I was enjoying a rather pleasant and quiet Father’s Day today. Then the telephone rang. On the line was a producer for British Broadcasting Company (BBC), inquiring if I was available to appear on a broadcast later in the day concerning an initiative for a countrywide smoking ban in Britain. Considering my recent reports about a new study concerning Environmental Tobacco Smoke (ETS) and lung cancer in nonsmokers published by the National Cancer Institute (NCI), I readily agreed to appear on the radio show. My E-Mail exchanges with Mr. Prout of BBC appear below this brief commentary. The final E-Mail below (my original response to Mr. Prout) outlines facts related to a highly significant and very important study recently published in the March 2, 2005 edition of the Journal of the National Cancer Institute (JNCI).

 

A March 21, 2005 article in the journal Science Daily reported the following conclusion concerning ETS and lung cancer in nonsmokers:

 

“These findings ‘support the hypothesis that at least two distinct molecular pathways are involved in the pathogenesis of lung adenocarcinomas, one involving EGFR TK domain mutations and the other involving KRAS gene mutations,’ the authors write. These results also ‘suggest that exposure to carcinogens in environmental tobacco smoke may not be the major pathogenic factor involved in the origin of lung cancers in never smokers but that an as-yet-unidentified carcinogen(s) plays an important role.’" (Underline, bold, italic added.)

 

Links to the Science Daily article, the abstract for the study, and an NCI editorial and press release concerning this new information are included in my E-Mail to Mr. Prout at BBC. What is material and significant the above conclusions is that they directly refute a conclusion reached in the December 1992 EPA report on secondhand smoke:

 

“ETS is a human lung carcinogen, responsible for approximately 3,000 lung cancer deaths annually in U.S. nonsmokers.”

 

It turns out that a study published by JNCI has concluded that ETS may not be the major factor in lung cancer in nonsmokers AND that “an as-yet-unidentified carcinogen(s) plays an important role.” In short, not only is secondhand smoke NOT considered to be the major factor in lung cancer in nonsmokers, but something else unrelated to ETS IS.

 

Bummer! What’s a good, strident “Anti-Mentality” activist to do? I guess “Secondhand Smoke Consultant” James Repace will need to re-calibrate his computer that regularly spits out “statistics” – notably for the Pierce County, Washington Board of Health -- about how may “Tornado Like” air exchanges per hour it takes to clear the air of ETS (it could be 35,000, 50,000 or 100,000, depending on whether his is in Toronto, New York or Pierce County’s City of Tacoma.) He’ll probably need to upgrade the Pentium chip in his computer to keep up with the rate at which his “scientific” Tornado Prognostications are collapsing. Soon enough, Tornado Jim. is going to find himself confronted with the figure of about two (2) air exchanges per hour – the “normal work environment” level at which the U.S. Occupational Safety and Health Administration (OSHA) has concluded ETS constituents “do not exceed Permissible Exposure Levels.” Then, even at those levels, the Journal of the National Cancer Institute has now published a study that concludes ETS ain’t the major factor factor in nonsmokers’ lung cancer and that something else not-yet-identifed IS.

 

I suspect that this most recent study will be responsible for causing a nationwide wave of acute heartburn among the anti-tobacco crowd. Here they sit, atop their priestly thrones with piles of “studies” to their left and mounds of mega-bucks looted from US consumers to the right, only to find their 1992 EPA report on secondhand smoke cornerstone has finally crumbled to dust. University of California at San Francisco statistics guru Stanton Glantz can commiserate with Tornado Jim. ‘Ol Stanton is one of the fellows who helped leverage EPA’s 1992 “estimate” of 3,000 nonsmoker deaths per year to first 38,000 in 1995, 53,000 later and then a whopping 73,200 in 2004. Problem is that in 1994 a nationwide push for smoking bans by Project ASSIST virtually wiped out exposure to ETS in all public places save, most hospitality trade businesses. So Guru Glantz et al would have us believe that as exposure decreases attributable deaths increase. Now, in order to buy the anti-tobacco party line after reading the study published by JNCI in March that smoking bans are necessary, we necessarily conclude what NCI says IS NOT a major cause of lung cancer in nonsmokers really IS, anyway AND that unidentified carcinogens that JNCI says probably ARE a cause of lung cancer in nonsmokers really isn’t. Way to go! For insight into some of the motivations that may cause such highly relevant thinking that produces overwhelmingly cogent thoughts fomr the best science minds that our universities can produce please see “The Tobacco Dance”  at Geocities.com (in the large green type at bottom of article):

