Behind that slo-mo smile? Big Tobacco.
Who would have guessed that even the stake to the heart of the tobacco industry would be at-risk of being removed in our rightward surge? And yet, there he is: Herman Cain, lackey to Big Tobacco, standing poised and ready to help out his old cronies, the people who made him, under the guise of removing excessive government regulation.
An in-depth article in Sunday’s New York Times, “Cain, Now Running as a Political Insider, Went to Washington as a Lobbyist,”got the ball rolling, and thinkprogress.org has dug a little deeper, but neither do more than scratch the surface of the 156 references to Herman Cain contained in the University of California at San Francisco Legacy Tobacco Documents Library.
Cain’s tobacco era began when he took over as CEO and executive lobbyist for the National Restaurant Association (the other NRA). Cain developed a money trail that culminated in contributions from R.J. Reynolds alone at a level of many hundreds of thousands of dollars in in-kind benefits to the NRA. This was stated clearly by Rob Meyne, former senior director of public affairs for the tobacco company. He wrote in a 1999 memo published by the Times that indicated R. J. Reynolds gave the National Restaurant Association “nearly $100,000 in cash and much more in in-kind support” on a more or less annual basis. One wonders what forms that in-kind support took, and how such support may have buoyed Mr. Cain’s premature foray into presidential politics in 2000.
In return, Herman Cain became a junkyard dog for Big Tobacco. According to Mr. Meyne in 1999 (from the Times article):
Bottom line: Herman Cain is certain, in one form or another, to be a political factor for a number of years to come. We have a good relationship with him, and that will certainly be to our benefit.
Mr. Meyne was certainly correct, if surprisingly so, on the first count. He must have known first-hand of Mr. Cain’s nascent passion for politics. And there is only one real way for the tobacco industry to have a good relationship with anybody, and that way is money. Interesting, how he is “certain” about two aspects of Mr. Cain’s trajectory.
Reviewing the record found in the tobacco archives, one thing is crystal clear: Mr. Cain was passionate about restaurant-industry initiatives most closely aligned with the interests of the tobacco industry. Cain put the restaurant industry on the map. He did so with tobacco industry money. He shilled for their interests above and beyond any logical, intrinsic interests of the restaurant industry. According to the New York Times article:
Under Mr. Cain’s leadership, the restaurant association opposed higher taxes on cigarettes and the use of federal money to prosecute cigarette makers for fraud — positions that Matt Myers, president of the Campaign for Tobacco-Free Kids said had little to do with the restaurant business.
And Mr. Cain argued vociferously that the decision about whether to go smoke-free was the province of individual restaurant owners, not the government. “The restaurant industry literally became the alter ego of the tobacco industry during that period of time,” Mr. Myers said in an interview.
Now, the restaurant industry’s legislative interests around smoking were reprobate enough on their own in those days. The industry was firmly fixated on the notion of maintaining each restaurant’s individual choice as to remain smoking or go smoke-free. This was cast in an anti-government argument. Cain himself was cast by Meyne as an “anti-government mandate” conservative. Apparently, the prospective medical fates of those forced to work in smoke-filled environments never once occurred to Mr. Cain.
His was a one-track mind, and he was a one-trick pony, authoring press release after release filled with the self-righteous rhetoric of the smoking industry. It was never, never, about food for Herman. Cain joined the board of Nabisco—in itself a weird appointment—not long before it merged with Reynolds. Rob Meyne joined the board of the National Restaurant Association. This was a marriage; a marriage of interests that formed—and forms—the potential to launch a candidate whose anti-regulation rhetoric is capable of upending a generation’s worth of anti-smoking efforts if her were to become president aligned with a Republican Congress.
And why shouldn’t it? Isn’t the right to smoke a perfect anti-gummint foil? Doesn’t the pendulum always swing in both directions? And who better to take it there than Herman Cain? He’s all about, “Look over here; 9-9-9!” Uh uh. Follow the money. And tail the guys that brung ya to the dance. Meyne’s proprietary and slightly condescending attitude toward Cain bleeds through his assessment of Cain as a fledgling candidate in 1999, “Nice to have goals, huh?” he writes, continuing, “In any event, Cain brings some positives. He is a genuine ‘antigovernment mandate’ conservative who happens to be an African-American. He is a wonderful speaker and would be an effective and charismatic candidate. He is also good on our issues.”
And Cain is duly appreciative of Mr. Meyne’s tobacco support, writing in a 1997 letter found in the tobacco archives, “Rob, as we head into a new millennium [sic], it will take courage and leadership from industry leaders like you if we are to Save American Free Enterprise.” Save American Free Enterprise, or SAFE, was one of Mr. Cain’s own anti-regulation initiatives, one of his supposedly catchy one-liners, like 9-9-9. But it was really Save American Tobacco.
Many of us on the progressive side of the fence have asked of this Republican pack, “What regulations are they referring to?” Obvious targets, like the EPA, go without saying. But anti-tobacco regulations? Who would have thought? So, as of today anyway, meet Herman Cain, leader of the pack and stealth candidate for Big Tobacco. His long-standing support for smoking rises to the level of a core belief and he should be hounded to address the subject. And you wonder why Mr. Cain’s Chief of Staff, Mark Block, was smoking in that ad? If you review Mr. Cain’s tenure as CEO and Lobbyist-in-Chief of the National Restaurant Association, you will realize that he never made an empty gesture.


Salon.com
Comments
This totalitarian urge on the left (and believe me, on other issues the right has it as well, although I'd argue that they don't have it on as many issues) is one of the reasons some of us have left the Democratic party. I understand that health is part of your religion. You are free to have it be a station of the cross. You should not, however, be free to force others to make that "pilgrimage" with you.
He is without equal it seems when it comes to being disingenous.
SAFE ? Really?
Not safe at all.
Words are insufficient to express the utter disdain I hold for the Rightwing these days, but "Have you at long last no shame?" begins to get there. And in fiction containing more truth than the news media category, there's the Jensen speech from the 1977 movie Network, that also contained the line "I'm mad as hell, and I'm not going to take it anymore!"
Despite their enormous differences, the Tea Party movement and the OWS movement are signs that people truly aren't going to take this crap any more. Not without a fight anyway.
bj, if you hadn't arrived here, someone would have had to write a comic book inventing you.
GREAT research, Steve. Please keep them coming.
-R-
My guess is that Rush will now say that "the Blacks" owe the "white man" reparations because "Blacks picked the tobacco."
Classic "2fer." And after Rush says this, you'll hear the following:
"This message was approved by Herman Cain."
Hey when you get the chance check out my October 17th tome: "Herman 'Bigsby' Cain: 'Black White Supremacist." Thanks!
Factories large and small obtain EPA permits to discharge pollutants,yet restaraunts are not, nor bars for having open alcohol present in an enclosed public space that also releases minute amounts of carcinogens.Yet we dont regulate nor outlaw restaraunt cooking smoke or carcenogenic alcoholic fumes! The same principle has always applied to cigarette smoke inside restaurants and bars.
Heres what cooking smoke equates too!
A study found that grilling four large steaks, four turkey cuts and eight large sausages for two hours can release the same level of dioxins as up to 220,000 cigarettes.
Dioxins are also found in ham, milk, children's balloons and tap water. Also, cooking a fish produces micrograms of these Dioxins yet only femptograms and nanograms in tobacco smoke!
Tobacco control claims endolethial dysfunction/heart disease from second hand smoke!
You get the same effect eating a thanksgiving dinner at a restaraunt or eating a cheeseburger or cereal and milk!
The lifetime lung cancer risk for eating red meat is over TEN TIMES HIGHER than the excess risk supposedly caused by constant daily exposure to high levels of secondhand smoke. Yet a non-smoker in a smoking diner might get the annual equivalency of half a cigarette per year.
You will also note that the smoking of 5-6 cigarettes a day has not been shown to increase the risk for any supposed tobacco related health risks!
Will the anti-tobacco lobby now support a ban on 4th of july cookouts in the parks of America or even push lawsuits against the restaraunts and dad for cooking outdoors based upon femptograms and nanograms of ficticous levels of harm!
Here are just some of the chemicals present in tobacco smoke and what else contains them:
Arsenic, Benzine, Formaldehyde.
Arsenic- 8 glasses of water = 200 cigarettes worth of arsenic
Benzine- Grilling of one burger = 250 cigarettes
Formaldehyde – cooking a vegetarian meal = 100 cigarettes
As I have said if you accept the idea of a smoking ban based upon their INSANITY of science then you accept the demise of your ow freedom and that of others and business by the hand of that same science you base your backing of indoor and outdoor bans on! Rediculous doesnt even come close to match such a reason for backing any smoking ban for the same non-sensical junk science can and will be used to crucify everybody else.
They deny 20-25% of the country the right to enjoy freedom and association with like minded people.. Its america and as Cain said its time to take her back!
Yeah? Then do it for, oh, 20 years and come talk to me.
Clearly, you never worked in clubs.
All in all you raise what might be called an inventory fallacy. You know the words, but not the facts, the context, or the outcomes of decades worth of study.
Deny climate change much?
Yeah? Then do it for, oh, 20 years and come talk to me.
Clearly, you never worked in clubs.
All in all you raise what might be called an inventory fallacy. You know the words, but not the facts, the context, or the outcomes of decades worth of study.
Deny climate change much?
No need to, the global warming emails already took care of that MYTHOLOGY OF SCIENCE!
As far 5-6 cigs heres the reference:
Regulatory Toxicology and Pharmacology, Vol. 14, No. 1. (August 1991), pp. 88-105.
Abstract
Environmental tobacco smoke (ETS) is derived from cigarette smoldering and active smoker exhalation. Its composition displays broad quantitative differences and redistributions between gas and respirable suspended particulate (RSP) phases when compared with the mainstream smoke (MSS) that smokers puff. This is because of different generation conditions and because ETS is diluted and ages vastly more than MSS. Such differences prevent a direct comparison of MSS and ETS and their biologic activities. However, even assuming similarities on an equal mass basis, ETS-RSP inhaled doses are estimated to be between 10,000- and 100,000-fold less than estimated average MSS-RSP doses for active smokers. Differences in effective gas phase doses are expected to be of similar magnitude. Thus the average person exposed to ETS would retain an annual dose analogous to the active MSS smoking of considerably less than one cigarette dispersed over a 1-year period. By contrast, consistent epidemiologic data indicate that active smoking of some 4–5 cigarettes per day may not be associated with a significantly increased risk of lung cancer. Similar indications also obtain for cardiovascular and respiratory diseases. Since average doses of ETS to nonsmoking subjects in epidemiologic studies are several thousand times less than this reported intake level, the marginal relative risks of lung cancer and other diseases attributed to ETS in some epidemiologic studies are likely to be statistical artifacts, derived from unaccounted confounders and unavoidable bias
http://www.citeulike.org/user/vmarthi...
...
Its been measured thru the 16 cities study and other studies that bartenders only get about 6-9 cigs by annual equivalency in their 8 hour shifts 40 hours a week! If you want the citations Ive got them.
But heres something you need to understand about the second hand smoke JUNK SCIENCE:
the "threshold" theory and the "no threshold" theory.
The threshold theory argues that below a certain level any exposures to carcinogens literally "disappear" because they get swallowed up in all the random chaos of how the body works at a microscopic level. The "no threshold" theory says that even the smallest possible event, such as a one second exposure to a small beam of sunlight, could be the "trigger" that later produces a deadly cancer. The "no threshold" theory applied in meteorology would say that yes, a single flap of a single butterfly's wings in the backwoods of Australia could have "caused" Hurricane Katrina. The "threshold" scientists say that such an idea is nonsense. The Antismokers' "no safe level" argument is a "no-threshold" argument: they're saying even very small exposures to ETS could have as big an effect on lung cancer as a butterfly's wings in Australia could have on US hurricanes.
All it takes is a few believers and its a fact given moment for the gullible!
Your PSYCHOSIS has been studied and found non-harmful and they can seek treatment!
Toxicol Rev. 2003;22(4):235-46.
Idiopathic environmental intolerance: Part 1: A causation analysis applying Bradford Hill's criteria to the toxicogenic theory.
