Dr. Siegel,
I all of this, did any of you, yourself included, take into consideration the diet of these so called people who are at risk? Were their diets high in fat and carbs and sugars? Were these confounders even figured in as possible major contributors to your "death watch list"?
Seriously, where is the proof, irrefutable proof beyond a reasonable doubt, that the 25% increase in risk is a guarantee of any illness?
Please, I have no medical training and even I can see through all this BS you all try to pass off as fact and science.
So, let's pretend I'm from Missouri, and "show me" the proof that can't be refuted.
This very morning on an ABC Daybreak news show (local), the newscaster reported on another reason for smokers to quit. He recited a study which said that once a smoker quits smoking, it only takes one year for the arteries to clear and be plaque free and they would look like the arteries of a never smoker. Sorry, but I didn't catch who did this study. So considering that the antis and tobacco control wants us to believe all this crap they call studies just for some grant money, I will believe this one study. Now adding some common sense to it, it should be evident that if it only takes 1 year for a smoker, then the time for a non smoker is nil, as there never was any danger for them in the first place.
As I said, I didn't catch who released this study, but one has to wonder if the truth is slowly leaking out and the American Cancer Society is in fear of being caught with their pants down around their knees. That is one plausible reason for all their latest doubletalk lately. This should be fun watching them all fall, for good this time!
Diane,
It will be delightful watching them fall. Now the latest to enter the dog fight is Babcock Endowment for Dermatologic Research and the National Institutes of Health which funded this study http://www.eurekalert.org/pub_re...h-
slw031907.php
There seems not end to their folly!!!
not=no
Diane-
Thanks for noting the results of that new study. It makes it obvious that brief exposure to secondhand smoke cannot possibly cause hardening of the arteries, as the ACS claims. If the effects of lifetime smoking on the arteries can clear up in a year or so, then certainly the effects of a brief exposure would clear up pretty instantaneously. From a scientific standpoint, the ACS statement is absurd. The only thing that baffles me is why the ACS would not correct the statement.
Sunz
I heard this on my daily health report too. You know the show, it use to be called the news. My first reaction to it was, "I wonder why no one, friends, family, neighbors, Doctors or nurses ever asked me if I was jaundiced?" I would love to see their faces when I told them that I felt fine, I am just a smoker!
"The only thing that baffles me is why the ACS would not correct the statement."
The only thing that baffles me is why grown-up, supposedly well educated human beings can even make up such statements. They MUST know they are wrong.
Dr Siegel ,why do you ALWAYS have to temper your comments-"brief exposure",1 second,2 seconds etc the term is meaningless in scientific terms ,is it to ensure that the rantis don't jump to ridiculous conclusions or is it because you wish to stamp your viewpoint ?Show us the evidence that suggests SHS causes harm,when epidemiological studies do not,unless you move the goalposts.
Sunz, thanks for the enlightening link to eurekalert.
Why for heavens sake would anybody be interested in such a study, to the point of financing it.
And look at the impressive list of "authors", just to handle a microscope and count wrinkles.
In addition to Helfrich, authors were Abena Ofori, M.D.; Ted A. Hamilton, M.S.; Jennifer Lambert, M.S.; Anya King, M.P.H.; John J. Voorhees, M.D.; and senior author Sewon Kang, M.D., all of the U-M Department of Dermatology; and Le Yu, M.D., now with Cedars Sinai Medical Center in Los Angeles.
Sunz;
This stuff is rediculous they should be cautioning smokers not to put lit smokes where the sun don't shine and no corelations would be found.
Maybe they could be similarly convinced to put their educational paperwork where the sun don't shine as well. Putting it to good use for a change.
If the ACS gets ahold of that stuff they will be asking for a curfew until the clouds disapate every time it rains.
I had a rather interesting experience with smoking questions last week. I had a cyst removed from my upper thigh. As usual i got the "Do u smoke and how much?" etc... question but even after i answered yes, i was then asked (for the first time) "Does anyone else in ur home smoke around u?" My concern here is that someone is trying to double dip statistics. I dont much care for those questions and i only answer them for my regular clinic. I could only see asking the second question if the answer to the first question is no. Since i am a smoker, what possible reason other than trying to double dip some fraudulent stats (prolly pinning my cyst falsely on smoking)would they have in asking me if anyone smokes around me, after i already told them im a smoker?
Sunz; Kevin
All I can say is that it serves those people right if they got wrinkly skin inside their upper arms.
I mean didn't anyone ever tell them that you get a more satisfying smoke if you put the cigarette in your mouth rather then in your armpit!
Then again, perhaps they are so used to hiding their lit cigarettes when the smoke gestapo come snooping round. 
On a more serious level, I noted that there were 77 participants in this 'study'.
77? Are they kidding?
"Researchers also collected data about the participants from interviews, such as their age, ethnicity, history of cigarette smoking, use of non-steroidal anti-inflammatory drugs, use of dietary or herbal supplements, sun exposure, sunscreen use, tanning bed use and, for women, how many children they had given birth to, hormone therapy use and oral contraceptive use." Oh yeah? What for?
So by the time they subdivided the participant group and 'adjusted' for all of the other factors, who was the (probably by now only one) poor bugger who had wrinkly skin one year after it had been as smooth as a baby's bum?
Really, this piece of junk is about as close to the bottom of the barrel as I've seen so far - and given the squalid nature of anti-smoking research in general, that's saying something!
.
Sunz,
I've been smoking for 39 years now. I'm 54 years old. I've had 2 kids. I sunbathe, have done tanning beds, etc. I can assure you, and prove it (please don't ask though hehehe) that my skin in NOT wrinkly, nor yellowed.
Now, I don't even have those creases around the mouth that they claim smoking gives you, and technically I should as it seems to be a genetic thing in my mothers family. My never smoked mother has those creases and has had them since her 40's. My never smoked sister has them also, and she's younger than me.
There, I just blew 2 fallacies out of the water.
more on the inside of 'toxic cars.'
http://www.msnbc.msn.com/id/1765...651756?
GT1=9145
branz, I want to know the dosage on the anti-anxiety meds these folks consume; everything is a fright to them.
Lynda, Seems we have about the same stats! Nothing but minor wrinkling here. Certainly not where I'd need that group of locusts' examinimining me to come up with a count, benpal!!
And you know Brian Bond, the antis could, in fact, cause us all to be using our armpit and any other availiable orafice to extinguish our smokes!!! Think of the liability!
Kevin, I know they have room enough for Egypt, so they can take all of their 'studies' and put them where the sun don't shine IMHO!
That reminds of this story my grandma told me once...back when my mom was 4 or 5 she wanted some of my grandma's coffee. Gran told mom it would make her knees turn green. At that age of course mom believed it, all the way up until she was about 10. Of course Gran made such a goofy claim as a joke...
One wonders at the mental capacity of anyone that would believe smoking turns you yellow lol
Jalestra
Everyone knows living in fear makes you Yellow and we all know who that would describe.
I would guess at this point the only thing left to do would be to contact as many newspapers and broadcast media outlets as possible informing them of the showdown calling our the ACS and their lapdogs.
