for that statement:


    The research, headed by Dr. Virender Rehan, a principal investigator at Los Angeles BioMed and UCLA and the corresponding author of the study, was published in the July 2011 issue of the American Journal of Physiology, and was, as usual for this sort of stuff, headlined all over the world. With “Thirdhand Smoke” abbreviated as THS here, some of the typical headlines were “THS hurts infant lungs,” “THS Dangerous for Babies,” “THS dangerous to unborn babies’ lungs,” and “THS affects infant’s lungs,” while quotes from those stories included such notes as:

    +++ {this +’s section contains highlighted quotes from the news stories}
    Prenatal exposure to toxic components of a newly recognized category of tobacco smoke—known as ‘thirdhand smoke’—can have as serious or an even more negative impact on an infant’s lung development as postnatal or childhood exposure to smoke … Thirdhand smoke is the newly formed toxins from tobacco smoke that remain on furniture, in cars, on clothing and on other surfaces—long after smokers have finished their cigarettes.… a stealth toxin because it lingers on the surfaces in the homes, hotel rooms, casinos and cars used by smokers… babies (are) especially vulnerable to the effects of thirdhand smoke … The dangers of thirdhand smoke span the globe … more damaging than secondhand smoke or firsthand smoke … the alarming data clearly highlight (that) pregnant women should avoid homes and other places where thirdhand smoke is likely to be found to protect their unborn children against the potential damage these toxins can cause to the developing infants’ lungs.

    Clearly a rather scary picture. An invisible stealth toxin. More damaging than firsthand smoke. Babies especially vulnerable. A danger that spans the globe. Several of the stories emphasized the concept that even touching a surface in a home where smokers might have smoked a long time in the past could lead to a lifetime of respiratory suffering for the innocent unborn.

    None of the stories went into any detail at all about the actual research other than occasionally mentioning a few of the scary chemical names of the “stealth toxins” left behind by smokers. In order to find out more, I had to request a copy of the study itself from the researchers. Given all that I’ve seen I should not have been surprised by what I found. Nonetheless, I was.

    The study didn’t examine mothers touching surfaces in homes where someone smoked in the past. It didn’t examine mothers being hugged by smokers. It didn’t even examine mothers being touched by someone who might have once walked through a room where George Washington might have smoked a pipe before sleeping and leaving one of his ubiquitous signs.

    The study simply once again examined rats. More specifically it examined baby rats. More specifically than that it examined tiny unborn baby rats who were bloodily ripped out of their mommy rats’ guts and then torn wide open so that their innocent little unborn rat lungs could be yanked out, thrown on a slab, chopped brutally into teenie-weenie one millimeter cubes, and then soaked with concentrated chemicals that can just barely be detected at picogram and nanogram levels in nitrous-acid filled rooms where people have smoked heavily. Those little bits of tortured fetal rats’ lungs were then examined and some of their cells were found to have suffered damages that could be related in some vaguely arguable way to abnormalities in human lungs that might sometimes correlate with conditions like asthma.

    None of that information was given in the news stories. Almost none of it was provided in the study abstract, and the little that was provided there would have been overlooked by most reporters after they were hit with the following opening line: “The underlying mechanisms and effector molecules involved in mediating in utero smoke exposure-induced effects on the developing lung…”

    If any reporters did manage to stay awake after that, rather than simply heading straight to the press release with all its juicy quotes (and no hint of rodents) they might have noticed the one mention of the word “rat” in the following excerpt: “Fetal rat lung explants were exposed to nicotine, 1-(N-methyl-N-nitrosamino)-1-(3-pyridinyl)-4-butanal (NNA), or 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)” Even that explicit mention however would have been blasted out of almost anyone’s consciousness once they hit “breakdown of alveolar epithelialmesenchymal cross-talk, reflecting lipofibroblast-to-myofibroblast transdifferentiation.”

    No one, anywhere in the world, reading any news stories that I was able to find in English, would have had the slightest clue that this study had done anything other than observe the horrible effects of thirdhand smoke exposure on human children who had suffered an unwise visit to grandmom in the old family home where grandpop had occasionally smoked a pipe by the fireplace 20 years earlier.


    Just another example of the lies used by Antismokers in building their hate campaign.