Staudenmayer H, Binkley KE, Leznoff A, Phillips S.
Source
Behavioral Medicine, Multi-Disciplinary Toxicology, Treatment and Research Center, Denver, Colorado 80222, USA. hstaudenmayer@comcast.net
Abstract
Idiopathic environmental intolerance (IEI) is a descriptor for a phenomenon that has many names including environmental illness, multiple chemical sensitivity and chemical intolerance. Toxicogenic and psychogenic theories have been proposed to explain IEI. This paper presents a causality analysis of the toxicogenic theory using Bradford Hill's nine criteria (strength, consistency, specificity, temporality, biological gradient, biological plausibility, coherence, experimental intervention and analogy) and an additional criteria (reversibility) and reviews critically the scientific literature on the topic. The results of this analysis indicate that the toxicogenic theory fails all of these criteria. There is no convincing evidence to support the fundamental postulate that IEI has a toxic aetiology; the hypothesised biological processes and mechanisms are implausible.
...
I am in favour of people being able to smoke in their own establishments and being free to CHOOSE if they will allow that or not. I think smoke alarms should be a choice also in free-standing buildings not adjacent to others. I am not against all building codes - because people do not KNOW if a building has been built safely or not, whereas they do KNOW if a building - that is privately owned - is one where smoking is allowed. And they CHOOSE to go there.
I am not against all regulation. That is dumb. Are you for regulation of EVERYTHING? Do you want the government to regulate everything you eat or drink or how much paper you use or whether you exercise? That would be the DUMB answer back to you. I am against most regulations that pertain to private actions where a third party is not harmed via casual association. (I.e., they put themselves in the environment unknowingly.) I am against the government telling me I can't allow smoking in my establishment where only those who CHOOSE to be there and CHOOSE to smoke (or be around smokers) are "harmed". AND, hate to break it to you genius, but that ain't so with traffic laws where third parties are hurt in situations where they do not CHOOSE to put themselves at risk.
Here is the bottom line on SMOKING - not building codes. It is MY restaurant. YOU don't have to enter it. YOU don't have to work there. No one ELSE is hurt by accident if I allow smoking in MY privately owned establishment. And if you think that smoke goes through the walls and into a shop next door, I'd ask what YOU are smoking.
And yes drugs should be decriminalized.
Just because someone is for the right of people to smoke in private establishment,s they want no anti-discrimination laws? Wow, you're really out there. No, babe, I'm fine with making it hard on racists. However, if some moron doesn't want to associate PRIVATELY with someone of another race, or have him in his home, that is his right. My right is to avoid him. And, by the way, I do. Wouldn't catch me near an OWS idiot holding up an anti-Semitic sign. Really. How about you?
People should have the right to smoke in privately-owned establishments in the US. Sorry to break it to the left, but that is a liberal position. And you all are afraid of the religious right? I have spent a lot of time at work around religious folk. I have never, really, found anyone as self-righteous and as restrictive of personal freedom among the religious at churches or temples as I have among the left. (Where, unfortunately, I have also spent time.)
Denialism: what is it and how should scientists respond?
EFFECT OF MATERNAL TOBACCO SMOKING OR EXPOSURE TO SECOND-HAND SMOKE ON THE LEVELS OF 4-(METHYLNITROSAMINO)-1-(3-PYRIDYL)-1-BUTANOL (NNAL) IN URINE OF MOTHER AND THE FIRST URINE OF NEWBORN
Florek, E
JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY 62 (3): 377-383 JUN 2011
Abstract: Tobacco smoking during pregnancy is associated with a variety of negative consequences not only for the mother, but also for the developing fetus. Many studies have shown that carcinogens contained in tobacco smoke permeate across the placenta, and are found in fetus. The aim of the study was to determine the prenatal exposure to tobacco-specific carcinogenic N-nitrosamines on the basis of measurements of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) in urine of smoking and second-hand smoke (SHS) exposed women and in the first urine of their newborns. A questionnaire documenting demographics and socio-economical data, smoking habits and exposure to SHS was completed by 121 delivering women near or at term. Maternal concentrations of cotinine and NNAL were measured in urine of the mother and the first urine of her newborn infant by liquid chromatography tandem mass spectrometry (LC/MS/MS). The mean concentration of cotinine was 439.2 ng/mg creatinine and NNAL concentration in urine of smoking women was 74.0 pg/mg creatinine, and for her newborn 78.6 pg/mg creatinine. Among mothers exposed to SHS, cotinine and NNAL mean concentration were 23.1 ng/mg creatinine, and 26.4 pg/mg creatinine. In newborns of SHS exposed mothers during pregnancy the mean concentration of NNAL was 34.1 pg/mg creatinine, respectively. Active tobacco smoking as well as passive exposure to smoking during pregnancy is an important source of tobacco specific N-nitrosamines to the fetuses as evidenced by increased concentrations of this carcinogen. Determination of NNAL in maternal urine samples can be a useful biomarker of prenatal exposure of newborn to carcinogenic nitrosamines.
Role of carbon monoxide in impaired endothelial function mediated by acute second-hand tobacco, incense, and candle smoke exposures.
Weber, Lynn P., Al-Dissi, Ahmad, Marit, Jordan S., German, Timothy N., Terletski, Sharilyn D.
Environmental Toxicology & Pharmacology May2011, Vol. 31 Issue 3, p453-459
Summary: Abstract: The aim of this study was to determine if carbon monoxide (CO) is responsible for acute adverse cardiovascular effects of different sources of smoke: second-hand tobacco smoke (SHS), incense and candle smoke. Endothelial function was tested using flow-mediated dilation (FMD) in pigs and was shown to be sensitive to nitric oxide synthase blockade. Subsequent experiments showed that FMD was significantly impaired compared to sham-exposed pigs at 30min after a 30-min exposure to all three sources of smoke. In contrast, SHS significantly increased systolic, diastolic and pulse pressures compared to sham-exposure, while both incense and candle smoke exposure had no effect. The FMD impairment correlated well with CO levels in the exposure chamber, but not total particulates or venous CO-hemoglobin. Therefore, this study suggests a gas phase component of smoke that accompanies CO, but not CO itself, is responsible for acute endothelial dysfunction after SHS, incense or candle smoke exposure.
The association between active smoking, smokeless tobacco, second-hand smoke exposure and insufficient sleep.
Sabanayagam, Charumathi
Sleep Medicine vol. 12, no. 1 (Jan 2011), p. 7
Summary: Background: Studies have shown that cigarette smoking is associated with sleep disorders in the general population. But studies examining the association between smokeless tobacco use, second-hand smoke exposure and insufficient rest/sleep are limited. Methods: We examined the association between smoking, smokeless tobacco use (n = 83,072), second-hand smoke exposure (n = 28,557) and insufficient rest/sleep among adults aged ≥ 20 years in the state-based 2008 Behavioral Risk Factor Surveillance System. Exposure to second-hand smoke was defined as >1day of exposure to cigarette smoking either at home or in the workplace in the preceding 7days. Insufficient rest/sleep was defined as not getting enough rest/sleep everyday in the preceding 30days. Results: Compared to never smokeless tobacco users, the odds ratio (OR; 95% confidence interval [CI]) of insufficient rest/sleep was 1.16 (1.00–1.36) and 1.74 (1.37–2.22) among former and current users. Compared to non-smokers/non-smokeless tobacco users, the OR (95% CI) of insufficient rest/sleep for those who were both current smokers and current smokeless tobacco users was 2.21 (1.66–2.94). Regarding second-hand smoke exposure among non-smokers, those with second-hand smoke exposure had higher odds for insufficient rest/sleep than those without. In contrast, the odds of insufficient rest/sleep were similar among current smokers with or without second-hand smoke exposure. Conclusions: In a multiethnic sample of US adults, compared to non-smokers/non-smokeless tobacco users, those who were both current smokers and current smokeless tobacco users had twice the odds of insufficient sleep. Second-hand smoke exposure was associated with insufficient rest/sleep among non-smokers.
Distinct tachykinin NK(1) receptor function in primate nucleus tractus solitarius neurons is dysregulated after second-hand tobacco smoke exposure.
Sekizawa S
British Journal of Pharmacology 163(4):782-91, 2011 Jun
Summary:
BACKGROUND AND PURPOSE: Second-hand tobacco smoke (SHS) exposure in children increases the risk of asthma and sudden infant death syndrome. Epidemiological and experimental data have suggested SHS can alter neuroplasticity in the CNS, associated with substance P. We hypothesized that exposure to SHS in young primates changed the effect of substance P on the plasticity of neurons in the nucleus tractus solitarius (NTS), where airway sensory information is first processed in the CNS.
EXPERIMENTAL APPROACH: Thirteen-month-old rhesus monkeys were exposed to filtered air (FA, n= 5) or SHS (n= 5) for >6 months from 50 days of their fetal age. Whole-cell patch-clamp recordings were performed on NTS neurons in brainstem slices from these animals to record the intrinsic cell excitability in the absence or presence of the NK(1) receptor antagonist, SR140333 (3 microM).
KEY RESULTS: Neurons were electrophysiologically classified based on their spiking onset from a hyperpolarized membrane potential into two phenotypes: rapid-onset spiking (RS) and delayed-onset spiking (DS) types. In RS neurons, SR140333 reduced the spiking response, similarly in both FA- and SHS-exposed animals. In DS neurons, SR140333 almost abolished the spiking response in FA-exposed animals, but had no effect in SHS-exposed animals.
CONCLUSIONS AND IMPLICATIONS: The contribution of NK(1) receptors to cell excitability depended on firing phenotype of primate NTS neurons and was disrupted by SHS exposure, specifically in DS neurons. Our findings reveal a novel NK(1) receptor function in the primate brainstem and support the hypothesis that chronic exposure to SHS in children causes tachykinin-related neuroplastic changes in the CNS.
Better luck next time, John. Are you sure you’re not self-projecting when you talk about being gullible? It’s obvious you are.
And to the author. Feel free to start the "You're hijacking my blog" stuff about now. This is a pretty typical leftist rant here at OS when people dare to disagree - especially if they post more than once. John E., watch out.
http://tobaccoanalysis.blogspot.com/2007/08/new-study-shows-mcdonalds-meal-causes.html
,,,,,,,,,,,,,,,,,,,,,
From: Glantz, Stanton A
Date: Sun Aug 19 2007 - 21:00:22 PDT
The finding of similar changes in endothelial function with a high cholesterol load is not new. It just shows that the high oxidant load has effects similar to SHS (which is probably also acting, at least in part through the oxidant load in the smoke). We pubished the first paper on this over ten years ago, when I was an associate editor of the Journal of the American College of Cardiology. (The "intervention there was an eg McMuffin.)
In addition to the acute effects, the associated insult to the vascular endothelium is important for the long-run development of atheroschlerosis.
Mike's comments are further evidence that he just does not understand modern vascular biology."
as to Glantz's comments that Dr. Siegel doesn't understand modern vascular biology well, one needs only compare the oxidant load of mass of SHS inhaled by a bystander to the mass of a McDonalds meal to realize it is really Glantz who does not understand modern vascular biology very well.
In addition Glantz ignores the fact that the McDonalds meal contains all the same components present in SHS, but in much greater quantities.
www.fda.gov/ohrms/dockets/dockets/99n1174/ts00020.pdf
Not only does Glantz conveniently ignore the more plausible science in attacking Doc, Glantz apparantly does not even acknowlege dosimetry exists.
..........................................
If dialation of the brachial artery is affected by something as normal and routine as eating a meal, is it even appropriate to refer to it as a "dysfunction"?
I feel quite confident that changes in bloodflow in the brachial artery could be measured in individuals who, say, jog a lap around the track, or maybe after taking an asprin, or even possibly while watching an hilarious movie. Are these "dysfunctions"?
Maybe it's just a normal physiological response. Not every measurable change in the human body needs to be pathologized.
..............................
www.fda.gov/ohrms/dockets/dockets/99n1174/ts00020.pdf
(a) Humans have many natural defenses that buffer against normal exposures to toxins
(3) and these are usually general, rather than tailored for each specific chemical.