Quoting Dr. Seigel and Dr. Enstom. and a cast of millions, Letting the press knowe the ACS has been lying to the public in an effort to scare people wqith lies and exagerations. Stuffing donations and Industry money into their coffers selling those fears.
Charities spending good will donations for political advocacy just has a ring of criminality about it there should be a law.
A major law...anybody got a rope?
Michael Siegel wrote:
"The only thing that baffles me is why the ACS would not correct the statement."
The ACS has nothing to brag about so why not divert attention elsewhere? Especially when the CEO (Seffrin) hauls in 600k a year.
Regarding smoking and wrinkles:
I believe the study's results. Nonsmokers are fatter than smokers and fat people don't have wrinkles because their fat pushes them out. (That's my guess anyway)
So it appears that tobacco funding is only acceptable when the results favor the anti side.
No bias there, nope, none at all {/s}
Michael The ACS has been selling the wrong message since it's formation. They have always supported the extremes and have never considered the idea of co-operation they demand the spotlight and attack anyone who does not agree. What the public is not aware of is exactly who these people are the ACS label alone gives them some god like perspective in al conversations regardless of how many huge mistakes they make in process.
Put your grown biasses aside for a few minutes and think in scisntific terms as a guy who only wants to reduce mortality rates and consider the following, let me know what you think;
I cannot understand why such a large controversy has grown in respect to cotenine as a marker for smoking. It is one of the most direct indicators. Yes it is found in other sources however the concentrations can be seen to be a divining factor, which can realistically draw a line. In the other court I believe failure to recognize concentration levels can also have a bias effect and be used to exaggerate numbers.
In the concentrations we have not seen any real studies, which assess concentration levels and how long they are sustained in a drunkenness perspective. If we look as with alcohol the morning after gives us a clear indication the body has been damaged and needs healing. That healing obviously does occur. How long cotenine stays in the body, and in what concentrations, may well find a new reality, which we seem to walk right past with all the research to date. Cotenine in urine demonstrates exit strategy and a measure no longer within the body. The detrimental effects of smoking we are told diminish after someone quits which indicates research proves nothing [or at least little] from a cigarette remains chronic within the body. This also could support if no accumulation occurs which is permanent Garbage in garbage out applies. Meaning if the body in younger years has an ability to purge the smoke effectively and later in life it looses or is diminished in varying degrees. That purge rate ability [input vs. output’ is a subject we should be discussing, and determined safe levels would be much less difficult to imagine.
We inhale a lot of things, which do not have a lasting effect including many Chemicals, which in concentration would kill immediately. Asthmatics use of the inhalers as a case in point. Or the fog machine at a rock concert.
There is little doubt heavy smokers find more adverse effects than light smokers lifetime. The Doll 50 year study of doctors who smoke, demonstrated this pretty effectively. I can think of dozens of life studies, which would also concur. If we took smoking as equated to drinking and moderation were considered it may well lead to some realistic reasons why some smokers can smoke for 90 years and not be affected while others die of cancers and lung ailments which are highly correlated to the smoking.
Just as I believe the numbers of smoking related disease categories are highly inflated I do not believe smoking does no harm. I believe the measure of harm could be tremendously minimized by supporting the idea and relaying it to the public moderation in smoking can have a beneficial effect of lowering risk, which I also do not believe even the most determined of anti smoking advocates would be able to credibly argue against.
Aster we get past that hurdle we could talk about minimizing the toxin levels in the product, which we should not be avoiding to please the politics alone. These are beneficial health issues, which should be prioritized above the egos of those who would be embarrassed.
If someone drinks in moderation it has been seen to have beneficial effects. I believe similarly smoking is self medication for many and it does without any doubt allow people to avoid hunger pains, Depression, Stress even ear aches and a host of other symptoms which otherwise would be selling a host of drug products with dangers of their own which would be needed to replace the universal benefits of smoking. Think of one stable target [Smoking] to deal with as opposed to thousands [replacement drugs] to deal with because we replacing the first target.
Personally I am not a stable smoker many times in heavy conversations or while drinking I may smoke 4 in an hour and at other times I may smoke 1 in an 8 hour day, The 4 per hour would be a norm for some which I believe should be cautioned against while the 1 in 8 hours might be closer to a norm for others which I believe would not raise a lot of concern. Concentrations as with drinking and how long they are sustained may well prove to be a much more effective way to deal with smoking than the extremes of “ I will, and no you wont” in respect to public health and smokers today. A common ground and co-operation of all would no doubt benefit everyone’s comfort levels.
Off Topic but a must be seen anyway:
And people wonder why I can’t trust doctors anymore?
Doctor uses ADHD drug Adderall, an amphetamine, to treat childhood obesity
CNN) -- When Alex Veith was 11 years old, he was in a bad spot.
He was 30 pounds overweight, and blood tests showed he was headed toward Type 2 diabetes. His parents say Alex was already physically active and eating a healthy diet. They didn't know what to do.
Their pediatrician didn't know either, so she referred Lisa and Hank Veith to Dr. Fuad Ziai, a pediatric endocrinologist in nearby Oak Lawn, Illinois. In the summer before Alex entered sixth grade, Ziai prescribed Adderall, an amphetamine used to treat attention deficit and hyperactivity disorder, or ADHD. Alex didn't have ADHD, but one of the drug's common side effects is weight loss. And that's what happened to Alex.
http://www.cnn.com/2007/HEALTH/0...rall/
index.html
I wonder if it ever occured to any of them to actually remove sugar from this boys diet and seriously lower his carb intake (especially the refined carb variety).
Lynda F asks...'And people wonder why I can’t trust doctors anymore?'
add or any 'science' for that matter!
The author states:
Critical thinking has left the building.
http://junkfoodscience.blogspot....t-
building.html
Lynda
Although the interviewed experts sought to protect the doctor in question and yes this is common practice. The doctor should be jailed and not just criticised.
Human experimentation is still against the law despite what they would like to imply.
Sunz: add or any 'science' for that matter!
The author states:
Critical thinking has left the building.
Actually, it's even worse than that.....a deliberate ignoring of facts or lack of them.
The most disturbing thing I'd read in a long time was this piece. Granted it's focused on global warming, but it goes along way to explain things that we're seeing in science in general now.
Here's a reasonably succinct definition of *shudder* post-normal science.
More junk science? Smoking study finds attention deficits "Teenagers exposed to cigarette smoke in the womb are at risk for attention problems, and the deficits worsen if the teens themselves smoke, according to a new study." See here http://www.newsday.com/news/heal...hnews-
headlines
Mike----A most interesting read on post normal science is here as well.
http://www.melaniephillips.com/diary/
?p=1469
Seems it is just fine to lie, ignore, invent with impunity when it 'makes your case' Shameful
I've just realized, that all this "junk science" is probably the reason for a majority of the apathy we all suffer from.
There's no way anymore to discern the real truth, and most people feel so overwhelmed at trying that they don't bother and stop caring.
I think "public health" needs to be done away with totally. They are obviously NOT interested in real public health anymore.
Thank goddess I am not 20 anymore, the prospect of another 50 years of this crap would be enough to make me suicidal.