    – MJM

    • Frank Davis says:

      Just another example of the lies used by Antismokers in building their hate campaign.

      Well, yes. But they’re also building a separate reality as well. One in which tobacco smoke can reach the placenta. They’re creating a new reality in which tobacco smoke has magical properties (I’m not the first to notice this, by any means). They’re creating an entire new, magical world. And this magical world is gradually dissolving the ‘real’ world in which magical things can’t actually happen.

      • harleyrider1978 says:

        Frank its fun busting that magical world ehh! Hats off to Mike for his in depth analysis of the junk science.

    • Margo says:

      MJM, this is a brilliant piece of writing.

  3. harleyrider1978 says:

    The common knowledge is nothing crosses the placental barrier! Thats what Ive read countless times and why these rabid nazis have been so set on finding some way to link a passage! How do you seperate the normal chemical constituents of tobacco smoke and the real world………Its simple you cant. Thats why these nazis chose nicotine as we all know to try and show exposures. There was one other chemical I read about somewhere that the tobacco companies said should be used during the OSHA discussion:

    OSHA: Proposed Standard For Indoor Air Quality: ETS Hearings, January 17, 1995

    Next, Paul Nelson, who obtained his Ph.D. in analytical chemistry from Georgia Tech in 1987, will talk about the severe limitations in the use of nicotine and cotinine to precisely predict ETS exposure.

    In her Figure 1, which I have reproduced here in slide 6, Dr. Hammond shows results from one experiment done by another researcher in which both nicotine and RSP increase more or less linearly with the number of cigarettes smoked. However, the data for 3-ethenylpyridine do not appear to increase in the same fashion. Not only is this result for 3-ethenylpyridine implausible, it is incorrect.

    Shown here in slide 7 are the ETS vapor phase marker results from a similar experiment conducted at R.J. Reynolds. These data demonstrate two points.

    First, 3-ethenylpyridine increases linearly with the number of cigarettes smoked. Second, 3-ethenylpyridine also tracks exactly the vapor phase of ETS, as measured by carbon monoxide and flame ionization detector response, which is an indication of the total volatile organic compounds present in ETS.

    As you can see, although nicotine increases in a similar fashion, it actually overestimates the vapor phase of ETS. This overestimation becomes more predominant with increasing levels of smoke.

    Myosmine also exhibits the same trend as nicotine, although to a lesser extent.

    Dr. Hammond levies an additional criticism against 3-ethenylpyridine. She claims that 3-ethenylpyridine is not as sensitive a marker as nicotine in detecting ETS. This also is not true.

    In 1992, we published limits of detection for both nicotine and 3-ethenylpyridine showing that the that 3-ethenylpyridine is actually twice as easy to detect as nicotine.

    Slide 8 shows the ETS particulate phase marker results from the same experiment at RJR. As for the vapor phase components, all markers increase linearly with increasing concentration. However, all particulate phase markers track each other very well. This is to be expected in this controlled experiment where all RSP comes from ETS.

    In addressing how to go about measuring ETS exposure, the NPR concludes that the use of an internal measure of individual exposure such as body fluid cotinine is preferable to actually measuring external exposure. I disagree with this statement.

    While an internal measure may be well suited to some experiments in the workplace, it is certainly not true with regard to ETS.

    First of all, of the potential biomarkers currently available for estimating exposure to ETS, cotinine is the only one that is even marginally useful.

    Of all biomarkers that have been proposed, cotinine is the most tobacco-specific. Also, cotinine has a half-life of approximately 17 hours, although it certainly can vary over a much wider range. This was discussed in more detail previously by Dr. Neil Benowitz.

    This half-life is the amount of time it takes for half of any nicotine inhaled to be eliminated from the body as cotinine. This means that at best cotinine provides an integrated estimate of exposure over the preceding one to three days.

    However, in the context of measuring workplace ETS exposure, cotinine is not to be preferred over air monitoring. There are several reasons for this, however, I will explain only one of them here in slide 9.

    A significant problem with the use of cotinine for workplace exposure assessment is this same relatively long half-life that I just mentioned. By relatively long half-life, I now mean relative to the continuous amount of time spent at work.