Thus they work against both natural and synthetic chemicals. Examples of general
defenses include the continuous shedding of cells exposed to toxins ——th—e surface layers
of the mouth, esophagus, stomach, intestine, colon, skin and lungs are discarded every
few days; DNA repair enzymes, which repair DNA that was damaged from many
different sources; and detoxification enzymes of the liver and other organs which generally
target classes of chemicals rather than individual chemicals. That human defenses
are usually general, rather than specific for each chemical, makes good evolutionary
sense. The reason that predators of plants evolved general defenses is presumably to be
prepared to counter a diverse and ever-changing array of plant toxins in an evolving
world; if a herbivore had defenses against only a set of specific toxins, it would be at a
great disadvantage in obtaining new food when favored foods became scarce or evolved
new chemical defenses.
The inconvenient truth is that the only studies of children of smokers suggest it is PROTECTIVE in contracting atopy in the first place. The New Zealand study says by a staggering factor of 82%.
“Participants with atopic parents were also less likely to have positive SPTs between ages 13 and 32 years if they smoked themselves (OR=0.18), and this reduction in risk remained significant after adjusting for confounders.
The authors write: “We found that children who were exposed to parental smoking and those who took up cigarette smoking themselves had a lower incidence of atopy to a range of common inhaled allergens.
“These associations were found only in those with a parental history of asthma or hay fever.”
They conclude: Our findings suggest that preventing allergic sensitization is not one of them.”
The Journal of Allergy and Clinical Immunology
Volume 121, Issue 1 , Pages 38-42.e3, January 2008
http://www.jacionline.org/article/S00...(07)01954-9/abstract
.
This is a Swedish study.
“Children of mothers who smoked at least 15 cigarettes a day tended to have lower odds for suffering from allergic rhino-conjunctivitis, allergic asthma, atopic eczema and food allergy, compared to children of mothers who had never smoked (ORs 0.6-0.7)
CONCLUSIONS: This study demonstrates an association between current exposure to tobacco smoke and a low risk for atopic disorders in smokers themselves and a similar tendency in their children.”
Clin Exp Allergy 2001 Jun;31(6):908-14
http://www.data-yard.net/30/asthma.htm
...
Lung function and exposure to workplace second-hand smoke during exemptions from smoking ban legislation: an exposure--response relationship based on indoor PM2.5 and urinary cotinine levels.
Hak-Kan Lai, Hedley, Anthony J., Repace, James, Ching So, Qiu-Ying Lu, McGhee, Sarah M., Fielding Richard, Chit-Ming Wong
Thorax Jul2011, Vol. 66 Issue 7, p615-623
Summary: Background The effects of workplace second-hand smoke (SHS) on lung function remain uncertain because of a lack of objective measures for SHS exposures. Objective To determine whether an exposureeresponse association exists between lung function and two different markers of SHS based on indoor fine particulate (PM2.5) and urinary cotinine levels in non-smoking catering workers. Design A cross-sectional study during a 1.5-year exemption of licensed catering premises from smokefree legislation. Participants 186 non-smoking catering workers aged 18-65 years in Hong Kong were recruited. A declared non-smoking status was accepted in workers with exhaled breath carbon monoxide levels 1 in litres), forced vital capacity (FVC in litres) and forced expiratory flow as 25-75% of FVC (FEF25-75 in l/s) were recorded. Results Indoor fine particulate (PM2.5) concentrations were 4.4 times as high in smoking premises (267.9 mg/m3) than in non-smoking premises (60.3 mg/m3) and were strongly associated with the probability of permitted smoking (R2=0.99). Smoking was the dominant source of particulates (R2=0.66). Compared with workers exposed to the lowest indoor PM2.5 stratum (3), lung function was lower in the three higher PM2.5 strata (25-75-175, >175 μg/m3) with FEV1 -0.072 (95% CI -0.123 to -0.021), -.078 (95% CI -0.132 to -0.024), -0.101 (95% CI -0.187 to -0.014); FEF25-75 -0.368 (95% CI -0.660 to -0.077), -0.489 (95% CI -0.799 to -0.179), -0.597 (95% CI -0.943 to -0.251); and FEV1/FVC (%) -2.9 (95% CI -4.8 to -1.0), -3.2 (95% CI -5.1 to -1.4) and -4.4 (95% CI -7.4 to -1.3), respectively. Urinary cotinine was associated positively with indoor PM2.5 but negatively with lung function. Consistently lower values for lung function per unit increase of indoor PM2.5 were found. Conclusion Lung function is inversely associated with workplace SHS. Workplace exemptions and delays in implementing smoke-free policies and current moves to relax legislation are a major threat to the health of workers.
Increased Tobacco Exposure in Older Children and Its Effect on Asthma and Ear Infections
Hawkins, SS
JOURNAL OF ADOLESCENT HEALTH 48 (6): 647-650 JUN 2011
Summary: Purpose: To examine selected social determinants of children's exposure to household tobacco use and smoking inside the home and to assess the effect of second-hand smoke exposure on asthma and ear infections across children's age groups.
Methods: A total of 90,961 parents of children aged 0-17 years from the 2007 National Survey of Children's Health were included in the study.
Results: In all, 26.2% of parents reported that anyone in the household used tobacco products. Parents of children aged 6-11 and 12-17 years were 1.97 (adjusted OR; 95% CI, 1.65-2.36) and 2.93 (2.46-3.49) times more likely, respectively, to report that someone smoked inside the house than parents of younger children. Second-hand smoke exposure varied by children's race/ethnicity, and children from more disadvantaged circumstances were more likely to be exposed. For all children, they were more likely to ever have asthma if someone in their household used tobacco. Although young children's likelihood of recurrent ear infections did not increase with household tobacco use, children aged 12-17 were 1.67 (1.02-2.72) times more likely to have recurrent ear infections if someone smoked inside their home. Conclusion: Family members are increasingly likely to smoke indoors as children age, which may increase adolescents' vulnerability to ear infections. Parents and health professionals should monitor second-hand smoke exposure at home and encourage a smoke-free environment.
Factors associated with second-hand smoke exposure in young inner-city children with asthma.
Butz AM
Journal of Asthma 48(5):449-57, 2011 Jun
Summary: OBJECTIVES: To examine the association of social and environmental factors with levels of second-hand smoke (SHS) exposure, as measured by salivary cotinine, in young inner-city children with asthma.
METHODS: We used data drawn from a home-based behavioral intervention for young high-risk children with persistent asthma post-emergency department (ED) treatment (N = 198). SHS exposure was measured by salivary cotinine and caregiver reports. Caregiver demographic and psychological functioning, household smoking behavior, and asthma morbidity were compared with child cotinine concentrations. Chi-square and ANOVA tests and multivariate regression models were used to determine the association of cotinine concentrations with household smoking behavior and asthma morbidity.
RESULTS: Over half (53%) of the children had cotinine levels compatible with SHS exposure and mean cotinine concentrations were high at 2.42 ng/ml (SD 3.2). The caregiver was the predominant smoker in the home (57%) and 63% reported a total home smoking ban. Preschool aged children and those with caregivers reporting depressive symptoms and high stress had higher cotinine concentrations than their counterparts. Among children living in a home with a total home smoking ban, younger children had significantly higher mean cotinine concentrations than older children (cotinine: 3-5 year olds, 2.24 ng/ml (SD 3.5); 6-10 year olds, 0.63 ng/ml (SD 1.0); p
Passive smoking and aortic arch calcification in older Chinese never smokers: the Guangzhou Biobank Cohort Study.
Xu L
International Journal of Cardiology 148(2):189-93, 2011 Apr 14
148(2):189-93, 2011 Apr 14
Summary: OBJECTIVE: To study whether passive smoking is a risk factor for aortic arch calcification (AAC) among never smokers.
BACKGROUND: We have previously reported that active smoking increases the risk of AAC, but the effect of passive smoking has not been reported.
METHODS: We used baseline data of the Phase 1 Guangzhou Biobank Cohort Study (GBCS). 7702 older Chinese never smokers from the Phase 1 GBCS were included. Information on passive smoking and potential confounders were collected by standardized interviews and laboratory assays. AAC was diagnosed from chest X-ray by two experienced radiologists. Unconditional logistic regression was used to estimate odds ratios of AAC for passive smoking with adjustment for potential confounders.
RESULTS: In women, the risk for aortic arch calcification (AAC) increased significantly with increasing duration of adulthood passive smoking exposure at home, at work and total duration of adulthood home and work exposure [adjusted odds ratio 1.24 (95% confidence interval 1.09-1.41) for high level of total exposure] (P for trend from 0.012 to 0.001). For passive smoking at home, at work and total exposure, significant trends of increasing severity of AAC with increasing duration of exposure were observed in men and women combined (P for trend from 0.05 to 0.002).
CONCLUSION: Passive smoking is a risk factor for aortic arch calcification. Studies of passive smoking and AAC, especially in developing countries can generate important local evidence to raise awareness and to support public health measures to protect non-smokers from second-hand smoke.
John, stop cut and pasting old studies from from bogus blog posts. You're becoming a parody of yourself.
Among mothers exposed to SHS, cotinine and NNAL mean concentration were 23.1 ng/mg creatinine, and 26.4 pg/mg creatinine. In newborns of SHS exposed mothers during pregnancy the mean concentration of NNAL was 34.1 pg/mg creatinine, respectively.
You whizz this stuff away every single day of your life. If it wasnt detected in their urinalysis I'd suspect they hasve more problems than anything as it shows up it means mom and babys systems are working fine!
They cant claim it comes from smoke either as its in the environment naturally everywhere and its no just specific to tobacco!
This study appears to be wall to wall junk science. They seem to be most worried about "carcinogenic tobacco-specific nitrosamines or TSNAs..nanograms of nitrosamines" (1)
Guess where Nitrosamines are also formed? Cooking fish, where TSNAs are measured in microgrammes, but in the study nanogrammes and picograms a factor of a thousand times and a million times smaller. (2)
Nitrosamines are also found in ham, milk, children's balloons and tap water. (3)
Then one has to ask what did these study participants eat for breakfast or lunch or dinner or even a week before as it would effect the chemistry!
Finally the World Health Organization's cancer mouthpiece the International Agency Research on Cancer says on Nitrosamines: "5.2 Human carcinogenicity data. No data were (sic) available to the Working Group." (4)
So we have a dose that is so low, cooking a fish produces 1,000 times more "carcinogens" on a chemical which has not been proven to cause cancer in the first place.
Junk science that insults the intelligence.
Just a little bit more about the N'-nitrosonornicotine found in SHS/ETS.
However, the dose makes the poison!!
This stuff is NOT present in quantities known to be hazardous!!!
The concentration of N'-nitrosonornicotine (NNN) ranged from not detected to 23 pg/l, that of N'-nitrosoanata-bine ranged from not detected to 9 pg/l, while 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) was detected in concentrations ranging from 1 to 29 pg/l.
Thus, non-smokers can be exposed to highly carcinogenic TSNA.
NNN = 0 to 23 picograms per liter
NNK = 0 to 29 picograms per liter
1 cubic meter = 1,000 liters
1 nanogram(NG) = 1,000 picograms
Thus, NNN of 0 to 23 picograms per liter is the same as 0 to 23 nanograms(ng) per cubic meter
NNK of 0 to 29 picograms per liter is the same as 0 to 29 nanograms(ng) per cubic meter.
The question is whether or not 0 to 29 nanograms(ng) per cubic meter of a carcinogenic substance is a dangerous level?
The Department of Health and Human Services (DHHS) has concluded that inorganic arsenic is known to be a human carcinogen.
The International Agency for Research on Cancer (IARC) cites sufficient evidence of a relationship between exposure to arsenic and human cancer. The IARC classification of arsenic is Group 1.
The EPA has determined that inorganic arsenic is a human carcinogen by the inhalation and oral routes, and has assigned it the cancer classification, Group A.
http://www.atsdr.cdc.gov/toxprof...iles/tp2- c6.pdf
6.4.1 Air
Mean arsenic levels in ambient air in the United States have been reported to range from 20 to 30 ng/m3 in urban areas (Davidson et al. 1985; EPA 1982c; IARC 1980; NAS 1977a).