Mike wrote:
"Being in a closed garage for several minutes with a car engine on exposes a person to carbon monoxide which causes measurable decrements in oxygen-carrying capacity of the blood. But we wouldn't say that such a person has been acutely poisoned?"
While Mike may not say that such a person has been acutely poisoned, I know of many others who disagree.
Whenever someone is exposed to even trace amounts of asbestos, lead, mercury, CO and/or other environmental contaminents, some healthcare professionals, public health officials, media, etc. refer to those events as poisoning.
Just because a person doesn't receive a lethal dose of something doesn't mean that they have been poisoned.
Perhaps Mike could provide us with what he considers to be a safe level of CO exposure for humans.
Just because a person doesn't receive a lethal dose of something doesn't mean that they have been poisoned.
So while you feel car exhaust put out by the millions of cars on the roads at any given moment every day is perfectly acceptable for us to breathe and be poisoned with; but a little bit of cigarette smoke isn't?
And people say MY thinking is twisted. pfffft
Bill...carbon monoxide is a normal product of normal human metabolism. Even people not exposed to any outside source have CO in their blood streams. Experiments trying to use CO as a marker of SHS exposure have always concluded there are too many other sources of exposure to be useful. also see page 3-40 of the 1992 EPA report Dave K
We can certainly go with Bill's definition of acute poisoning (by the way, I'm not saying this statement is a lie - I'm just saying it's misleading), but if we do, then the statement becomes completely meaningless. Because then just walking down a traffic-filled street causes one to become acutely poisoned, drinking alcohol of any amount represents acute poisoning, and eating a hamburger is also acute poisoning.
We can defend the ACS statement if we want by claiming that technically it is correct, but it should be obvious to all that doing so renders the statement completely meaningless.
Given the doubt, I stick with my opinion that the ACS intended to use the word acute poisoning to conjure up a particular sentiment in the public. I say this, in part, because the context of this document is how to craft the message in a way that maximizes its emotional appeal and sense of urgency.
By the way, I have no problem with crafting effective communications (that's what I in fact teach here at BU), but I teach my students to be accurate in their statements, not to mislead the public (worst-case scenario in interpreting this ACS statement) or to make statements that are meaningless (best-case scenario). I don't see any way in which a meaningless statement represents an effective communication.
Bill - I applaud your tenacity in defending the ACS. However, I think you're giving them far more credit than they deserve. I believe they themselves would admit that the statement was misleading if pressed on this.
A lie is a lie however you try to gloss over it.The truth of the matter is the large majority of these organisations have made comments that are scientifically unfounded, all in order to hit the headlines and help the cause.Add them all together and Total Control are the proverbial crock of sh1t.The audacity to state the Tobacco Companies are the lowest of the low is but one of their corkers,when they themselves are placed alongside for comparison.
"some healthcare professionals, public health officials, media, etc. refer to those events as poisoning"
Wait, Bill, you just referred to the use of "some say" as ambiguous in an earlier thread, as something ANR didn't necessarily endorse but knew other people said. If it was ambiguous then, it is now, and without facts and definition of what can be considered poisoning, it's just an emotive word.
It's like discussing tobacco "fumes" from a cigarette 15 feet away. "Well, they're still fumes. Many people say so."
Mike wrote:
"Bill - I applaud your tenacity in defending the ACS. However, I think you're giving them far more credit than they deserve."
I wasn't defending the ACS, but rather was simply pointing out the fact that many people consider (and refer to) nonlethal exposures to various environmental contaminents as "poisoning".
When I worked at our local health department 20 years ago, we had a brochure entitled "Carbon Monoxide Poisoning" that indicated that even a few minutes of exposure to a running car in an enclosed garage could result in CO poisoning.
Similarly, the health department had another brochure entitled "Childhood Lead Poisoning" that stated that even trace exposures to old paint chips could cause lead poisoning in children.
I noticed that while Mike misrepresented the purpose of my posting, he failed to answer my entirely reasonable question of what he considers a safe (or acceptable) level of CO exposure.
Bill since you are referring to poison,what about the adage,"the poison is in the dose".You're half way there Bill,better change the subject before you admit more than you may wish to.
Bill,
As an aside might I suggest to prevent any of the poisons you may encounter simply you should try wearing an aluminum foil hat. I wear one, and it keeps the aliens and our government, and all of TC from doing mind control. I just know this could work for you too.
I also string paper clips together and hang them from my belt to keep me grounded. This prevents any further shocks to my delicate system from various kooks I meet.
Sorry to go 'off-topic' but you sounded so stressed; I thought you'd just love some unsolicited advise in how to conduct your life.
si wrote:
"Bill since you are referring to poison,what about the adage,"the poison is in the dose"."
That adage is exactly what I was thinking about in my posting.
Government agencies, health and/or environmental advocacy groups, scientists and others can and do disagree (sometime by wide margins) about what amounts of exposure (to various contaminents) constitute "safe" and/or "unsafe" levels.
Since Mike has criticized the levels of tobacco smoke pollution that ACS and others consider "unsafe", it is only reasonable for Mike to disclose the levels of tobacco smoke pollution (and/or levels of various constituents in tobacco smoke) that he considers "safe" and "unsafe".
Actually Bill i was thinking more of the 222,000 cigarettes needed in order to reach OSHA's threshold limit for benzopyrene,or 25,555 for dimethylamine,based on an unventilated,sealed room 100m3 at STP.COMPLETED BY lITTLEWOOD & FENNEL Independant Public & Health Policy research group.The poison is in the dose.
I don't see this as an issue of what levels of ETS are safe or unsafe. After all, the ACS statement does not say that brief exposure to secondhand smoke is "unsafe." I wouldn't take issue with that (although I also wouldn't find it particularly meaningful).
What is at issue here is whether a brief exposure to secondhand smoke represents acute poisoning, and whether it is appropriate to characterize it as such.
My feeling is that in order to call something acute poisoning, there really should be clinically meaningful harm done. In Bill's examples, there is clinically signficant harm done. Low levels of lead have been shown to cause measurable clinical deficits.
However, I am questioning whether there is any clinically meaningful damage from a brief exposure to ETS that could reasonably constitute acute poisoining. Otherwise, I think the use of that term is very misleading.
So far, I haven't heard any solid evidence of clinically meaningful harm that would generally be recognized as representing acute poisoning.
Finally, regardless of the semantics, take a step back and tell me that the public is going to interpret the phrase "acute poisoning" as simply meaning that there are physiologic deficits that have no clinical significance in and of themselves. Forget about it!
Human experimentation is still against the law despite what they would like to imply. - Kevin
Of course it is!!
http://www.guardian.co.uk/aids/
s...1185358,00.html
UK firm tried HIV drug on orphans
GlaxoSmithKline embroiled in scandal in which babies and children were allegedly used as 'laboratory animals'
By the way, I have no problem with crafting effective communications (that's what I in fact teach here at BU), - Doc
Well Doc, in my opinion if "effective communications" equates to "scientifically correct" but presented and designed to illicit a disproportionate response from laypeople or legislators then it is nothing short of morale bankruptcy.