 

“At the Seventh World Conference on Tobacco and Health held in Perth, Australia in 1990, Stanton Glantz gave the keynote address in which he said, among other things: "The main thing the science has done on the issue of ETS, in addition to help people like me pay mortgages, is it has legitimized the concerns that people have that they don't like cigarette smoke. And that is a strong emotional force that needs to be harnessed and used. We're on a roll, and the bastards are on the run. And I urge you to keep chasing them." (Emphasis added)

 

I hope that Mr. Glantz doesn’t get caught in the shorts by rising interest rates on his mortgages and a distinct fall-off of revenues derived by pushing Junk Science.

 

But I digress. The news segment on BBC was broadcast as scheduled late this afternoon. My opponent was the President of the West Virginia, USA chapter of the American Lung Association (ALA) (the group that Maryetta Ables at Forces West Virginia has been twisting the tail of on a regular basis for the past year.) There were five segments to the show. The BBC presenter (known in the USA as a reporter) began by reporting that some newspapers are reporting that the British government is considering a nationwide smoking ban. The ALA spokes-person then presented her views, including promotion of the horrible human toll caused by persons lawfully consuming legal tobacco products in public places. I rebutted her arguments with the observation that smoking ban legislation rises and falls on the credibility of science about ETS and an announcement of the study published in Match by JNNCI. The lady from ALS responded that she had never heard of such a study, that even if one removes nonsmokers’ lung cancer from the table we are still left with 35,000 deaths from heart disease, and that no one has a Constitutional right to smoke. My response was that one person’s personal preference is not another’s legal mandate and that the Constitution does guarantee all citizens equal protection of the laws. I added that smoking ban laws require bona fide material risk from ETS. I was given the closing final statement, wherein I emphasized the points about the study published by JNCI and personal preference versus legal mandate. I close with the observation that considering this latest study about ETS current science to support smoking bans has been crushed.

 

Readers may want to peruse the E-Mails with BBC below. There are many more important points about that new study published by the Journal of the National Cancer Institute included in that text that should be of immediate interest.

I appreciate the unexpected Father’s Day present from BBC.

 

Norman E. Kjono

From: norm kjono [mailto:normkarl@earthlink.net]
Sent: Sunday, June 19, 2005 2:04 PM
To: 'Geoff Prout'
Subject: RE: Norman E. Kjono: BBC Radio Appearance June 19, 2005

 

Mr. Prout,

You bet it is. Thanks for the opportunity.

Best Always,

Norm Kjono

 

PS: I believe that the Downing Street Memo angle is very, very, important. Beyond which, of course, it ties the story to a current hot political story in Britain.

From: Geoff Prout
Sent: Sunday, June 19, 2005 1:58 PM
To: norm kjono
Subject: RE: Norman E. Kjono: BBC Radio Appearance June 19, 2005

 

Thank you very much.   We are trying to book a American Lung Association spokesperson to debate with you.  Is that okay with you?

 

Geoff Prout
Producer
Up All Night
BBC Radio Five Live
London
UK

From: norm kjono [mailto:normkarl@earthlink.net]
Sent: Sunday, June 19, 2005 1:26 PM
To: 'geoff.prout@bbc.co.uk'
Subject: Norman E. Kjono: BBC Radio Appearance June 19, 2005

 

Mr. Prout,

 

Thank you for your telephone call early this afternoon concerning my participation in an BBC radio broadcast concerning a proposal to ban smoking in public places in Britain, scheduled for about 5:05 PM Seattle, Washington USA time today. I appreciate the opportunity to comment.