NOTE: 20 to 30 ng/m3 is NOT stated to be a hazardous level of exposure to this known human carcinogen.
What's this I hear? ETS can also cause heart disease? Okidokie. Let's take a look at that. From the CDC's own estimates, http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5644a2.htm here's who gets heart disease:
Coronary heart disease: Current Smokers 29.3% Former smokers 31.8% Never smokers 38.9%
Stroke: Current smokers 30,1%, Former smokers 23% Never smokers 47%
So current smokers who also breathe their own second hand smoke and everyone else's since they don't avoid smoke laden places get less heart disease than never smokers?
UTILIZING MAXIMUM ALLOWABLE EXPOSURE RATES!
64 oz/8 glasses = 18,000ng
1 cig max arsenic = 32ng
18000/32 = 562.5 cigs not 200
Everything is a dose response relationship when it comes to harm thats why its best to use the maximum safe limits when doing comparisons and thats what anti-tobacco doesnt want let known! Why do you think you will never see a smokefree web site admitting the actual levels or percentages of tobacco smoke and its constituents!
IT WOULD MAKE THEM A LAUGHING STOCK!
About 90% of secondary smoke is composed of water vapor and ordinary air with a minor amount of carbon dioxide. The volume of water vapor of second hand smoke becomes even larger as it qickly disperses into the air,depending upon the humidity factors within a set location indoors or outdoors. Exhaled smoke from a smoker will provide 20% more water vapor to the smoke as it exists the smokers mouth.
4 % is carbon monoxide.
6 % is those supposed 4,000 chemicals to be found in tobacco smoke. Unfortunatley for the smoke free advocates these supposed chemicals are more theorized than actually found.What is found is so small to even call them threats to humans is beyond belief.Nanograms,picograms and femptograms......
(1989 Report of the Surgeon General p. 80).
They did the figures for what it takes to meet all of OSHA'S minimum PEL'S on shs/ets.......Did it ever set the debate on fire.
They concluded that:
All this is in a small sealed room 9x20 and must occur in ONE HOUR.
For Benzo[a]pyrene, 222,000 cigarettes
"For Acetone, 118,000 cigarettes
"Toluene would require 50,000 packs of simultaneously smoldering cigarettes.
Acetaldehyde or Hydrazine, more than 14,000 smokers would need to light up.
"For Hydroquinone, "only" 1250 cigarettes
For arsenic 2 million 500,000 smokers at one time
The same number of cigarettes required for the other so called chemicals in shs/ets will have the same outcomes.
So,OSHA finally makes a statement on shs/ets :
Field studies of environmental tobacco smoke indicate that under normal conditions, the components in tobacco smoke are diluted below existing Permissible Exposure Levels (PELS.) as referenced in the Air Contaminant Standard (29 CFR 1910.1000)...It would be very rare to find a workplace with so much smoking that any individual PEL would be exceeded." -Letter From Greg Watchman, Acting Sec'y, OSHA
The US Department of Energy wired up restaurant and bar workers with air sampling devices to get a better picture of worker exposure to ETS. Their conclusions, published in "Exposure to Environmental Tobacco Smoke in Sixteen Cities in the United States As Determined by Personal Breathing Zone Air Sampling", appearing in the Journal of Exposure Analysis and Environmental Epidemiology, were that inhalation exposure to ETS was so low as to render health hazards negligible to improbable. The study showed that typical exposure rates taken for granted by anti-ETS lobbyists are 2 to 5 times the actual exposure rate, over an 8 hour exposure period. Respirable suspended particulate matter exposure was 1/4 the threshold level OSHA considers significant. These findings were later replicated by the Oak Ridge National Laboratories in ""Determination of Exposure to Environmental Tobacco Smoke in Restaurants and Tavern Workers in One U.S. City" in 2000. Additional studies suggest that, in opposition to the anti-smoking forces' claim that bartenders involuntarily inhale half a pack a day of cigarette smoke, bartenders annual exposure to smoke rises, at most, to the equivalent of 6 cigarettes/year. The question must be asked, then: if exposure to environmental tobacco smoke was so low for individuals working eight-hour shifts in restaurants and bars, how much lower would be the exposure to individuals exposed only during the course of a meal?
The 2006 standards tighten the 24-hour fine particle standard from 65 micrograms per cubic meter (µg/m3) to 35 µg/m3, and retain the current annual fine particle standard at 15 µg/m3.
EPA has decided to retain the existing 24-hour PM10 standard of 150 µg/m3. Due to a lack of evidence linking health problems to long-term exposure to coarse particle pollution, the Agency has revoked the annual PM10 standard.
The Agency selected the levels for the final standards after reviewing thousands of peer-reviewed scientific studies about the effects of particle pollution on public health and welfare. External scientific advisors and the public examined EPA's science and policy review documents. The Agency also carefully considered public comments on the proposed standards. EPA held three public hearings and received over 120,000 written comments.
While EPA provisionally assessed new, peer-reviewed studies about particulate matter and health (including some studies received during the comment period), these studies were not the basis for the final decision. EPA will consider those studies during the next review of the PM standards.
http://www.epa.gov/pm/naaqsrev2006.html
If you feel that smoking is that harmful that it should be very limited as to where people can do it, then why don't you ban it? We can ban stuff we don't like can't we? What happens when Cain gets elected and decides he doesn't like you? Maybe he can issue an executive order to outlaw your writing.
BTW, I'm a non-smoker who has never tried smoking. I also had a smoke free restaurant. That was my choice, not the governments, as it should be.
The actual standard to use is OSHA'S
The EPA standard is to be used for OUTSIDE ambient air quality and it is the average over a period of 3 years.
The proper standard to compare to is the OSHA standard for indoor air quality for respirable particulate (not otherwise specified) for nuisance dusts and smoke. That standard is 5000 ug/m3 on a time-weighted average (8 hours a day, 5 days a week) and is intended to be protective of health over an average working life of 30 years!
on carbon monoxide
1) The OSHA permissible exposure limit (PEL) for carbon monoxide is 50 ppm
2) No bar, restaurant, or "public" space is unventilated. In the US, ASHRAE standards require at least 15 cfm of outdoor air into building spaces, in the hypothetical test room described with 20 occupants there would have been 300 cubic feet per MINUTE of fresh air required to be pumped into the space, additionally the furnace or air conditioning systems would be providing 4 - 10 air changes per hour into that same space, diluting those indoor air pollutants with 172 to 400 cubic meters of ventilation.
3) the ambient (naturally occurring) level of carbon monoxide OUTDOORS is 9 ppm,
Also found online here:
http://docs.google.com/viewer?a=v&q=cache:0RykGN4sbpUJ:www.bartlett.ucl.ac.uk/web/ben/CO%2520Measurement%2520Protocols.doc+what+is+the+ambient+co+level+indoors&hl=en&gl=us&pid=bl&srcid=ADGEESiob-1tuv-C8CuhxImBICzCmVITI9VnhqasAV9QtRKeoiXpKL5pflJxu_hlzpvfSK75z1MFL7l_UqWfqlWMbohxwnes7gVHyjqeMXsXBL5vnOzeLp6a9ZhiKPZNoH9w6RaFdzSr&sig=AHIEtbSoTI_AkF-s0pcYFa-cjCdJRlJy7A pg 12
CO is CO is produced in the body primarily by the action of heme oxygenase-1, which continuously breaks down heme proteins of all kinds (hemoglobin in blood, myoglobin in muscle, cytochromes in mitochondria, etc) into iron (which is stored as ferritin until the body uses it to make more heme) and equal parts of biliverdin (a potent anti-oxidant that is converted to bilirubin) and CO, which is bioactive in the body as a neurotransmitter, vasodilator and key catalyst in over 100 pathways.
HO-1 is known as the “universal stress enzyme” because its activity (and resulting CO production) are quickly and greatly increased from ten to hundred-fold by human exposures to mental, physical and environmental stressors of any kind, including infections of all kinds, many chronic diseases (including asthma, diabetes and heart disease), and sensory stressors such as bright lights, loud sounds, strong odors, and hot weather.
Several studies report that CO levels in exhaled breath are maximized in the range of parts per million—and thus are detectable with the type of CO detectors recommended in Chapter 1
Mark
43 cubic meters is 1518 cubic feet, assuming a standard residential ceiling height (8') this room would have been 10' x 18' x 8' approx. if it were unventilated, after 78 minutes of near suffocating conditions, the 20 inhabitants would have been stressed which as reported below causes the body to produce higher levels of carbon monoxide.
HO-1 is known as the “universal stress enzyme” because its activity (and resulting CO production) are quickly and greatly increased from ten to hundred-fold by human exposures to mental, physical and environmental stressors of any kind,
You started it,I was done til you hit it with junk studies that when you look are simply QUESTIONAIRE STUDIES........continine levels arent even adequate for measuring exposure anyway,foods like potatoes and egg plant,tomatoes all have nicotine in them and continine is what the body turns it into! Make a note,nicotine is NOT A CARCINOGEN. The levels your studies point to arent hazardous to anyone and can even be the result of a heavy meal where it concerns nitrosomines or anything else folks claim is in tobacco,everything in tobacco is also in everything else around us some more some less.
Benzo-a- pyrene is in tobacco smoke thats a PAH,its also that sweet smell you get from gassing your car up from gasoline and your getting equal to thousands of cigs of that same benzo just in one fill up!
These anti-tobacco funded studies are mere junk and what they normally do is take a normal bodily function that occurrs to any natural stimuli and try and spin it as caused by second hand smoke......even the SIDS THING is a myth,SIDS is caused by low serotonin levels in a babys brain that regulates breathing patterns!
I could go on and on all nite destroying the myth of second hand smoke and even the 3rd hand smoke junk science being spouted off now but instead heres some links:
Scientific Evidence Shows Secondhand Smoke Is No Danger
Written By: Jerome Arnett, Jr., M.D.
Published In: Environment & Climate News
Publication Date: July 1, 2008
Publisher:
http://www.heartland
.org/policybot/resul
ts/23399/Scientific_
Evidence_Sho...
myth-of-second-hand-
smoke
http://yourdoctorsor
ders.com/2009/01/the
-myth-of-second-hand
-smoke
BS Alert: The 'third-hand smoke' hoax
http://www.examiner.com/public-policy-in-louisville/bs-alert-the-third-hand-smoke-hoax
The thirdhand smoke scam
http://velvetgloveironfist.blogspot.com/2010/02/thirdhand-smoke-scam.html
Heart attacks Frauds and Myths..
http://www.spiked-on
line.com/index.php/s
ite/article/7451/
New study: No evidence linking SHS and lung cancer
http://fightantismok
ertyranny.blogspot.c
om/2010/11/new-study
-no-evidence...
Dial 9-9-9 for nonsense.
To clarify. If one is talking about this comparison at all, (raised, by the way by one of the anti-smoking, pro-ban people here) one has to do this:
If a ban on Jim Crow is based on its (Jim Crow's ) badness and one FAVORS SUCH A BAN;
And a ban on smoking is also based on its (smoking's) badness and one, DOES NOT FAVOUR SUCH A BAN,
The logical assumption is that one thinks Jim Crow WORSE than smoking. I.e., one favours the BAN on the worse item/situation.
BTW, as said, the comparison is not mine, but that would be how the logic would play out.
You certainly write… I mean copy and paste a lot for someone who doesn’t have anything substantial to say.
Is this the best you can do? You must be shoveling air.
Wow, this is what we call reliable sources:
Scientific Evidence Shows Secondhand Smoke Is No Danger
http://www.heartland
.org/policybot/resul
ts/23399/Scientific_
Evidence_Sho...
http://yourdoctorsor
ders.com/2009/01/the
-myth-of-second-hand
-smoke
http://www.examiner.com/public-policy-in-louisville/bs-alert-the-third-hand-smoke-hoax
http://velvetgloveironfist.blogspot.com/2010/02/thirdhand-smoke-scam.html
http://www.spiked-on
line.com/index.php/s
ite/article/7451/
http://fightantismok
ertyranny.blogspot.c
om/2010/11/new-study
-no-evidence...