People deserve honesty and perspective.
GreatScot
I noticed that while Mike misrepresented the purpose of my posting, he failed to answer my entirely reasonable question of what he considers a safe (or acceptable) level of CO exposure.
For someone who rarely answers direct questions to put to him, I don't think you are in any position to demand answers from anyone. OR is it just us disgusting, murdering, abusive, rapist smokers you ignore?
Since Mike has criticized the levels of tobacco smoke pollution that ACS and others consider "unsafe"
Maybe that's because your (yes you are included there) idea of "unsafe" tobacco smoke pollution is anything above ZERO, while having no problems with the brown haze hanging over every community in this country due to your precious motor vehicles, etc.
And since you consider even a small whiff of smoke to be deadly, our opinion hardly matters at all. I mean who are we? Just living, breathing proof of the lies being told.
This is part of a letter that has been sent to all the senators and representatives in the states of Oregon, Texas, Tennessee, Virginia, Mississippi, Alabama, Illinois, New Hampshire, South Carolina, North Carolina, Hawaii, Maryland, Pennsylvania, Wisconsin, Michigan, Kansas, Iowa, Minnesota, Wisconsin and many city councils around the country as they consider new restricitions on public smoking. When they vote, at least they have seen Dr. Enstrom's research.
The longest-running and highest-quality secondhand smoke study ever done, completed too late (2003) to be included in Surgeon General Carmona’s report, found no link between secondhand smoke and lung cancer or heart disease. http://bmj.bmjjournals.com/cgi/c...l/326/7398/
1057
A study by the Oak Ridge National Laboratory found that restaurant
ventilation/filtration systems can make the air of a nonsmoking section of a smoking restaurant as clean as the air of smoke-free restaurant.
http://www.data-yard.net/2/21/rtp.pdf
Another Oak Ridge National Laboratory study of tavern workers in 16 major cities found that the tobacco smoke exposure of bar and restaurant workers to be minimal. No bartender was found to breathe more than the equivalent of a single cigarette per 40 hour work week. The average bartender breathed .1 of a cigarette per 40 hour week.
http://www.ornl.gov/info/press_r...r=mr20000203-
00
http://www.ehponline.org/members...nkins-
full.html
A huge recent study of heart attack rates in California and New York has
proven that smoking bans do not lead to a reduction in heart attack rates:
http://tobaccoanalysis.blogspot....claim-
that.html
In an estimate of health benefits of the New York City smoking ban,
American Counsel on Science and Health President, Elizabeth M. Whelan Sc. D., M.P.H., admits that “There is no evidence that any New Yorker * patron or employee * has ever died as a result of exposure to smoke in a bar or
restaurant.” Whelan further states that “The link between secondhand smoke and premature death, however, is a real stretch.”
http://www.acsh.org/factsfears/
n...news_detail.asp
Surgeon General Carmona’s report and press statements have come under
severe criticism from respected public health authorities even within the antismoking movement. The Surgeon General’s contention that there in no safe level of exposure to secondhand smoke is especially disputed. The Surgeon General’s report needs much more analysis and scrutiny before it can become the proper basis for law. It is important to remember that the
EPA Report which declared secondhand smoke to be a human carcinogen was
subject to years of scrutiny by scientists and epidemiologists before
being vacated as a fraud by a federal judge four years after its release.
http://www.acsh.org/factsfears/
n...news_detail.asp
http://
tobaccoanalysis.blogspot....unications.html
http://www.forces.org/evidence/e...iles/
osteen.htm
Dear Dr. Siegel,
I have been reading your blog with great respect over quite some time now. As I have just started my own blog on German politics (in German, though) I have been posting a couple of times on the current debate on Secondhand smoke in Germany. The Rest of the Story has been very helpful indeed. I wonder whether you might want to link TRotS to www.fette-henne.info?
Yours
Uwe Alschner
Uwe-
Thanks. I added a link under Reader's Blogs.
The instructions which came with my carbon monoxide detector NightHawk) say that OSHA considers any level below 50 ppm safe for healthy adults in an 8 hour period.
I smoke in our home. I have never seen our carbon monoxide detector register even 1 ppm when the house is closed up, say in the winter.
How about you other smokers who post here? have any of you ever seen your home carbon monoxide detectors register any readings which could be attributed to your smoking?
Of course not, yet Bill suggests this could be acute poisoning posting that : "I noticed that while Mike misrepresented the purpose of my posting, he failed to answer my entirely reasonable question of what he considers a safe (or acceptable) level of CO exposure.
Bill Godshall | Homepage | 03.22.07 - 3:03 pm | # "
So, I ask you Bill, if your so concerned, then why have you never asked anyone who smokes if they have a CO detector at home, and if they've ever set it off? and did you happen to have a CO detector in your home back when you smoked? and did you ever set it off?
The evidence is so easily obtainable, that cigarette smoke components never reach critical levels, even indoors, that claims to the contrary, are positively senseless.
We've even invited guests into our home and smoked cigars, never gotten any reading on our CO detector.
The evidence is so overwhelming that CO from SHS is not a problem, that Bill's insisance that CO is an issue which should be debated here has no merit. Dave K
Dave wrote:
"The instructions which came with my carbon monoxide detector NightHawk) say that OSHA considers any level below 50 ppm safe for healthy adults in an 8 hour period.
I smoke in our home. I have never seen our carbon monoxide detector register even 1 ppm when the house is closed up, say in the winter."
The EPA's 8 hour standard for CO in outdoor air is 9 ppm, and the EPA's 1 hour standard for CO in outdoor air is 35 ppm.
According to the 1986 SG Report and the 1992 EPA report, CO levels in indoor tobacco smoke pollution ranged from 4 ppm to 66 ppm, with the highest levels found in cars.
But CO in tobacco smoke pollution isn't the only health hazard, as levels of respirable particulates in tobacco smoke pollution indoors greatly exceed EPA outdoor air quality standards.
Bill,you haven't spouted this bullshit for a while have you ? Not since you were made well aware that your little speech means absolutely nothing.OSHSA standards are the be all and end all,and they are NOT EXCEEDED.Don't you recollect Marcus Aurelias,Bill ? Why not re-visit his website (it is listed) and his article will ONCE AGAIN BLOW YOUR LITTLE RESPIRABLE PARTICLES INTO TOUCH.
Dr. Siegel, it breaks my heart to watch you answer Bill with care when it's quite obvious that ultimately Bill has no more respect for you than he does for us when he tries to play the very same tricks on you (i.e. demanding you prove what isn't when science demands one prove what is).
And since Bill has such a hard time with this concept let me put it into terms he might be able to understand:
I say there's a pink elephant in the room. Laws of Science say I'm the one that has to prove it IS really there. But I'm feeling goofy today. I think I'll use Laws of Bill. So I insist that Bill prove there ISN'T a pink elephant in the room.
Bill, Bill, Bill...
The typical size of the interior compartment of a compact car is roughly 3 cubic meters.(1)
A car with the heater control set to outside air, and the fan set on high will give you approximately 30 Air Changes per Hour.
