How do they know? By sending 'healthy' volunteers into such spaces.
During this time, researchers measured participants’ total respiratory impedance, resistance, and reactance with the use of an impulse oscillometry, a noninvasive way of measuring the physical properties of respiratory movement during quiet breathing. Results showed that short-term exposure to concentrated secondhand smoke significantly and immediately impacted participants’ airways, invoking such physiologic changes as increased airway impedance and resistance. Participants showed no clinical signs or feelings of discomfort during the test.What did their test add to current knowledge?
Well, the Environmental Protection Agency has already declared secondary smoke to be a danger to health. But it has also declared all particulates under a certain size (PM2.5) to be dangerous to the same degree:
- There is no safe level of exposure to PM2.5;
- Inhaling PM2.5 can kill within hours of exposure; and that
- PM2.5 can also cause cancer…
So what is the difference between secondary smoke and PM2.5 from any other source, in the eyes of EPA? None, it would seem. Why yet another study telling us what we already know, that scientists have decreed that PM2.5 and secondary smoke are a danger to our health that we must never be subjected to, and against which regulations already exist. Especially since the research involves exposing subjects to these substances like the EPA does here.
Why don't they show us how effective air cleaning would be in such a situation? Now that would be worth doing. We might learn something that we don't already know.
6 comments:
I posted this on their facebook page:
http://www.facebook.com/accpchest
Where can I find the latest second hand smoke and breathing study in its complete form. Secondhand Smoke in Cars, Bars Impairs Breathing Within 20 Minutes There seems to be no link to the actual study nor do they indicate the actual levels of smoke induced in the chamber.
harley
It hasn't been published Harley. It was presented at some meeting. And all the references I've seen to it just refer to "highly concentrated" cigarette smoke. Typical junk science. It was probably at concentrations hundreds of times greater than is ever found in reality, much like their experiments with animals.
SESSION TYPE: Physiology/PFTs/ Rehabilitation Posters
PRESENTED ON: Wednesday, October 24, 2012 at 01:30 PM - 02:30 PM
PURPOSE: Exposure to secondhand smoke (SHS) is a significant threat to personal, occupational and public health. Research has indicated that exposure to SHS within a car or bar can lead to very potent levels of exposure, with particulate matter smaller than 2.5 microns (PM2.5), commonly used as a marker of exposure. With the above in mind the purpose of this study was to assess how different levels of short term exposure to SHS may induce a change is respiratory flow resistance and pulmonary oxidative stress.
METHODS: After written informed consent, participants (n=15) were exposed for 20 minutes to SHS exposure at a PM2.5 concentration of 500 μg/m3 within an exposure chamber (simulating exposure in a moving car with limited ventilation, or in a smoke filled bar). The participants’ total respiratory impedance (Z5Hz), resistances (at R5Hz, R10Hz, R20Hz) and reactance (X5Hz, X10Hz, X20Hz) were measured with the use of an impulse osscilometry (IOS) system. Analysis was performed with SPSS 20.
RESULTS: Short term exposure to SHS at these concentrations was found to have a significant impact on the subjects airway impedance (Z5Hz), which was found to increase by 0.037[kPa/(L/s), and as also was airway resistance at R5Hz by 0.034[kPa/(L/s)], at R10Hz by 0.036[kPa/(L/s)] and at R20Hz by 0.039[kPa/(L/s)] respectively. In all cases a p<0.01 was noted. Overall central airway resistance was also found to increase by 0.028[kPa/(L/s)], as was peripheral airway resistance by 0.037[kPa/(L/s)], albeit non statistically significantly (p=0.054 and p=0.102, respectively)
CONCLUSIONS: Short term exposure to SHS at bar or car levels of exposure lead to immediate adverse changes in pulmonary mechanics, inducing airway restriction over a number of frequencies. While the above results are promising, further research is needed to assess the impact of SHS exposure on overall airway resistance with a larger study population.
CLINICAL IMPLICATIONS: These findings may indicate an additional mechanistic link between SHS exposure and the development of pulmonary disease.
DISCLOSURE: The following authors have nothing to disclose: Hara Stathopoulou, Constantine Vardavas, Vassiliki Evangelopoulou, Anna Tzwrtzi, Gregory Connolly, Panagiotis Behrakis
http://journal.publications.chestnet.org/article.aspx?articleid=1376724
Harley
Daniel
from the ads you linked to:
It does this by changing the HABIT FORMING centers of your brain and helps reprogram your brain to hate smoking!
Is this a Well Formed Outcome?
I do hope a reprogrammed brain doesn't generalize this.
(As you may be aware there are patterns that do use these techniques, you may also consider, now :), the implications)
'While the above results are promising, further research is needed to assess the impact of SHS exposure on overall airway resistance with a larger study population'.
Interesting use of the word 'promising'. It's almost as if they want non smokers to be harmed. Well, we know they do - crucial part of the war.
I'm interested in this seemingly accepted use of PM2.5 as a marker for passive smoking, which I was previously unaware of. I came across it last week when a BBC article on smoking in cars referred to a paper by Sean Semple of Aberdeen University. The WHO has published accepted levels of these particles and it is clear that any sort of air cleaning device will satisfy them. This contradicts the WHO claim that there is no safe level of passive smoking. If you weren't dealing with the warped and corrupt forces of the anti tobacco industry, getting the law changed to allow smoking with adequate ventilation would be pushing at an open door.
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