    The continuous amount of time spent in the workplace for most workers is only about eight hours. This continuous amount of time would even be less for workers who may leave their workspace to run errands, go out to eat, et cetera.

    In order to use cotinine or any other biomarker with a similar half-life to infer anything about exposure at work requires the implicit assumption that all out-of-workplace exposures are the same for everyone.

    This is, of course, an illogical assumption. An individual’s body fluid levels of cotinine cannot distinguish between nicotine inhaled at work, at lunch, at home or anywhere else.

    I would like to cite one specific example from my own research that illustrates how relying solely on cotinine levels would have resulted in a serious error concerning potential workplace exposures.

    This study, outlined in slide 10, was conducted in Columbus, Ohio in 1991. The results were presented to OSHA in May 1993, and were published later that year.

    Among all non-smoking subjects who were exposed to ETS at home, a statistically significant difference in cotinine levels was found between those who worked outside the home and those who did not work outside the home. In short, the subjects who were spousal-exposed to ETS at home and who also worked outside the home had higher cotinine levels than subjects who were spousally exposed at home and who did not work outside the home.

    If I had relied solely on cotinine data, I would have attributed this increased cotinine to ETS exposure at work. However, I would have been wrong.

    Air monitoring in the homes revealed higher concentrations of nicotine and 3-ethenylpyridine in the home of the working subject. Thus, the difference in cotinine was truly attributable to a difference in home exposure and was not due to a workplace effect.

    Personal monitoring of workers going about their daily activities in their workplace is a much better way to determine actual exposure.

    I would like to offer this specific advice to OSHA: If you want to know what exposure is in the workplace, measure it.

    With readily available materials and methods, a number of informative constituents of ETS can be measured, including 3-ethenylpyridine, solanesol and even nicotine.

    From the quote in slide 11, you can see that Meridian Research reached the same conclusion regarding ETS exposure in the workplace. This was in a 1988 report which was commissioned by OSHA.

    Moving to my next point in slide 12, now let’s examine the proper definition of exposure and contrast that to what was actually used in the NPR.

    Since it is critical in evaluating the merits of this entire section of the NPR, the correct definition of exposure must first be given.

    Exposure can correctly be defined simply as being equal to concentration times time. This equation defining exposure is explicit in that exposure in any given environment is equally dependent upon both the time spent in that environment and the concentration level of the contaminant in that environment. Without assessment of both variables, exposure cannot be determined.

  4. harleyrider1978 says:

    “Fetal rat lung explants were exposed to nicotine, 1-(N-methyl-N-nitrosamino)-1-(3-pyridinyl)-4-butanal (NNA), or 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)”

    Were EXPOSED after they were removed I gather is that correct.

    But really the best example of it all being Bullshit is the real life world,werent we all born to smoking mothers or fathers during the baby boom generation!

    But I must always remember TC isnt concerned with proving anything,they just want an avenue to say the word linked to! Thats the headline they want……..But on the part of nicotine exposed lung tissue Id have to offer this study that David Atherton found a while back:

    Make note this study is of rats or mice too

    In 2008 this paper was produced in America and concludes that nictotine and hence active smoking and passive smoking leads to less asthma. It also gives the aetiology (causation) why nicotine and the biologial process that reduces asthma in recipients.

    The results unequivocally show that, even after multiple allergen sensitizations, nicotine dramatically suppresses inflammatory/allergic parameters in the lung including the following: eosinophilic/lymphocytic emigration; mRNA and/or protein expression of the Th2 cytokines/chemokines IL-4, IL-5, IL-13, IL-25, and eotaxin; leukotriene C4; and total as well as allergen-specific IgE. unequivocally show that, even after multiple allergen sensitizations, nicotine dramatically suppresses inflammatory/allergic parameters in the lung including the following: eosinophilic/lymphocytic emigration; mRNA and/or protein expression of the Th2 cytokines/chemokines IL-4, IL-5, IL-13, IL-25, and eotaxin; leukotriene C4; and total as well as allergen-specific IgE. ”

  5. Lately I’ve taken to using the term ‘ambiotic generation’ to describe the kids born between 1965 and the present in writing and in conversation. It pretty well depicts the scared-to-death-of-their-own-shadow worldviews of both the parents and their second coming of Christ offspring. You know, the kind of thumb-sucking readers this doctor aimed this study at and who eat this stuff up like organically-grown, free-trade Gerbers Baby Food.