A cigarette produces somewhere between 26 and 61mg of Carbon Monoxide(3). For the sake of argument we will say 50mg of CO per cigarette.
Using the handy dandy calculator 50 mg of Carbon Monoxide will yield a concentration of 39ppm in 1 cubic meter, or 13 parts per million in 3 cubic meters, the size of the interior of a compact car.
It would take roughly 5 cigarettes chain smoked in a hermetically sealed car before the concentration of carbon monoxide concentration to reach 66 parts per million.
This would indicate Bill was trying to commit a fallacy of trying to compare an instantaneous measurement against a time weighted average. If one were to measure the temperature of a candle at the flame, they would find a very high temperature, but that heat is quickly dissipated by the volume of the room. Gases dissipate much the same, until you get to the point of open air which is almost infinite. What Bill is essentially doing is comparing heat at the candle, and comparing that against the temperature of the entire room.
The typical anti smoking zealot respires approximately 694 mg of carbon dioxide per minute (1kg/day). Converting this is approximately 537ppm per cubic meter. In the 6 minutes it takes to smoke a cigarette, the anti smoking zealot would have produced over 1074 ppm of carbon dioxide in that same vehicle. In the time it takes to smoke 5 cigarettes, the anti-smoking zealot would have contributed 5370ppm of Carbon Dioxide inside of that same vehicle. It should be noted the OSHA prolonged exposure limit is 5000ppm, and the ASHRAE standard for workplace is 1000ppm for Carbon Dioxide.
So we should prevent children from riding in vehicles with anti-smoking zealots?
Actually the answer is much simpler, we dilute the automobile cabin with fresh air. Since the contribution of CO from cigarettes is approximately 13ppm, and even assuming a typical person smokes twice as much while driving (4 cigarettes per hour) Before dilution is approximately 54 ppm/hr, while Anti Smoking Zealot will contribute 11140ppm/hr to that environment. Since one Air Change per Hour effectively halves the concentration, and n changes per hour can be expressed as 1/2^n.
Solving for n to reach the ASHRAE guideline of 1000ppm of CO2 we would see we need 1/2^n = 1/11.14 or 2^n=11.14 or n=log(11.14)/log(2) or approximately 3.47 changes per hour. But conversely the contribution from the cigarette would also be decreased by a factor of 11.14 so it's effective hourly concentration would be around 4.85 ppm of Carbon Monoxide.
What I've shown here is the contribution by source. One should not that the basic assumption here is the outside air contains neither CO or CO2, but since the air we are diluting it with is higher than the contribution by the source, then the effects will be an increase by the concentration of the outside air. Hence this is why EPA guidelines on outside air, are much lower than OSHA guidelines as this is what we must dilute the indoor air with. If the air is dirtier outside, then is being produced inside, the outside air will raise the concentration to at least that of the outside. In other words, the concentration contributed by the cigarette is smaller than the contribution from the outside air. In other words, it's your car, and all the cars around you which is creating the real hazard. The contribution by the cigarette is only a fraction of the total from other sources.
This is also why I take such exception to the misrepresentation being done by Bill and others like them when thy try to use outdoor air quality standards and apply them to an indoor environment which is being refreshed by outside air. Any time one of these zealots makes such a comparison with EPA outdoor air,quality standards, they are deliberately trying to deceive the public.
(1) http://en.wikipedia.org/wiki/
Veh...icle_size_class (approximately 35 cubic feet = 1 cubic meter)
(2) http://www.lenntech.com/calculat...per-
million.htm
(3) http://www.cdc.gov/niosh/91108_54.html (26 - 61mg)
Holy cow, Walt H.! May I steal this? It's a work of art. But even in stealing it I'd want to give it proper attribution. Will "Walt H., 'Rest of the Story' contributor" do? Or would you choose to be more forthcoming with your name and background?
JTF, feel free to use it as you see fit. As for a work of art, I'm flattered, but it's just some calculations to show what a huge impact turning over the air a few times does, and the fallacies being promoted by the TCI.
I know antz love to use emotional arguments conjuring up the idea that an automobile is a sealed capsule, but the reality of it, is for comfort from ourselves, we have to have air exchange, even if we don't smoke. I don't think the TCI has ever taken this into consideration while testing static models, as it has been my experience that most smokers open windows, and run the outside air through their climate controls in their cars, for obvious reason. Their worst case scenarios rarely if ever take these into account.
I remember reading in one air quality model trying to determine the "average" window open based on observation. One of the "unanswered" observations were that it appeared that more windows down conditions were observed in cars with people smoking. Imagine that... too bad they didn't incorporate that into the model, as a car with the windows even cracked, has a huge increase in the number of air changes per hour, and also remember that the effective concentration above ambient is divided by 2 to the Nth where N is the exchanges per hour. At 10 that is 1024 or 1/1024th of the sum of the sources for that hour over ambient. At 20 it's 1/1,000,000.
The other big fallacy I see used quite frequently is to use transient spikes, and compare those to time weighted averages. While most gaseous components reach equilibrium fairly quickly in terms of a seconds for a small environment, minutes for a very large environment, the concentration at the source will diminish with the square of the distance, again another exponential distribution. So when you look at Bill's graphs of his RSP's, you can tell the monitor was placed and is being highly influenced by someone smoking in a very close proximity.
More of the deceit and fraud being used by those in the TCI.
Hi, guys.
Thought as long as I'm here, witnessing the efforts made to present hazardous particulate in and around vehicles as provided by human choice, rather than fossil fuels...
And while money pours into this effort, the 2005 exposure assessment study with snippets quoted below points out that:
'Despite the increasing concerns about the health impacts of UFPs, very little information is available on their concentrations or physical/chemical properties in places where people live and work, such as in community air, homes, schools, workplaces, restaurants, or vehicles. It is therefore essential to develop and deploy technologies that can assess the nature and extent to which people are exposed to these particles in these microenvironments. The complexity of the sources and nature of UFPs suggest that considerable characterization efforts will be needed to either discover and/or refine our understanding of linkages between exposures and various types of health outcomes.'
However, such studies make it very clear that the concern is with fossil fuel emissions, not tobacco smoke, all that seems to be mentioned, publicized, or claimed as an issue by those presenting themselves as public health rulers...
Anyway, tossed in a few examples for thinking people
http://www.cleanairsys.com/
airzo...0pollution.html
'Research Finds Diesel Exhaust Kills Throat Cells
'Press Release:
'September 11 - Researchers at Deakin University have found that diesel exhaust is far more damaging to our health than exhaust from biodiesel, the plant-based fuel.
'Associate Professor Leigh Ackland, Associate Head of Deakin’s School of Life and Environmental Sciences, led a team of researchers who compared the effects of diesel exhaust and biodiesel exhaust on human airway cells. They found that diesel exhaust damaged and killed the cells, while biodiesel exhaust had little effect.'
...
'"The fumes from burning fuels, including diesel, contributes to pollution and can cause heart disease, bronchitis and asthma. Efforts are underway to replace petrol and diesel with cleaner biofuels, such as biodiesel, but there is considerable resistance to this.