Two points are very clear:
1. You don’t even understand what you’re copying, even less the real studies on this topic.
2. You’re a fraud and a poser.
When you write this “I could go on and on all nite destroying the myth of second hand smoke and even the 3rd hand smoke junk science being spouted off now”. You haven’t met me yet. I could also go on all night and day hands down, if I wanted to.
Here’s another taster:
The association between second hand smoke and low birth weight and preterm delivery.
Khader, Yousef S.
Maternal and Child Health Journal vol. 15, no. 4 (May 2011), p. 453
Summary: To determine the association between maternal exposure to SHS and low birth weight and preterm delivery. This cross-sectional study was carried out in the four main governmental hospitals dealing with deliveries in the north of Jordan. A consecutive 8,490 women who delivered in these hospitals between April 2007 and September 2007 were included in the study after excluding those who reported active smoking during the current pregnancy. Prestructured questionnaire and review of hospital records were used to collect data about maternal background, obstetric history, medical history, and data related to second hand smoke exposure. Overall, 13.8% of women gave birth to a preterm baby and 10.0% gave birth to a low birth weight baby. About 12.6% of women who were exposed to SHS delivered low birth weight babies compared to 7.7% for non exposed women. The rate of preterm delivery among the exposed group was significantly higher than that among the non-exposed group (17.2 vs. 10.6%). In the multivariate analysis, exposure to SHS during pregnancy was significantly associated with increased odds of low birth weight (OR = 1.56 (95% CI 1.31, 1.89)) and preterm delivery (OR = 1.61 (95% CI: 1.30, 1.99)). Exposure of women to SHS during pregnancy is associated with increased odds of low birth weight and preterm delivery.
Health care professionals should carry out educational programs to increase awareness and understanding of pregnant women and their husbands about the harmful effects of second hand smoke on birth outcomes.
Smoking and endothelial progenitor cells: a revision of literature.
Author: Di Stefano R
Current Pharmaceutical Design 16(23):2559-66, 2010
Summary: Accumulating evidence indicates that circulating endothelial progenitor cells (EPCs) derived from bone marrow contribute to reendothelialization of injuried vessels as well as neo-vascularization of ischemic lesions in either a direct or an indirect way. Moreover, the number and/or the functional activity of EPCs are inversely correlated with risk factors for cardiovascular disease. Among the different risk factors, cigarette smoking is a major cause of reducing the numbers and function of circulating EPCs. This review is a revision of recent literature on EPC alteration associated with smoking. In particular, we show the recent observation on the effects of active and second hand smoke (SHS) exposure on EPC number and functional activity. This review also considers the effects of nicotine and other smoke compounds on EPC number and activity, in in vitro and in vivo models.
Development of an ultrasensitive immunochromatography test to detect nicotine metabolites in oral fluids
Gonzalez, JM
ANALYTICAL AND BIOANALYTICAL CHEMISTRY 400 (10): 3655-3664 JUL 2011
Summary: Passive exposure to tobacco smoke causes a variety of illnesses ranging from allergic responses to cancer. Assessment of exposure to second-hand tobacco smoke (SHS), particularly among vulnerable populations enables intervention and prevention of future disease. A minimally invasive oral fluids-based onsite test to detect such exposure would create a valuable tool for researchers and clinicians. Here we describe the development of a test that uses an inexpensive reader that utilizes a CMOS image sensor to reliably quantify a reporter signal and determine nicotine exposure. The rapid lateral flow test consists of a nitrocellulose strip with a control line containing goat anti-rabbit IgG, used as an internal standard, and a test line containing BSA-cotinine conjugate. To run the test, diluted sample containing antibodies against cotinine, the major metabolite of nicotine, is mixed with protein A-gold nanoparticles and placed on the sample pad. As the sample runs up to the nitrocellulose pad, antibodies in the running buffer bind to available cotinine. If cotinine is absent, the antibodies will bind to the BSA-cotinine derivative immobilized on the test line, resulting in an intense purple-red band. The concentration of cotinine equivalents in the sample can be estimated from interpretation of the test line. In this article we describe the effect of different cotinine derivatives, oral fluid pretreatment, and application and running buffers on assay sensitivity.
The test can reliably detect as little as 2 ng mL(-1) cotinine equivalents. The assay is sensitive, simple, rapid, inexpensive, and easily implementable in point-of-care facilities to detect second-hand smoke exposure.
The case for a worldwide ban on smoking in public places.
Menzies D
Current Opinion in Pulmonary Medicine 17(2):116-22, 2011 Mar
17(2):116-22, 2011 Mar
Summary: PURPOSE OF REVIEW: Second-hand smoke (SHS) is a major cause of morbidity and mortality on a global scale. Governments have increasingly sought to mitigate the effects of SHS by introducing legislation that restricts tobacco consumption in public places. There is emerging evidence that such legislation leads to direct and indirect health benefits.
RECENT FINDINGS: Exposure to SHS is now shown to be associated with development of cardiovascular disease, and poorer health outcomes in patients with established chronic obstructive pulmonary disease. Childhood (including in-utero) exposure to SHS has recently been linked with increased risk of cleft palate, demonstrable signs of atherosclerosis, and the development of emphysema and lung cancer in adulthood. Comprehensive bans on smoking in public lead to a reduction in overall exposure to SHS for both adults and children and have also been shown to immediately attenuate the incidence of myocardial infarction and paediatric hospital attendances with acute asthma.
SUMMARY: Banning smoking in public places is an effective tool for reducing tobacco-related morbidity across a multiplicity of diseases. Countries that have not already done so should introduce legislation to enforce effective legislation that prohibits smoking in public places.
Development of an ultrasensitive immunochromatography test to detect nicotine metabolites in oral fluids
Gonzalez, JM
ANALYTICAL AND BIOANALYTICAL CHEMISTRY 400 (10): 3655-3664 JUL 2011
Summary: Passive exposure to tobacco smoke causes a variety of illnesses ranging from allergic responses to cancer. Assessment of exposure to second-hand tobacco smoke (SHS), particularly among vulnerable populations enables intervention and prevention of future disease. A minimally invasive oral fluids-based onsite test to detect such exposure would create a valuable tool for researchers and clinicians. Here we describe the development of a test that uses an inexpensive reader that utilizes a CMOS image sensor to reliably quantify a reporter signal and determine nicotine exposure. The rapid lateral flow test consists of a nitrocellulose strip with a control line containing goat anti-rabbit IgG, used as an internal standard, and a test line containing BSA-cotinine conjugate. To run the test, diluted sample containing antibodies against cotinine, the major metabolite of nicotine, is mixed with protein A-gold nanoparticles and placed on the sample pad. As the sample runs up to the nitrocellulose pad, antibodies in the running buffer bind to available cotinine. If cotinine is absent, the antibodies will bind to the BSA-cotinine derivative immobilized on the test line, resulting in an intense purple-red band. The concentration of cotinine equivalents in the sample can be estimated from interpretation of the test line. In this article we describe the effect of different cotinine derivatives, oral fluid pretreatment, and application and running buffers on assay sensitivity.
The test can reliably detect as little as 2 ng mL(-1) cotinine equivalents. The assay is sensitive, simple, rapid, inexpensive, and easily implementable in point-of-care facilities to detect second-hand smoke exposure.
The case for a worldwide ban on smoking in public places.
Menzies D
Current Opinion in Pulmonary Medicine 17(2):116-22, 2011 Mar
17(2):116-22, 2011 Mar
Summary: PURPOSE OF REVIEW: Second-hand smoke (SHS) is a major cause of morbidity and mortality on a global scale. Governments have increasingly sought to mitigate the effects of SHS by introducing legislation that restricts tobacco consumption in public places. There is emerging evidence that such legislation leads to direct and indirect health benefits.
RECENT FINDINGS: Exposure to SHS is now shown to be associated with development of cardiovascular disease, and poorer health outcomes in patients with established chronic obstructive pulmonary disease. Childhood (including in-utero) exposure to SHS has recently been linked with increased risk of cleft palate, demonstrable signs of atherosclerosis, and the development of emphysema and lung cancer in adulthood. Comprehensive bans on smoking in public lead to a reduction in overall exposure to SHS for both adults and children and have also been shown to immediately attenuate the incidence of myocardial infarction and paediatric hospital attendances with acute asthma.
SUMMARY: Banning smoking in public places is an effective tool for reducing tobacco-related morbidity across a multiplicity of diseases. Countries that have not already done so should introduce legislation to enforce effective legislation that prohibits smoking in public places.
Prestructured questionnaire and review of hospital records were used to collect data about maternal background, obstetric history, medical history, and data related to second hand smoke exposure.
Smoking and endothelial progenitor cells: a revision of literature.
Endothelium-dependent and -independent vasodilations were determined by high-resolution ultrasound.
They measured how big an artery got and never ever discounted other causes that would effect the the dialation of a artery to another stimulus like a big mac or cold air or running on a treadmill. Nor do they explain other mechanisms going on that affect the proginator cells of bone marrow in endolthium!
Development of an ultrasensitive immunochromatography test to detect nicotine metabolites in oral fluids
Who cares so now they can tell you,you either smoked or ate potatoes for dinner lastnite.......Its a simple sensitivity test no diferent than a western blot or ELISA test!
The case for a worldwide ban on smoking in public places.
RECENT FINDINGS: Exposure to SHS is now shown to be associated with development of cardiovascular disease,
Low levels of exposure, including exposures to secondhand tobacco smoke, lead to a rapid and sharp increase in endothelial dysfunction and inflammation, which are implicated in acute cardiovascular
events and thrombosis."
And when we move beyond fear mongering by half truths, we realize that a hearty thanksgiving dinner, results in identical effects almost universally.
A big mac, walking from the heat into the cold and a number of other physical activities that require that body to regulate blood flow and heart rate, will also fall into this same category. It is simply your body's natural defense mechanism working splendidly as it should.
And that is the health risk?
Junk Science is what its called! Normal reactions by the body to natural occurring events is what the smokefree insanity has been using to claim second hand smoke causes! Its all pure make believe!
........................
and poorer health outcomes in patients with established chronic obstructive pulmonary disease.
The evidence is suggestive but not sufficient to infer a causal relationship between secondhand smoke exposure and acute respiratory symptoms including cough, wheeze, chest tightness, and difficulty breathing among persons with asthma.
The evidence is suggestive but not sufficient to infer a causal relationship between secondhand smoke exposure and acute respiratory symptoms including cough, wheeze, chest tightness, and difficulty breathing among healthy persons.
The evidence is suggestive but not sufficient to infer a causal relationship between secondhand smoke exposure and chronic respiratory symptoms.
The evidence is suggestive but not sufficient to infer a causal relationship between short-term secondhand smoke exposure and an acute decline in lung function in persons with asthma.
The evidence is inadequate to infer the presence or absence of a causal relationship between short-term secondhand smoke exposure and an acute decline in lung function in healthy persons.
The evidence is suggestive but not sufficient to infer a causal relationship between secondhand smoke exposure and a worsening of asthma control.
The evidence is suggestive but not sufficient to infer a causal relationship between secondhand smoke exposure and risk for chronic obstructive pulmonary disease.
SG REPORT 2006
....................
Do Smoking Bans Reduce Heart Attacks?
“In contrast with smaller regional studies,” says a RAND Corporation study, “we find that smoking bans are not associated with statistically significant short-term declines in mortality or hospital admissions for myocardial infarction [heart attack] or other diseases.”
In fact, “An analysis simulating smaller studies using subsamples reveals that large short-term increases in myocardial infarction incidence following a smoking ban are as common as the large decreases reported in the published literature.”
In other words, although heart attacks do decline in some places with smoking bans, there are just as many places where they rise. On average, the difference between jurisdictions with smoking bans and jurisdictions without smoking bans is essentially zero.
http://healthblog.ncpa.org/do-smoking...
...
They use tricks to say we have LINKED it or say it has a causal effect!
PROOF AS IN MICROSCOPE PROOF!