 

Pursuant to our discussion please find below the excerpts and links regarding new conclusions concerning Environmental Tobacco Smoke (ETS) as published in the Journal of the National Cancer Institute (NCI) March 2, 2005 that I promised to send to you. Please note that the excerpts include links to NCI’s press release, the study abstract, and a March 2005 editorial published by the journal about the study. According to a March 21, 2005 article in Science Daily the following conclusions are stated:

 

“These findings ‘support the hypothesis that at least two distinct molecular pathways are involved in the pathogenesis of lung adenocarcinomas, one involving EGFR TK domain mutations and the other involving KRAS gene mutations,’ the authors write. These results also ‘suggest that exposure to carcinogens in environmental tobacco smoke may not be the major pathogenic factor involved in the origin of lung cancers in never smokers but that an as-yet-unidentified carcinogen(s) plays an important role.’" (Underline, bold, italic added.)

 

The “Justification” for smoking bans in the United States (see, for example, ASSIST94.PDF attached) has been based on large part on claims about ETS arising from or based on the December 1992 U.S. Environmental Protection Agency’s report on secondhand smoke, which concluded that “ETS is a human lung carcinogen, responsible for approximately 3,000 lung cancer deaths annually in the USA.” (see EPAPOST.PDF attached, page 2) The EPA report referenced was issued in the final months of the second George H.W. Bush administration. That report was later ordered vacated by U.S. District Court Judge William L. Osteen July 17, 1998 (see EPAPOST.PDF attached, page 1), based on severe criticism by our federal courts of EPA’s methodologies. Despite such criticism by our federal courts, efforts to aggressively promote smoking bans – and thereby produce a coerced consumer choice of “Smoke Free” pharmaceutical nicotine delivery gums, patches, lozenges and inhalers – proceeded apace. Notably, Britain’s GlaxoSmithKline (Nicorette gumm, NicoDerm CQ patches) has been a principal supporter of smoking bans in the United States, paying an annual fee to the American Cancer Society for use of the society’s seal to promote sales of the company’s products.

 

The recent conclusions published by the U.S. National Cancer Institute that Environmental Tobacco Smoke “may not be the major pathological factor involved in the origin of lung cancers in never smokers” and that “an as yet unidentified carcinogen(s) plays an important role” are highly significant in terms of the U.S. EPA’s report on secondhand smoke, and therefore with respect to smoking bans allegedly “justified” by promoting exaggerated risks of ETS. That significance rises from the fact that the 1992 EPA report was a meta-analysis of several reports that primarily focused on the spouses (by and large female) of persons who smoke in the 1980s. The 1992 EPA report, and therefore all exaggerated claims about the alleged risks of ETS touching it, have been dealt a significant, perhaps fatal, blow for several reasons:

 

First, the study explicitly states that another “as-yet-unidentified carcinogen,” clearly other than ETS, “plays an important role” in nonsmokers’ lung cancer;

 

Second, a gene mutation that appears to be associated with lung cancer in nonsmokers, and that is unique to the preponderantly female sample population of the EPA report, has been identified;

 

Third, the importance of Environmental Tobacco Smoke as a contributing factor to lung cancer in nonsmokers has clearly been brought into question, at the least dramatically diminished;

 

Fourth, when adjusting for this confounding factor in the 1992 EPA report meta-analysis it is virtually certain that all or more of the 3,000 estimated deaths would disappear on EPA’s epidemiological model’s output;

 

Fifth, with a negative population deaths figure (virtually certain when considering this new study), and a therefore a negative correlation, we arrive at the rather bizarre conclusion that lung cancer deaths in nonsmokers are inverse, opposite, to exposure to ETS.