' "This study provides clear evidence that diesel exhaust is more harmful to our health than biodiesel exhaust." '
(Carbon from vegetative sources being entirely different to that of combusted fossil fuels, although both are termed 'organic carbon' and its presence generally claimed by certain anti interests to be only from tobacco smoke, or nearly all so - even when 'testing' smoking emissions outdoors in high-traffic areas.)
'"We saw hardly any cell death after treatment with biodiesel particulates." '
http://www.sciencedaily.com/
rele...50921082651.htm
'Scientists studying air pollution levels in 10 Southern California cities found that the closer children live to a freeway, the greater their chance of having been diagnosed with asthma. They report their findings in the November issue of the journal Epidemiology.
'Researchers also found that children who had higher levels of nitrogen dioxide, or NO2, in the air around their homes were more likely to have developed asthma. NO2 is a product of pollutants emitted from combustion engines, such as those in cars and trucks.'
http://www.cleanairnet.org/caias...icle-
70498.html
'Taxi travel pollution "highest"
Taking a taxi may be a relatively luxurious form of transport - but it might also increase your exposure to common pollutants. (from BBC)'
'A team at Imperial College London found taxi travel resulted in more exposure to pollutants than travelling by car or bus, riding a bike, or walking.
'The study, in the journal Atmospheric Environment, found car travel was the best way to minimise exposure.
'The researchers measured exposure to ultrafine pollution particles.
'POLLUTANT EXPOSURE
'Taxi: over 100,000 pt/cm3
Bus: just under 100,000 pt/cm3
Cycling: 80,000 pt/cm3
Walking: just under 50,000 pt/cm3
Car: 40,000 pt/cm3
Measure is: ultrafine particles counts per cubic centimetre
'These particles - less than 100 nanometres in diameter - are particularly dangerous because they are so small that it is possible to inhale them in large quantities, and they can penetrate deep into the respiratory system.
'The Imperial team developed a visualisation system which allowed them to play back video images of an individual's activities alongside a read-out of the ultrafine particle concentrations to which they were exposed at any each given moment.
'This enabled them to pinpoint which activities were associated with the highest levels of exposure to pollutants.
'On average, while travelling in a taxi, passengers were exposed to over 100,000 ultrafine particles counts per cubic centimetre (pt/cm3).
'This compared to an average reading of just under 50,000pt/cm3 for walkers.
'Surprise'
'Lead researcher Dr Surbjit Kaur said: "The higher exposure from travelling in taxis may come from actually sitting in the vehicle while being stuck in traffic where you are directly in the path of the pollutant source.
'"Also the fact that taxis are probably on the road for much longer than your average car could cause an accumulation of ultrafine particles."
'Dr Richard Russell, of the British Lung Foundation, said his own research had shown higher levels of carbon monoxide and nitric oxide among people who travelled to his clinic by taxi, rather than walking.
'"We would encourage people to walk as much as possible, as exercise is good for you," he said.
'Richard Massett, of the Licensed Taxi Drivers Association, said: "We have concerns for taxi drivers, who are driving around all day in roads with the highest levels of pollution.
' "We would like to see pollution lowered."
'The study was carried out as part of the DAPPLE (Dispersion of Air Pollution & Penetration into the Local Environment) project.
'This was set up to provide a better understanding of the relationship between air, traffic, people and pollution.
'Source: http://news.bbc.co.uk/2/hi/healt...lth/
4598388.stm '
Please note below- little info garnered on real health threats, such as that from fossil fuel emissions, especially in and around cars.
All we get is the protective smokescreen...
'Exposure Assessment for Atmospheric Ultrafine Particles (UFPs) and Implications in Epidemiologic Research
Constantinos Sioutas,1 Ralph J. Delfino,2 and Manisha Singh1
1Department of Civil and Environmental Engineering, University of Southern California, Los Angeles, California, USA
2Epidemiology Division, Department of Medicine, University of California, Irvine, California, USA'
http://www.pubmedcentral.nih.gov...i?
artid=1280332
(Snippets below; the differences between particle types - and the vast differences in constuents and potential results - are often unmentioned, or deceptively claimed to be the same, where anti-smoking advocates are concerned.
So here's a good study.)
'These three particle modes have distinctly different chemical composition, sources, and lifetimes in the atmosphere. Particles in the coarse mode are produced by mechanical processes (grinding, erosion, and resuspension by the wind). Because of their relatively larger size, they have higher gravitational settling velocities and are thus removed from the atmosphere within hours. Particles in the accumulation mode are mostly anthropogenic in origin; they are generated through gas-to-particle conversion mechanisms, including homogeneous and heterogeneous nucleation, and by condensation onto preexisting particles in the accumulation-size mode. Because they are too small to settle out, particles of the accumulation mode have lifetimes in the atmosphere on the order of days (Hinds 1999), and they can be transported over long distances. The major chemical constituents of fine particles are sulfate, nitrate, ammonium, organic carbon, and elemental carbon (EC), as well as a variety of trace metals formed in combustion processes.
'Because of their increased number and surface area as well as their high pulmonary deposition efficiency, UFPs are particularly important in atmospheric chemistry and environmental health. For example, the UFP’s surface can carry large amounts of adsorbed or condensed toxic air pollutants (oxidant gases, organic compounds, and transition metals) (Oberdörster 2001). Many of these toxic air pollutants have been identified as having pro-inflammatory effects, yet relevant exposure data are rarely available to epidemiologists. Results from several recent studies in mostly urban areas (Jones et al. 2000; Kim et al. 2002; Morawska et al. 1998; Shi et al. 2001; Woo et al. 2001) showed that a large proportion of urban UFPs consists of primary combustion products from mobile source emissions (particularly diesel and automobile exhaust) and includes organic compounds, EC, and metals. Because exposure to mobile emissions can vary across short distances and depends on personal activity patterns, assessing such exposures requires methods that go beyond the use of government monitoring data alone.'
(TBC)
(Con't - apologies for the length, but these are important and oft-ignored facts beautifully laid out.)
'Evidence now supports the view that UFPs carry considerable amounts of air toxics. Kim et al. (2002) studied composition of size-fractionated particulate air pollution in urban sites of Los Angeles, California, with considerable mobile source emissions. They found a large proportion of UFPs are made up of organic carbon, followed by EC as primary products from mobile source emissions, particularly diesel and automobile exhaust. Other studies showed that UFPs contain the largest fraction of polycyclic aromatic hydrocarbons (PAHs) by mass (Eiguren-Fernandez et al. 2003; Li et al. 2003). Overall PAH concentrations are likely to be higher where there is a greater traffic density, such as downtown Los Angeles where diesel exhaust was found to make up 32.7% of the fine particle mass (Glovsky et al. 1997). Given these findings, if PAHs and other organic compounds are major causal components of the inflammatory response to PM, then greater responses from UFPs compared with larger particle fractions are expected at urban areas in the proximity of mobile sources. This expectation is further supported by the greater PN and surface area of UFPs, and greater internal doses due to the higher respiratory deposition of UFPs (Kim and Jaques 2000, 2004).