Not 1 Death or Sickness Etiologically Assigned to Tobacco. All the diseases attributed to smoking are also present in non smokers. It means, in other words, that they are multifactorial, that is, the result of the interaction of tens, hundreds, sometimes thousands of factors, either known or suspected contributors - of which smoking can be one!
JOINT STATEMENT ON THE RE-ASSESSMENT OF THE TOXICOLOGICAL TESTING OF TOBACCO PRODUCTS"
7 October, the COT meeting on 26 October and the COC meeting on 18
November 2004.
http://cot.food.gov.
uk/pdfs/cotstatement
tobacco0409
"5. The Committees commented that tobacco smoke was a highly complex chemical mixture and that the causative agents for smoke induced diseases (such as cardiovascular disease, cancer, effects on reproduction and on offspring) was unknown. The mechanisms by which tobacco induced adverse effects were not established. The best information related to tobacco smoke - induced lung cancer, but even in this instance a detailed mechanism was not available. The Committees therefore agreed that on the basis of current knowledge it would be very difficult to identify a toxicological testing strategy or a biomonitoring approach for use in volunteer studies with smokers where the end-points determined or biomarkers measured were predictive of the overall burden of tobacco-induced adverse disease."
In other words ... our first hand smoke theory is so lame we can't even design a bogus lab experiment to prove it. In fact ... we don't even know how tobacco does all of the magical things we claim it does.
The greatest threat to the second hand theory is the weakness of the first hand theory.
Im a simple american fighting for the simple right to smoke!
nothing more,nothing less!
"Women who wait in public bar-rooms and smoking-saloons. though not themselves smoking, cannot avoid the poisoning caused by inhaling smoke continually. Surely gallantry, if not common honesty, should suggest the practical inference from this fact."
--- Dr. Charles R. Drysdale in 1875.
That's EIGHTEEN seventy five.
Heres today:
A letter from a doctor on shs
Robert E. Madden MD, FACS. I am also a non-smoker. HOWEVER I am a passionate opponent smoking bans. Most of the opposition to the smoking bans has been based upon economic factors such as loss of business revenue, even closings. My opposition is due to loss of individual freedom and abuse of scientific fact.
I am a practicing chest surgeon, a teacher and a former cancer researcher. I am also past president of the NY Cancer Society. I will not tell you that smoking is harmless and without risk, in fact one in eight hundred smokers will develop lung cancer. Asthmatics should avoid tobacco smoke. What I will say is: 1) it’s a personal choice and 2) so called second smoke (ETS) is virtually harmless. One may not like the smell but it has not been shown to cause cancer, even in bartenders. If people do not like the odor then they may go elsewhere. Those who support the ban have no right to deny 24% of the adult population their enjoyment of a popular product based on dislike, possibly hatred of smoking. This attitude is that of a bigot, akin to anti-Semitism or racism.
To me the most offensive element of the smoking bans is the resort to science as “proving that environmental smoke, second hand smoke, causes lung cancer”. Not only is this unproven but there is abundant and substantial evidence to the contrary. It is frustrating, even insulting, for a scientist like myself to hear the bloated statistics put out by the American Cancer Society (of which I am a member) and the American Lung Association used to justify what is best described as a political agenda. Smokers enjoy smoking. Most non-smokers are neutral. Anti-smokers hate smoking. It is this last group that drives the engine of smoking bans. Smoking sections in restaurants, ventilated bars and the like have been satisfactory and used for years. To those who choose to smoke they do so at their own risk. To those eschew smoking let them patronize establishments whose owners prohibit smoking. To impose a city wide or a state wide ban is to deny people of their rights.
Respectfully,
Robert E. Madden, M.D
...
This docs near 75!
Jack is in fact the poster boy of people who are easily manipulated by bogus experts:
When peons are easily manipulated by bogus "experts"
Would anyone rely on a nobody, such as
“ A letter from a doctor on shs
Robert E. Madden MD, FACS. I am also a non-smoker. HOWEVER I am a passionate opponent smoking bans. Most of the opposition to the smoking bans has been based upon economic factors such as loss of business revenue, even closings. My opposition is due to loss of individual freedom and abuse of scientific fact.
I am a practicing chest surgeon, a teacher and a former cancer researcher. I am also past president of the NY Cancer Society. I will not tell you that smoking is harmless and without risk, in fact one in eight hundred smokers will develop lung cancer. Asthmatics should avoid tobacco smoke. What I will say is: 1) it’s a personal choice and 2) so called second smoke (ETS) is virtually harmless. One may not like the smell but it has not been shown to cause cancer, even in bartenders. If people do not like the odor then they may go elsewhere. Those who support the ban have no right to deny 24% of the adult population their enjoyment of a popular product based on dislike, possibly hatred of smoking. This attitude is that of a bigot, akin to anti-Semitism or racism.
To me the most offensive element of the smoking bans is the resort to science as “proving that environmental smoke, second hand smoke, causes lung cancer”. Not only is this unproven but there is abundant and substantial evidence to the contrary. It is frustrating, even insulting, for a scientist like myself to hear the bloated statistics put out by the American Cancer Society (of which I am a member) and the American Lung Association used to justify what is best described as a political agenda. Smokers enjoy smoking. Most non-smokers are neutral. Anti-smokers hate smoking. It is this last group that drives the engine of smoking bans. Smoking sections in restaurants, ventilated bars and the like have been satisfactory and used for years. To those who choose to smoke they do so at their own risk. To those eschew smoking let them patronize establishments whose owners prohibit smoking. To impose a city wide or a state wide ban is to deny people of their rights.
Respectfully,
Robert E. Madden, M.D”
Or people who know their stuff, such as those below
Recent contributions of air- and biomarkers to the control of secondhand smoke (SHS): A review
Prignot, J.J.
International Journal of Environmental Research and Public Health, Volume 8, Issue 3, March 2011, Pages 648-682.
Abstract
Since the publication of the US Surgeon General Reports in 1996 and 2006 and the report of the California Environmental Protection Agency in 1999, many reports have appeared on the contribution of air and biomarkers to different facets of the secondhand smoke (SHS) issue, which are the targets of this review. These recent studies have allowed earlier epidemiological surveys to be biologically validated, and their plausibility demonstrated, quantified the levels of exposure to SHS before the bans in various environments, showed the deficiencies of mechanical control methods and of partial bans and the frequently correct implementation of the efficient total bans. More stringent regulation remains necessary in the public domain (workplaces, hospitality venues, transport sector, etc.) in many countries. Personal voluntary protection efforts against SHS are also needed in the private domain (homes, private cars). The effects of SHS on the cardiovascular, respiratory and neuropsychic systems, on pregnancy and fertility, on cancers and on SHS genotoxicity are confirmed through experimental human studies and through the relationship between markers and prevalence of disease or of markers of disease risk.
Quantification of ETS exposure in hospitality workers who have never smoked
Kolb, S., Brückner, U., Nowak, D., Radon, K.
Environmental Health: A Global Access Science Source, Volume 9, Issue 1, 2010, Article number 49
Abstract
Background. Environmental Tobacco Smoke (ETS) was classified as human carcinogen (K1) by the German Research Council in 1998. According to epidemiological studies, the relative risk especially for lung cancer might be twice as high in persons who have never smoked but who are in the highest exposure category, for example hospitality workers. In order to implement these results in the German regulations on occupational illnesses, a valid method is needed to retrospectively assess the cumulative ETS exposure in the hospitality environment. Methods. A literature-based review was carried out to locate a method that can be used for the German hospitality sector. Studies assessing ETS exposure using biological markers (for example urinary cotinine, DNA adducts) or questionnaires were excluded. Biological markers are not considered relevant as they assess exposure only over the last hours, weeks or months. Self-reported exposure based on questionnaires also does not seem adequate for medico-legal purposes. Therefore, retrospective exposure assessment should be based on mathematical models to approximate past exposure. Results. For this purpose a validated model developed by Repace and Lowrey was considered appropriate. It offers the possibility of retrospectively assessing exposure with existing parameters (such as environmental dimensions, average number of smokers, ventilation characteristics and duration of exposure). The relative risk of lung cancer can then be estimated based on the individual cumulative exposure of the worker. Conclusion. In conclusion, having adapted it to the German hospitality sector, an existing mathematical model appears to be capable of approximating the cumulative exposure. However, the level of uncertainty of these approximations has to be taken into account, especially for diseases with a long latency period such as lung cancer.
Risks for heart disease and lung cancer from passive smoking by workers in the catering industry
Hedley, A.J.a , McGhee, S.M.a , Repace, J.L.b , Wong, L.-C.a , Yu, M.Y.S.c e , Wong, T.-W.d , Lam, T.-H.a
Toxicological Sciences, Volume 90, Issue 2, April 2006, Pages 539-548
Abstract
Workers in the catering industry are at greater risk of exposure to secondhand smoke (SHS) when smoke-free workplace policies are not in force. We determined the exposure of catering workers to SHS in Hong Kong and their risk of death from heart disease and lung cancer. Nonsmoking catering workers were provided with screening at their workplaces and at a central clinic. Participants reported workplace, home, and leisure time exposure to SHS. Urinary cotinine was estimated by enzyme immunoassay. Catering facilities were classified into three types: nonsmoking, partially restricted smoking (with nonsmoking areas), and unrestricted smoking. Mean urinary cotinine levels ranged from 3.3 ng/ml in a control group of 16 university staff through 6.4 ng/ml (nonsmoking), 6.1 ng/ml (partially restricted), and 15.9 ng/ml (unrestricted smoking) in 104 workers who had no exposures outside of work. Workers in nonsmoking facilities had exposures to other smoking staff. We modeled workers' mortality risks using average cotinine levels, estimates of workplace respirable particulates, risk data for cancer and heart disease from cohort studies, and national (US) and regional (Hong Kong) mortality for heart disease and lung cancer. We estimated that deaths in the Hong Kong catering workforce of 200,000 occur at the rate of 150 per year for a 40-year working-lifetime exposure to SHS. When compared with the current outdoor air quality standards for particulates in Hong Kong, 30% of workers exceeded the 24-h and 98% exceeded the annual air quality objectives due to workplace SHS exposures.
More to follow…
Kenfield, S.A.a b , Wei, E.K.b c , Rosner, B.A.b d , Glynn, R.J.d e , Stampfer, M.J.a b , Colditz, G.A.f
Tobacco Control, Volume 19, Issue 3, June 2010, Pages 248-254
Abstract
Objective The burden of smoking on six causes of death in women was evaluated using various novel modeling approaches. Design A prospective US-based nationwide cohort study. Participants 102 635 women in the Nurses' Health Study followed biennially from 1980 to 2004. Methods The relation between cigarette smoking and cause- specific death was compared using baseline versus biennially updated smoking status. The authors used competing risk survival analysis to formally compare associations of smoking-related variables on risk of death as a result of coronary heart disease (CHD), cerebrovascular diseases, lung cancer, other respiratory diseases, other smoking- caused cancers and other causes.& Results The associations of current and former smoking were stronger with most cause-specific mortality when using updated information. The effect of each smoking related variable differed significantly (ph
Second-hand smoke, cotinine levels, and risk of circulatory mortality in a large cohort study of never-smokers
Gallo, V.a , Neasham, D.a , Airoldi, L.b , Ferrari, P.c , Jenab, M.c , Boffetta, P.c , Overvad, K.d , Tjønneland, A.e , Clavel-Chapelon, F.f , Boeing, H.g , Pala, V.h , Palli, D.i , Panico, S.j , Tumino, R.k , Arriola, L.l , Lund, E.m , Bueno-De-Mesquita, B.n , Peeters, P.H.o , Melander, O.p , Hallmans, G.q , Riboli, E.a , Saracci, R.r , Vineis, P.a
Epidemiology, Volume 21, Issue 2, March 2010, Pages 207-214
Abstract
BACKGROUND:: Exposure to second-hand smoke has been shown to be associated with increased cardiovascular mortality in several, but not all, epidemiologic studies. Our aim was to investigate the risk of circulatory death associated with exposure to second-hand smoke in never-smokers in a very large prospective study, the European Prospective Investigation into Cancer and Nutrition. A secondary aim was to use cotinine levels for cross-validating self-reported second-hand smoke exposure. METHODS:: Cox proportional hazard models were used to investigate the risk of death due to circulatory causes associated with second-hand smoke exposure in 135,233 never-smokers. Exposure to second-hand smoke was assessed through a questionnaire at enrollment and then validated against plasma cotinine measurements in a subsample. RESULTS:: Study participants who reported second-hand smoke exposure at home had higher cotinine levels (median plasma cotinine concentration in exposed = 0.82 μg/L; in those unexposed 0.02 μg/L). Second-hand smoke exposure at home was associated with an increased risk of dying from cardiovascular diseases (hazard ratio [HR] = 1.38 [95% confidence interval = 1.01-1.90]), all circulatory diseases (1.28 [0.98-1.69]), and coronary heart disease (1.31 [0.83-2.08]) after adjustment for age, sex, education, physical activity, and body mass index. Dose-response relationships were observed between exposure to second-hand smoke at home and risk of circulatory death (HR per each additional hour/d = 1.25 [1.04-1.50]). Having a partner who smokes more than 30 cigarettes per day considerably increased the risk of a circulatory death (2.94 [1.11-7.78]). Second-hand smoke exposure at home was not associated with total mortality (1.03 [0.93-1.13]). DISCUSSION:: Exposure to second-hand smoke at home (as confirmed by plasma cotinine levels) increases the risk of cardiovascular mortality.