    I’ve been watching the exhibition football (American style) games on TV with a new eyes as of late. It is only a matter of time until the sport is banned because of the danger of concussion to the little darlings. Shark toothed lawyers like John Banzhaf are circling the waters as we speak just waiting to strike.

    Have you ever seen the picture of Obama bicycling with his regulation crash helmet on juxtaposed to President Reagan on horseback? Really says it all.

    There’s just far too many life threatening products outside the womb it would seem. Better to just stay in there all warm and safe and secure.

    • nisakiman says:

      Completely OT, but an old friend of mine (he’s Canadian) was the model baby that was on all the Gerbers baby food jars way back when. :) Just thought I’d throw that one in. I bask in the second-hand fame! :)

  6. smokervoter says:

    Okay, that would be ‘amniotic generation’ and not ambiotic. And while I’m at it, I’m watching the games with ‘a new set of eyes’.

    And I’m really just smokervoter, singular. No Mister Mister silliness intended.

  7. beobrigitte says:

    But I always had the impression that babies don’t actually start breathing until they are born, very often with a smack on the back to help them get started, as shown in countless movies. And the reason the little critters don’t breathe is because there isn’t any air in there, and they float in amniotic fluid. Perhaps an experienced mother reading this can help out here.

    Actually, babies do practice “breathing” in the womb. I have even been lucky enough to observe it in one of the later scans (had them due to carrying very big babies and not being diabetic) of my offspring.

    Babies do not actually breathe in the womb—at least, not in the usual sense. Fetal lungs are not fully functional, and are not even able to fully expand, until after birth. During the later stages of gestation, the fetus may “practice” breathing by inhaling and exhaling amniotic fluid. The fetal lungs do not process the amniotic fluid, the way fully formed lungs process air, but experts believe this “breathing” is important to fetal lung development. The fetus gets all of its oxygen and nutrients through the placenta and umbilical cord—a process called fetal circulation.

    Read more:

    The “crown jewel” of anti-smoker fear-mongering:

    Atherosclerosis in children can begin in the womb as passive tobacco smoke crosses the placenta, leading to low birth-weight and impaired lung development. The condition can lead to blood clots and strokes later on in life.

    There we have it; all strokes are due to having been exposed in the womb to ultra-dangerous “third hand smoke”.
    The anti-smokers are getting desperate – more and more non-smokers are getting fed up with the constant idiot-bombardment of the dangers of “passive smoking”. They need the non-smokers to act out their hate against smokers.

    There should be a HUGE WARNING: “This publication kills common sense” and a picture of a rabid anti-smoker attached to this “study”.

    PS: Thanks, Michael J. McFadden for the preview of “TobakkoNacht. Looking forward to reading it.

  8. Rose says:

    Brought forward.

    “Re the COPD in India, it would seem that 94% of sufferers being non-smokers is quite significant. I’m not sure what smoking prevalence in India is, but when I was there in the 60s, it was a hell of a lot more than 6%. From memory, 60% would be closer!

    Whatever, it would seem likely that both smokers and non-smokers alike would have been squatting around those dung patty fires, and yet it was predominantly the non-smokers who suffered from COPD as a result……… Why?”

    Good question.

    The only thing I can think of that could be even slightly protective would be the greater amount of glutathione that smokers are reported to produce in response to regular smoking.

    Normal alveolar epithelial lining fluid contains high levels of glutathione
    “The epithelial cells on the alveolar surface of the human lower respiratory tract are vulnerable to toxic oxidants derived from inhaled pollutants or inflammatory cells. Although these lung cells have intracellular antioxidants, these defenses may be insufficient to protect the epithelial surface against oxidants present at the alveolar surface. This study demonstrates that the epithelial lining fluid (ELF) of the lower respiratory tract contains large amounts of the sulfhydryl-containing antioxidant glutathione (GSH). The total glutathione (the reduced form GSH and the disulfide GSSG) concentration of normal ELF was 140-fold higher than that in plasma of the same individuals, and 96% of the glutathione in ELF was in the reduced form.