'Experimental data show that compared with larger particles, UFPs are capable of avoiding phagocytosis by alveolar macrophages and gain entry to pulmonary interstitial sites, including vascular endothelium. Therefore, UFPs may induce pulmonary inflammation at both epithelial and interstitial sites, as well as enter the circulation to reach other target sites, including the cardiovascular system (Nemmar et al. 2002, 2004; Oberdörster 2001; Oberdörster et al. 2002). Additionally, organic components of PM such as PAHs, which comprise a large proportion of both freshly emitted exhaust and secondary aerosols, have been shown to induce a broad polyclonal expression of cytokines and chemokines in respiratory epithelium. As discussed, this effect may be due to the action of metals, PAHs, and related compounds that lead to the production of cytotoxic ROSs (Nel et al. 1998, 2001). ROSs induce oxidant injury and inflammatory responses (Pritchard et al. 1996), including the production of nuclear transcription factor κB, which increases the transcription of cytokines and acute phase proteins (Nel et al. 2001). These inflammatory and oxidant stress responses are expected to occur at extra-pulmonary sites as well, including the vascular endothelium of the heart. Evidence for the importance of oxidant stress responses to cardiovascular effects is that antioxidant therapy is protective against the development of hypertension, aetherosclerosis, cardiomyopathies, coronary heart disease, and congestive heart failure (Dhalla et al. 2000). Li et al. (2003) showed that UFPs in Los Angeles were most potent toward inducing cellular heme oxygenase-1 (HO-1) expression and depleting intracellular glutathione, both important in oxidant stress responses. A separate study in Los Angeles by Cho et al. (in press) used the dithiothreitol assay as a quantitative measure of in vitro ROS formation. That study also showed that UFPs had the highest ROS activity. Li et al. (2003) also showed that UFPs and, to a lesser extent, accumulation-mode particles localize in mitochondria where they induce major structural damage, which may contribute to oxidative stress. Xia et al. (2004) showed that suspensions of urban UFPs as well as diesel exhaust particles on epithelial cells decreased membrane potential and induced both loss of mitochondrial membrane mass and apoptosis. Interestingly, commercial polystyrene nanoparticles failed to exert a mitochondrial effect. Together, these studies provide strong evidence that the increased biologic potency of UFPs is related to the content of redox cycling organic chemicals and ability to damage mitochondria.'
'UFPs may be formed in the atmosphere by at least three processes: a) UFPs may be formed during combustion processes associated mostly with traffic or industrial sources, and emitted directly to the atmosphere as UFPs (Kittelson 199
; b) these combustion processes may also emit hot supersaturated vapors, which undergo nucleation and condensation while being cooled to ambient temperatures; and c) chemical reactions in the atmosphere may lead to chemical species with low vapor pressure at ambient temperature. The former sources produce UFPs that are more “localized,” with their concentrations decreasing with distance to their emissions sources, whereas the latter processes tend to produce UFPs that are more regionally (thus homogeneously) dispersed over an urban or rural area. UFPs sources and their impact on human exposure are discussed in the following sections.
'Emission inventories suggest that motor vehicles are the primary direct emission sources of fine and UFPs to the atmosphere in urban areas (Hitchins et al. 2000; Zhu et al. 2002b). Most PNs from vehicle exhaust are in the size range of 20–130 nm for diesel engines (Morawska et al. 199 and 20–60 nm for gasoline engines (Ristovski et al. 199. In addition to UFP formation by direct emission, recent studies show that photochemically driven atmospheric reactions lead to the formation of low-volatility species at ambient temperature. These chemical species may form UFPs by a variety of nucleation processes (Kulmala et al. 2004; Stanier et al. 2004). Nucleation may sometimes occur on ions and probably involves more than one species (i.e., is a multicomponent process). There is strong evidence that sulfuric acid vapor sometimes participates in nucleation, and there is growing consensus that ammonia and water vapor are also involved. However, the atmosphere probably also contains other trace gases, including organic compounds, that either participate in the nucleation process or react in the atmosphere to form compounds that nucleate. Because they may be present at extremely low concentrations, the identity and concentrations of those gases are not yet known. Kulmala et al. (2004) have written an excellent review on this topic. A variety of different nucleation mechanisms have been proposed for the atmosphere, including binary water–sulfuric acid nucleation (Kulmala and Laaksonen 1990), ternary water–sulfuric acid–ammonia nucleation (Kulmala et al. 2000), and ion-induced nucleation (Yu and Turco 2000).
'In urban areas, nucleation events have been observed in Atlanta, Georgia (Woo et al. 2001), Pittsburgh, Pennsylvania (Stanier et al. 2004), and Los Angeles (Fine et al. 2004). Stanier et al. (2004) showed in their study in Pittsburgh that the nucleation events are fairly well correlated with the product of ultraviolet intensity and sulfur dioxide concentration and can depend on the effective area available for condensation. This indicates that sulfuric acid (H2SO4) is a component of the new particles. However, they noted that published correlations for nucleation by binary H2SO4–H2O could not explain the observed nucleation frequency and intensity, suggesting that an additional component (perhaps ammonia) is participating in the particle formation, thus supporting the notion of a ternary process. Kulmala et al. (2004) indicate that after nucleation, UFPs grow at rates ranging from 1 to 20 nm/hr (increase in physical diameter), depending on season and locale. It is of particular note that recent evidence supports the notion that the species that dominate growth may be different from the species responsible for particle formation, with particle growth being attributed to the concentration of “nonvolatile” vapors. Our current understanding of atmospheric nanoparticle processes suggests that growth of these particles to larger sizes within the UFP mode occurs by condensation of low-volatility organic species. These species are products of photochemical oxidation of volatile organic precursors on these preexisting nuclei (Kulmala et al. 2004; O’Dowd et al. 1999). Recent studies by Zhang et al. (2004) showed that nucleation rates of sulfuric acid are greatly increased in the presence of organic acids (including products of atmospheric photochemical reactions), by forming unusually stable organic–sulfuric acid complexes, thereby reducing the nucleation barrier of sulfuric acid.'
'Because of the importance of traffic sources in the overall emission rates of UFPs and the resulting human exposure, it has been essential to determine UFP behavior after emission as they are transported away from the emission source, namely, busy roads and freeways.'
(TBC)
(Con't)
'Measurements of PN size distribution in the range of 11–452 nm were conducted on the side of a busy road in central London, over a period from April 1998 to August 2001 by Charron and Harrison (2003). The data were analyzed to demonstrate the influences of meteorologic factors on the overall size distribution. The relationship to traffic volumes indicated that accumulation-mode particles are associated with emissions from heavy-duty traffic (mainly diesel vehicles), whereas particles in the range of 30–60 nm showed a stronger association with light-duty traffic (Figure 5). The concentrations of both these particle size fractions decreased with increasing wind speed as a result of increased atmospheric dilution. Meteorologic parameters such as low temperatures and high relative humidity were shown to favor the formation of new particles. The relative number of particles ranging in size from 11 to 30 nm measured during the morning rush hour is strongly influenced by the prevailing temperature and humidity conditions. The strong dependence on the temperature corroborates the idea that these nanoparticles are not primarily emitted but formed during the cooling and dilution of the vehicle exhausts. By contrast no obvious relation was found between PN concentrations and relative humidity, despite the inverse correlation of temperature and relative humidity. Higher relative humidity is expected to favor homogeneous binary nucleation of sulfuric acid and water; ternary nucleation involving ammonia is expected to be independent of relative humidity, whereas the potential nucleation from organic compounds should be independent of relative humidity. The lack of a dependence on the relative humidity suggests that the binary nucleation from sulfuric acid and water is not a major factor in particle production.'