Association of environmental tobacco smoke exposure with elevated home blood pressure in Japanese women: The Ohasama study
Seki, M.a , Inoue, R.b , Ohkubo, T.c , Kikuya, M.a , Hara, A.a , Metoki, H.a , Hirose, T.c , Tsubota-Utsugi, M.d , Asayama, K.c , Kanno, A.a , Obara, T.a e , Hoshi, H.f , Totsune, K.a , Satoh, H.g , Imai, Y.a
Journal of Hypertension, Volume 28, Issue 9, September 2010, Pages 1814-1820
Abstract
Objective: Only a few of numerous epidemiological studies have demonstrated a positive association between environmental tobacco smoke (ETS) exposure and blood pressure (BP), despite experimental studies showing such a positive association. The association between home blood pressure (HBP) and ETS exposure was investigated in the general population. Methods: Five hundred and seventy-nine nonsmoking Japanese women were enrolled. The participants were classified into four categories according to their responses to a self-administered questionnaire: unexposed women (non-ETS), women exposed at home [ETS(home)], at the workplace/other places [ETS(work/other)] and at home and at the workplace/other places [ETS(both)]. Variables were compared using analysis of covariance adjusted for age, marital status, body mass index, diabetes mellitus, stroke, heart disease, hyperlipidemia, alcohol intake, salt intake and activity levels. Results: In participants without antihypertensive medication, systolic morning HBP in ETS(both) was 4 mmHg higher than that in non-ETS (116.8 ± 1.01 vs. 113.1 ± 1.08 mmHg, P = 0.02) and systolic morning HBP in ETS(home) and systolic evening HBP in ETS(both) were 3 mmHg higher than those in non-ETS (116.2 ± 1.07 vs. 113.1 ± 1.08 mmHg, P = 0.04; and 115.3 ± 1.02 vs. 111.9 ± 1.09 mmHg, P = 0.03, respectively). In participants with antihypertensive medication, ETS exposure status was not significantly associated with increased HBP levels. Conclusions: A positive association between HBP levels and ETS exposure was confirmed. HBP measurement is recommended in population-based studies investigating the effects of ETS exposure. ETS exposure may increase BP, thereby synergistically contributing to unfavorable cardiovascular outcomes along with other deleterious effects of ETS.
Cardiovascular effects of secondhand smoke: Nearly as large as smoking
Barnoya, J.a b , Glantz, S.A.a c
Circulation, Volume 111, Issue 20, 24 May 2005, Pages 2684-2698
Abstract
Background - Secondhand smoke increases the risk of coronary heart disease by ≈30%. This effect is larger than one would expect on the basis of the risks associated with active smoking and the relative doses of tobacco smoke delivered to smokers and nonsmokers. Methods and Results - We conducted a literature review of the research describing the mechanistic effects of secondhand smoke on the cardiovascular system, emphasizing research published since 1995, and compared the effects of secondhand smoke with the effects of active smoking. Evidence is rapidly accumulating that the cardiovascular system - platelet and endothelial function, arterial stiffness, atherosclerosis, oxidative stress, inflammation, heart rate variability, energy metabolism, and increased infarct size - is exquisitely sensitive to the toxins in secondhand smoke. The effects of even brief (minutes to hours) passive smoking are often nearly as large (averaging 80% to 90%) as chronic active smoking. Conclusions - The effects of secondhand smoke are substantial and rapid, explaining the relatively large risks that have been reported in epidemiological studies.
Secondhand smoke exposure and inflammatory markers in nonsmokers in the trucking industry
Chiu, Y.H.M.a b , Spiegelman, D.c d , Dockery, D.W.a c , Garshick, E.b e , Katharine Hammond, S.f , Smith, T.J.a , Hart, J.E.b c , Laden, F.a b c
Environmental Health Perspectives, Volume 119, Issue 9, September 2011, Pages 1294-1300
Abstract
Background: Few studies have directly assessed the association of secondhand smoke (SHS) with cardiovascular disease-related inflammatory markers, and the findings are inconsistent. Objectives: We assessed the association between SHS exposure and the inflammatory markers high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), and soluble intercellular adhesion molecule-1 (sICAM-1) in 199 nonsmoking U.S. trucking industry workers. Methods: Participants provided blood samples either by mail (blood drawn at local health care provider near home) or at the work site (blood drawn by research staff on-site) and completed a health and work history questionnaire at the time of blood draw. Exposure to SHS was measured by plasma cotinine concentrations. We used multivariate regression analyses to assess the associations between levels of cotinine and inflammatory markers. Results: The median cotinine level was 0.10 ng/mL (interquartile range, 0.04-0.23 ng/mL). The odds ratios of elevated hs-CRP (above highest CRP tertile, 1.5 mg/L) were 2.85 [95% confidence interval (CI), 1.03-7.89] for the high-cotinine group (> 0.215 ng/mL) and 2.80 (95% CI, 1.11-7.10) for the moderate-cotinine group (0.05-0.215 ng/mL), compared with the low-cotinine group (
Secondhand smoke (SHS) exposure is associated with circulating markers of inflammation and endothelial function in adult men and women
Jefferis, B.J.a , Lowe, G.D.O.b , Welsh, P.b , Rumley, A.b , Lawlor, D.A.c , Ebrahim, S.d , Carson, C.d , Doig, M.e , Feyerabend, C.e , McMeekin, L.e , Wannamethee, S.G.a , Cook, D.G.f , Whincup, P.H.f
Atherosclerosis, Volume 208, Issue 2, February 2010, Pages 550-556
Abstract
Aims: Secondhand smoke (SHS) exposure is associated with elevated CHD risks. Yet the pathways through which this may operate have not been investigated in epidemiologic studies with objective SHS exposure measures and a wide range of CHD risk factors associated with active smoking. Therefore we investigate associations between SHS exposure and CHD risk factors, to clarify how SHS exposure may raise risk of CHD. Methods: Cross-sectional population-based study of 5029 men and women aged 59-80 years from primary care practices in Great Britain. Smoking, behavioural and demographic information was reported in questionnaires; nurses made physical measurements and took blood samples for analysis of serum cotinine and markers of inflammation, hemostasis and endothelial dysfunction. Results: Active cigarette smokers had lower albumin and higher triglycerides, CRP, IL-6, white cell count, fibrinogen, blood viscosity, factor VIII, VWF and t-PA than non-smokers. Among non-smokers, serum cotinine levels were independently positively associated with CRP, fibrinogen, factor VIII, VWF and t-PA and inversely associated with albumin, after adjustment for age, gender, social and behavioural factors. The differences in CRP, fibrinogen and albumin between cotinine ≤0.05 and >0.7 ng/ml were one-third to one half the size of differences between cotinine ≤0.05 ng/ml and current smokers, but were of similar magnitude for VWF and t-PA. Conclusions: Endothelial, inflammatory and haemostatic markers related to CHD risk showed independent associations with SHS exposure in the same direction as those for active smoking. Results aid understanding of the associations between SHS exposure and elevated CHD risks.
Steve, you might also be interested in this following interview why physicist Dr. Lisa Randall
http://www.thedailyshow.com/watch/wed-october-26-2011/lisa-randall
Drinking and driving is safe,driving impaired or drunk is not safe and there is a diference!
The ones driving the bans at the ROBERT WOODS JOHNSON FOUNDATION are also behind NEO-PROHIBITION where they have taken over or bought outright groups like MADD!
Robert Wood Johnson Foundation: Financier of Temperance
by David J. Hanson, Ph.D.
The temperance-oriented Robert Wood Johnson Foundation (RWJF) "seeks to drive adult beverage consumption underground, away from mainstream culture and public places." 1 It attempts to stigmatize alcohol, de-legitimize drinking, marginalize drinkers, and create a de facto quasi-prohibition of the legal product.
The Robert Wood Johnson Foundation spent over a quarter of a billion (that's billion, not million) dollars ($265,000,000.00) in just four years alone further developing and funding a nation-wide network of anti-alcohol organizations, centers, activist leaders, and opinion writers to promote its long-term goal.
An in-depth report, Behind the Neo-Prohibition Campaign: The Robert Wood Johnson Foundation, demonstrates that "nearly every study disparaging adult beverages in the mass media, every legislative push to limit alcohol marketing or increase taxes, and every supposedly 'grassroots' anti-alcohol organization" is funded by the Robert Wood Johnson Foundation. 2 The foundation supports numerous temperance-oriented activists and groups including:
•The Rand Corporation, whose studies in support of roadblocks and limiting access to alcohol are funded by RWJF.
•The Center on Addiction and Substance Abuse (CASA), now calling itself the National Center on Addictions and Substance Abuse at Columbia University, whose many flawed studies have been widely refuted. CASA has received more than $35 million from RWJF since 1991.
•The Center on Alcohol Marketing and Youth (CAMY), which exists for one purpose: to accuse alcohol ads of “targeting' underage drinkers” and “create public outrage” against them. RWJF established CAMY with a $5 million grant.
•The Department of Education's Higher Education Center for Alcohol and Other Drug Prevention (HEC), which argues for "changing people's knowledge, attitudes, and behavioral intentions regarding alcohol use," It also supports "reducing alcohol availability" and "reducing alcohol promotion and marketing." HEC -- an agency of the federal government -- receives “supplemental” funding from RWJF.
•Ralph Hingson, formerly Vice President for Public Policy at Mothers Against Drunk Driving (MADD), who published a deeply flawed report claiming that alcohol causes 1,400 deaths among college students each year. These findings were repudiated by the federal government's General Accountability Office or GAO. Hingson received a $300,000 fellowship from RWJF.
more at the link:
http://alcoholfacts.org/RWJfoundation.html
World-renowned pulmonologist, president of the prestigious Research Institute Necker for the last decade, Professor Philippe Even, now retired, tells us that he’s convinced of the absence of harm from passive smoking. A shocking interview.
What do the studies on passive smoking tell us?
PHILIPPE EVEN. There are about a hundred studies on the issue. First surprise: 40% of them claim a total absence of harmful effects of passive smoking on health. The remaining 60% estimate that the cancer risk is multiplied by 0.02 for the most optimistic and by 0.15 for the more pessimistic … compared to a risk multiplied by 10 or 20 for active smoking! It is therefore negligible. Clearly, the harm is either nonexistent, or it is extremely low.
It is an indisputable scientific fact. Anti-tobacco associations report 3 000-6 000 deaths per year in France ...
I am curious to know their sources. No study has ever produced such a result.
Many experts argue that passive smoking is also responsible for cardiovascular disease and other asthma attacks. Not you?