    Compared with nonsmokers, cigarette smokers had 80% higher levels of ELF total glutathione, 98% of which was in the reduced form.”

    But why inhaling smoke from biomass generally appears not to have the same effect, I have no idea.

    Stepping outside the mainstream

    Inhaled glutathione for the prevention of air pollution-related health effects: a brief review.

    “Exposure to air pollution is associated with significant adverse health effects, such as cardiovascular disease and asthma. Most current research trends focus on quantifying illnesses or deaths attributable to air pollutants, but limited research has examined potential methods of preventing these effects.

    The mainstay of conventional therapies lies in the treatment of exposure-related diseases, not prevention strategies. Few medical interventions seek to protect the lungs directly. Complementary and alternative medicine (CAM) practitioners are widely recognized, and often criticized, for administering therapeutic substances based on biochemical plausibility or pre-clinical studies.

    One widely used CAM intervention that specifically targets the lung is inhalation of the antioxidant glutathione. Inhaled glutathione is commonly used in the CAM community to treat a number of conditions, such as asthma, chronic obstructive pulmonary disease, bronchitis, sinusitis, and chemical sensitivity. Evidence suggests that inhaled glutathione rapidly increases pulmonary glutathione levels, providing a potential preventive intervention in the presence of environmental oxidants (eg, air pollutants).

    Enhancing pulmonary glutathione levels may reduce or eliminate systemic effects of air pollutants; however, no controlled studies have evaluated this potential. This article briefly reviews a major air pollutant (particulate matter) and the natural defense system against its toxicity and propose a pilot study to investigate the potential of inhaled glutathione to blunt its adverse effects.”


    Epidemiologic studies indirectly suggest that the inhalation of carbonaceous particulate matter impairs lung function in children. Using the carbon content of airway macrophages as a marker of individual exposure to particulate matter derived from fossil fuel, we sought direct evidence of this association.

    “To ensure that the carbon content of airway macrophages reflected exposures in Leicester, we also excluded children who had spent more than 5 days outside the city in the previous 3 months (the half-life of particles in airway macrophages after a single instilled dose is 3.9 months”


    “have not proved that the black material in airway macrophages is elemental carbon. In a previous study, our group found that particles in alveolar macrophages from healthy children were morphologically identical to aggregates of carbon nanoparticles from emissions of primary diesel exhaust,36 and a preliminary analysis by means of electron energy-loss spectroscopy of the airway macrophages in the present study found no spectra indicating the presence of iron, titanium, silica, or sulfur (Geiser M: personal communication).

    It is therefore likely that a major proportion of the black-pigmented material is inhaled elemental carbon.

    In conclusion, in this cross-sectional study, we found a dose-dependent, inverse association between the carbon content of airway macrophages and FEV1, FEF25–75, and FVC in healthy children.

    Since we directly assessed the carbon content of airway macrophages, our data strengthen the evidence for a causal association between the inhalation of carbonaceous particles and impaired lung function in children.”

    I would have thought it showed that it worked the other way around, healthy children don’t have a problem beacuse their macrophages are doing exactly what they should be doing.

    Then again I’m not a scientist.

    1] Human macrophages are about 21 micrometres (0.00083 in) in diameter.[2] Monocytes and macrophages are phagocytes. Macrophages function in both non-specific defense (innate immunity) as well as help initiate specific defense mechanisms (adaptive immunity) of vertebrate animals. Their role is to phagocytose, or engulf and then digest, cellular debris and pathogens, either as stationary or as mobile cells. They also stimulate lymphocytes and other immune cells to respond to pathogens. They are specialized phagocytic cells that attack foreign substances, infectious microbes and cancer cells through destruction and ingestion.”

    • harleyrider1978 says:

      It seems that the TC folks like to take normal bodily reactions to natural stimuli and say its caused by tobacco or second hand smoke. When its actually the body working as its suppose to work! The big problem would be if it didnt react!

    • nisakiman says:

      Another good bit of research there Rose. I’m going to have to see if I can absorb and understand all that! The glutathione thing is particularly interesting, and deserves further investigation.

  9. magnetic01 says:


    A horribly botched attempt to restore a 102-year-old fresco in Spain is proving to be quite a drawcard for tourists.


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