'The high concentrations of PM and gaseous co-pollutants in the proximity of freeways raise concerns on population exposure level (and its health implications) during commute. Time spent in and near vehicles is an important route of exposure to air pollution, but few studies of UFP concentrations in vehicle-related settings have been conducted, especially inside moving vehicles. Investigators in southern California used an electric vehicle to house and power a suite of particle and gaseous pollutant measurements (Westerdahl et al., in press). Measurements were conducted on a variety of streets and freeways in Los Angeles from February through April 2003. Diesel-powered vehicles, as expected, were often a major source of high UFP count concentrations, especially when being directly followed. However, gasoline-powered vehicles were also often observed to produce comparably high UFP counts, particularly when the vehicles were older; when vehicles were accelerating hard or from a standing start, such as after waiting at a stop light; and when vehicles were driven and/or accelerated at high speeds (Figure 8A). Because of the ubiquitous nature of gasoline-powered vehicles and the frequency of such types of driving, they may be the predominate source of in-vehicle, roadway, and near-roadway UFP concentrations. Figure 8B presents a comparison of in-vehicle and roadway UFP number–based concentrations and estimates of overall UFP contributions by vehicle type for various types of roads, driving conditions, and meteorology. As evident from Figure 8, the UFP concentrations are higher than the urban background measurements by at least an order of magnitude in the freeway affected by diesel traffic (I-710) or the mostly gasoline engine freeway (I-110).'
'All the aforementioned studies indicate clearly that, besides contributions from vehicular sources, photochemical secondary formations are also a source of PM in urban atmosphere. What is important from the standpoint of human exposure is that, unlike vehicular emissions, which by nature have a strong local character whereby concentration decreases rapidly with increasing distance from their source, secondary formation of UFPs is more regional in nature, which implies a more uniform population exposure to UFPs generated by this mechanism.'
'Despite the increasing concerns about the health impacts of UFPs, very little information is available on their concentrations or physical/chemical properties in places where people live and work, such as in community air, homes, schools, workplaces, restaurants, or vehicles. It is therefore essential to develop and deploy technologies that can assess the nature and extent to which people are exposed to these particles in these microenvironments. The complexity of the sources and nature of UFPs suggest that considerable characterization efforts will be needed to either discover and/or refine our understanding of linkages between exposures and various types of health outcomes. At one extreme is the need to determine how large, spatially dispersed populations experience ultrafine exposures over prolonged periods of study. At the other extreme is the need to determine how individuals experience the hour-to-hour or minute-to-minute dynamics of ambient UFPs as they move within the aforementioned microenvironments. The analytic technologies required to characterize the physical and chemical nature of UFPs in these various microenvironments are largely unavailable or untested outside the controlled environment of the laboratory.'
'When exposure models are developed and employed to estimate UFP exposures, it is important to consider both indoor and outdoor sources. For the purpose of estimating exposures related to time spent indoors, it is useful to gather data on infiltration of UFPs from outside sources. The extent of particle penetration into indoor environments is governed by indoor and outdoor sources, exchange rates, and particle physicochemical characteristics. Indoor particle concentrations, therefore, depend on the dynamics of the transport and fate of outdoor particles in indoor environments. Previous research in this area has focused on PM2.5 and PM10 properties and behavior (Jones et al. 2000; Thatcher and Layton 1995). These studies indicated that concentrations of indoor particles of outdoor origin are significant. In addition, the building shell was found to be ineffective in removing infiltrating particles. Considering health implications of UFP exposure, it is important to assess particle penetration characteristics into indoor environments and the relationship between their physical and chemical properties and infiltration.
'Although experiments have been performed to investigate penetration properties of submicrometer particles, these laboratory-based studies have assumed that particles are spherical and rigid (Liu and Nazaroff 2003). Results indicated that particle size and building gap dimensions were most important factors determining particle penetration. Furthermore, real-world UFP penetration studies conducted thus far have examined infiltration properties for a limited set of conditions. For example, Long et al. (2001) evaluated penetration efficiencies in only suburban neighborhoods. Franck et al. (2003) studied indoor and outdoor UFP size distributions at one location. Vette et al. (2001) measured indoor and outdoor particle size distributions of a single residence at urban background concentrations. However, characterization of urban particle infiltration should consider recent studies showing that UFPs exhibit great spatial variations near sources (Zhu et al. 2002a). Sakurai et al. (2003) studied the chemical composition and volatility of nanoparticles emitted from diesel vehicles and found that these aerosols consist of residual species, which may represent nonvolatile cores or low-volatility organic compounds as well as more volatile, smaller particles thought to be products of condensation of hot supersaturated organic vapors associated with fuel and lube oils. The volatile fraction constitutes about 90% of the total aerosol emitted by vehicles based on number concentrations. Such findings suggest that at least the volatile particles of outdoor origin can experience substantial changes and may be lost to building walls during indoor penetration. This notion is further supported by a recent study investigating the transformation of labile ambient ammonium nitrate aerosols in indoor environments, which has shown that measured indoor concentrations were considerably lower than the values predicted based only on penetration and deposition losses (Lunden et al. 2003). Because of the public health implications of UFPs and their spatial variations near pollutant sources such as freeways, it is therefore important to evaluate outdoor UFP size distributions, volatility properties, and penetration efficiencies into indoor environments.
(TBC)
(Con't - also extra-strong HINT)
'In conclusion, exposure assessment issues for UFPs are complex and need to be considered before undertaking epidemiologic investigations of their health effects. For instance, because of the high spatial variability of UFPs, the use of central site concentration data alone may not reveal its relative importance compared with other PM-size fractions or compared with gaseous pollutants. Particular attention needs to be given to indoor sources and infiltration of UFPs from outside sources, as well as meteorology because of the potentially high seasonal variability in UFP PN concentrations, sources, and chemical composition, including volatility.'
'This work was supported by grant ES-12243 from the National Institute of Environmental Health Sciences (NIEHS), National Institutes of Health (NIH); the contents of this article are solely the responsibility of the author and do not necessarily represent the official views of the NIEHS, NIH. This work was also supported by the Southern California Particle Center and Supersite (SCPCS) funded by the U.S. Environmental Protecton Agency (U.S. EPA; STAR award R82735201).
This manuscript has not been subjected to the U.S. EPA peer and policy review and therefore does not necessarily reflect the views of the agencies. No official endorsement should be inferred.'
Under the circumstances, with so many industry appointments in these agencies - no, I wouldn't expect official endorsement of anything not blaming individuals rather than industry profit-makers.
Generally, one tends to get spin following each such publication, with the media presenting the findings but with tobacco smoke or other personal choice as the culprit instead.
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