They don’t base it on any solid scientific evidence. Take the case of cardiovascular diseases: the four main causes are obesity, high cholesterol, hypertension and diabetes. To determine whether passive smoking is an aggravating factor, there should be a study on people who have none of these four symptoms. But this was never done. Regarding chronic bronchitis, although the role of active smoking is undeniable, that of passive smoking is yet to be proven. For asthma, it is indeed a contributing factor ... but not greater than pollen!
The purpose of the ban on smoking in public places, however, was to protect non-smokers. It was thus based on nothing?
Absolutely nothing! The psychosis began with the publication of a report by the IARC, International Agency for Research on Cancer, which depends on the WHO (Editor's note: World Health Organization). The report released in 2002 says it is now proven that passive smoking carries serious health risks, but without showing the evidence. Where are the data? What was the methodology? It's everything but a scientific approach. It was creating fear that is not based on anything.
Why would anti-tobacco organizations wave a threat that does not exist?
...
The anti-smoking campaigns and higher cigarette prices having failed, they had to find a new way to lower the number of smokers. By waving the threat of passive smoking, they found a tool that really works: social pressure. In good faith, non-smokers felt in danger and started to stand up against smokers. As a result, passive smoking has become a public health problem, paving the way for the Evin Law and the decree banning smoking in public places. The cause may be good, but I do not think it is good to legislate on a lie. And the worst part is that it does not work: since the entry into force of the decree, cigarette sales are rising again.
Why not speak up earlier?
As a civil servant, dean of the largest medical faculty in France, I was held to confidentiality. If I had deviated from official positions, I would have had to pay the consequences. Today, I am a free man.
Le Parisien
...
Here's some other findings that have been taken so far out of context it defies the imagination:
2006 Surgeon General's Report (excerpts)
The evidence is inadequate to infer the presence or absence of a causal relationship between maternal exposure to secondhand smoke and female fertility or fecundability. No data were found on paternal exposure to secondhand smoke and male fertility or fecundability.
The evidence is inadequate to infer the presence or absence of a causal relationship between maternal exposure to secondhand smoke during pregnancy and spontaneous abortion.
The evidence is inadequate to infer the presence or absence of a causal relationship between exposure to secondhand smoke and neonatal mortality.
The evidence is inadequate to infer the presence or absence of a causal relationship between exposure to secondhand smoke and cognitive functioning among children.
The evidence is inadequate to infer the presence or absence of a causal relationship between exposure to secondhand smoke and behavioral problems among children.
The evidence is inadequate to infer the presence or absence of a causal relationship between exposure to secondhand smoke and children’s height/growth.
The evidence is inadequate to infer the presence or absence of a causal relationship between maternal exposure to secondhand smoke during pregnancy and childhood cancer.
The evidence is inadequate to infer the presence or absence of a causal relationship between exposure to secondhand smoke during infancy and childhood cancer
The evidence is suggestive but not sufficient to infer a causal relationship between parental smoking and the natural history of middle ear effusion.
The evidence is inadequate to infer the presence or absence of a causal relationship between parental smoking and an increase in the risk of adenoidectomy or tonsillectomy among children.
The evidence is suggestive but not sufficient to infer a causal relationship between secondhand smoke exposure from parental smoking and the onset of childhood asthma.
The evidence is inadequate to infer the presence or absence of a causal relationship between parental smoking and the risk of immunoglobulin E-mediated allergy in their children.
The evidence is suggestive but not sufficient to infer a causal relationship between exposure to secondhand smoke and an increased risk of stroke.
Studies of secondhand smoke and subclinical vascular disease, particularly carotid arterial wall thickening, are suggestive but not sufficient to infer a causal relationship between exposure to secondhand smoke and atherosclerosis.
The evidence is suggestive but not sufficient to infer a causal relationship between secondhand smoke exposure and acute respiratory symptoms including cough, wheeze, chest tightness, and difficulty breathing among persons with asthma.
The evidence is suggestive but not sufficient to infer a causal relationship between secondhand smoke exposure and acute respiratory symptoms including cough, wheeze, chest tightness, and difficulty breathing among healthy persons.
The evidence is suggestive but not sufficient to infer a causal relationship between secondhand smoke exposure and chronic respiratory symptoms.
The evidence is suggestive but not sufficient to infer a causal relationship between short-term secondhand smoke exposure and an acute decline in lung function in persons with asthma.
The evidence is inadequate to infer the presence or absence of a causal relationship between short-term secondhand smoke exposure and an acute decline in lung function in healthy persons.
The evidence is suggestive but not sufficient to infer a causal relationship between secondhand smoke exposure and a worsening of asthma control.
The evidence is suggestive but not sufficient to infer a causal relationship between secondhand smoke exposure and risk for chronic obstructive pulmonary disease.
And finally.....
The evidence is sufficient to infer a causal relationship between secondhand smoke exposure and odor annoyance.
Source: http://www.surgeongeneral.gov/library....
If you actually read the surgeon generals report it used mostly "The evidence is suggestive but not sufficient to infer a causal relationship" and even then if you read page 21 they admit that the use of meta-analysis on observational studies is not a widely accepted and controversial practice and yet they do it anyway.
http://www.surgeongeneral.gov/library....
...
And you, given your claim to be the former dean of the largest medical faculty in France need to identify yourself and connect that identity to some public C.V. or just go away. Because your medical peers need to see the crap you espouse.
Nick is the well paid lobbyist for the tobacco industry:
Joey Naylor: ...so what happens when you're wrong?
Nick Naylor: Whoa, Joey I'm never wrong.
Joey Naylor: But you can't always be right...
Nick Naylor: Well, if it's your job to be right, then you're never wrong.
Joey Naylor: But what if you are wrong?
Nick Naylor: OK, let's say that you're defending chocolate, and I'm defending vanilla. Now if I were to say to you: 'Vanilla is the best flavour ice-cream', you'd say...
Joey Naylor: No, chocolate is.
Nick Naylor: Exactly, but you can't win that argument... so, I'll ask you: so you think chocolate is the end all and the all of ice-cream, do you?
Joey Naylor: It's the best ice-cream, I wouldn't order any other.
Nick Naylor: Oh! So it's all chocolate for you is it?
Joey Naylor: Yes, chocolate is all I need.
Nick Naylor: Well, I need more than chocolate, and for that matter I need more than vanilla. I believe that we need freedom. And choice when it comes to our ice-cream, and that Joey Naylor, that is the defintion of liberty.
Joey Naylor: But that's not what we're talking about
Nick Naylor: Ah! But that's what I'm talking about.
Joey Naylor: ...but you didn't prove that vanilla was the best...
Nick Naylor: I didn't have to. I proved that you're wrong, and if you're wrong I'm right.
Joey Naylor: But you still didn't convince me
Nick Naylor: It's that I'm not after you. I'm after them.
[points into the crowd]
What is Nitrogen Oxide?
•Nitrogen Oxide, aka NOx, is a group of different gases made up of different levels of oxygen and nitrogen
•Two of the most common nitrogen oxides are: Nitrogen Dioxide and Nitric Oxide
•NOx is given off in many forms, such as smog or particles
How are Nitrogen Oxides Formed?
•NOx is formed when certain fuels (oil, gas and coal) are burned at a high temperature, such as combustion
•NOx is also formed from the plants that manufacture explosives
Why is there such a high level of Nitrogen Oxide Pollution?
•Because many factories, past and present, use coal-burning plants for power and/or energy or give off NOx from a certain processes
•Because NOx is commonly formed from motor vehicles (combustion in the engine)
Mechanisms of Diesel-Induced Endothelial Nitric Oxide Synthase Dysfunction in Coronary Arterioles
Background and objective: Increased air pollutants correlate with increased incidence of cardiovascular disease potentially due to vascular dysfunction. We have reported that acute diesel engine exhaust (DE) exposure enhances vasoconstriction and diminishes acetylcholine (ACh)-induced dilation in coronary arteries in a nitric oxide synthase (NOS)-dependent manner. We hypothesize that acute DE inhalation leads to endothelial dysfunction by uncoupling NOS.
Methods: Rats inhaled fresh DE (300 µg particulate matter/m3) or filtered air for 5 hr. After off-gassing, intraseptal coronary arteries were isolated and dilation to ACh recorded using videomicroscopy.
Results: Arteries from DE-exposed animals dilated less to ACh than arteries from air-exposed animals. NOS inhibition did not affect ACh dilation in control arteries but increased dilation in the DE group, suggesting NOS does not normally contribute to ACh-induced dilation in coronary arteries but does contribute to endothelial dysfunction after DE inhalation. Cyclooxygenase (COX) inhibition did not affect ACh dilation in the DE group, but combined inhibition of NOS and COX diminished dilation in both groups and eliminated intergroup differences, suggesting that the two pathways interact. Superoxide scavenging increased ACh dilation in DE arteries, eliminating differences between groups. Tetrahydrobiopterin (BH4) supplementation with sepiapterin restored ACh-mediated dilation in the DE group in a NOS-dependent manner. Superoxide generation (dihydroethidium staining) was greater in DE arteries, and superoxide scavenging, BH4 supplementation, or NOS inhibition reduced the signal in DE but not air arteries.
Conclusion: Acute DE exposure appears to uncouple NOS, increasing reactive oxygen species generation and causing endothelial dysfunction, potentially because of depletion of BH4 limiting its bioavailability.
http://ehp03.niehs.nih.gov/article/fetchArticle.action;jsessionid=16CAEF820312206AF426693F83851464?articleURI=info%3Adoi%2F10.1289%2Fehp.1002286
You're not making any point!
Again, this is the best you can up with?
Your opinions are getting dumber by the number of posts.
Self-projecting I see.
but if we are going to live in a dense society we have to adopt wide tolerance of social regulation, or else be continually assaulted by other people's ideas of how to behave. once you grasp the utility of allowing brown people into your restaurant, the principle of social regulation can be extended to anywhere the sovereign authority decides.
i believe that sovereign authority should be the electorate, acting in referendum. it is not. so people like bj say they don't like the gummint telling them what to do. i quite agree, because i despise politicians. unlike burger-flippers, they chose moral degradation, leaving behind more respectable occupations like law and street corner pimping.
hard to believe tobacco is still hopeful of a come-back, but if there is a dollar to be earned at some schoolyard, rjreynolds will be there, and some herman cain will spring up like mold after a rain, eager to spread the word.
the mayan empire lasted much longer than the usa has or will. i think it's because they didn't use money.
"but if we are going to live in a dense society we have to adopt wide tolerance of social regulation, or else be continually assaulted by other people's ideas of how to behave. ..."
That comment, had you left it there, would have been amongst the best you have ever made here.
However, Jack might be enlightened by talking to my wife, who has lung cancer and can no longer work. She is going through the living hell of chemotherapy, and she will likely die 20-30 years too soon -- given her family history -- as a result of smoking. Those numbers are far more meaningful to me than any studies put out by researchers -- likely in the employ of Big Tobacco.
I'd also recommend the film The Insider, for a look at what a head researcher inside that despicable industry had to say about the claim that tobacco is harmless. As far as I'm aware, cigarettes are the only product that when used as directed will kill you.
The quality of the English writing is at par with your understanding of this topic, which explains why after writing more than 30 comments under different pennames, you could not even come close to “show” that second-hand smoke is completely harmless.
After running out of arguments… I mean opinions (which are not facts), it all comes down to what people eat for breakfast, lunch and dinner. You should stick to your opinions about the eating habits of people and leave the actual understanding of the risk associated with smoking to those who do. No amount of cut and pasting from right-wing blog posts or tobacco lobbyist websites will help you in this regards. You can pack your shovel. It hasn’t been useful at all.
You want to see some cigarette smokers, go stand outside a hospital. That's right, I have to pass them every day. And they're not going away despite all your harping.
Besides, what is it all you libs smoke? Oh, thats' ok right. Just keep sending all our $ abroad and South.
A wide tolerance of social regulation indeed. No guys, a liberal wants as little social regulation via legislation in private spheres as possible. He leaves it up to the individual , absent harm to third parties who are forced to be in the environment, how much they will regulate their social activities.
You leftists really crack me up. Watch what you wish for, cause morons on the right can use your love of illiberality against you come tomorrow.
Strike OS -whoring – one tag only -OWS