 

In short, EPA and anti-tobacco activists have been hoist on their own exaggerated ETS risk petard by the National Cancer Institute. It is important to note that NCI was the federal sponsor for the George H.W. Bush administration’s 1991 to 1998 Project ASSIST in the United States (see ASSIST94.PDF attached for that programs “justifications” for smoking bans.)

Were we to rely on the “statistics” produced in the EPA model by removing nonsmoking females with lung cancer exposed to ETS, then further adjust for the “as-yet-unknown carcinogen(s)” the negative number of deaths and negative correlation would suggest that every nonsmoker in Britain should ask their friends who smoke to light up in their presence, and deeply then inhale the ensuing fragrance of tobacco smoke, to protect themselves from lung cancer!

 

Based on the foregoing I respectfully suggest that those who still look to secure employment by establishing a credible link between ETS and lung cancer in nonsmokers would be better advised to apply for a job on the Iraq Weapons of Mass Destruction (WMD) search team. Not only would they be employed for an indefinite period but their chances of success appear to be greater.

 

Downing Street Memos meet the March 2, 2005 issue of the Journal of the National Cancer Institute. I believe that both are of equal importance when considering fabrications exported by the USA to influence British policy.

 

Thank you again, I look forward to participating in the BBC broadcast late this afternoon.

 

Norman E. Kjono

 

Columnist, Forces.org

(425) 497-8187

Study Published By National Cancer Institute: From Science Daily, March 21, 2005, "Study Examines Role of EGFR Gene Mutations In Lung Cancer Development,"  about a study published by the Journal of the National Cancer Institute  (NCI):

 

“A new study has found that mutations in either of two genes are involved in the development of lung cancer. One of them is the first known mutation to occur specifically in never smokers, according to a new study in the March 2 issue of the Journal of the National Cancer Institute. Studies have found that the epidermal growth factor receptor (EGFR) gene is mutated in many non–small-cell lung cancers and that these mutations are associated with increased sensitivity to gefitinib (Iressa) or erlotinib (Tarceva), tyrosine kinase (TK) inhibitors that target EGFR. Recent studies have found that EGFR gene mutations are more common among females, patients from Japan, never smokers, and patients with adenocarcinomas, which are the same groups that have the highest response rates to TK inhibitors. However, little is known about how EGFR gene mutations affect lung cancer development. . . . In lung cancer patients, mutations in the TK domain of the EGFR gene were more common in never smokers than in smokers (51% versus 10%), adenocarcinomas versus other types of lung cancer (40% versus 3%), in patients of East Asian ancestry than in other ethnicities (30% versus 8%), and in females versus males (42% versus 14%). . . . These findings "support the hypothesis that at least two distinct molecular pathways are involved in the pathogenesis of lung adenocarcinomas, one involving EGFR TK domain mutations and the other involving KRAS gene mutations," the authors write. These results also "suggest that exposure to carcinogens in environmental tobacco smoke may not be the major pathogenic factor involved in the origin of lung cancers in never smokers but that an as-yet-unidentified carcinogen(s) plays an important role." (Underline, italic added.)

 

a.) March 2, 2005 NCI Press Release, “Study Examines Role of AGFR Gene In Lung Cancer Development,”   concerning this study was published by the Journal of the National Cancer Institute. That Press Release says, in part:

“A new study has found that mutations in either of two genes are involved in the development of lung cancer. One of them is the first known mutation to occur specifically in never smokers, according to a new study in the March 2 issue of the Journal of the National Cancer Institute.” (Underline added.)

 

b.) The Abstract for the above-referenced study, “Clinical and Biological Features Associated With Epidermal Growth Factor Receptor Gene Mutations in Lung Cancers,”    published by NCI presents the following conclusions:

“Conclusions: Mutations in either the EGFR TK domain or the KRAS gene can lead to lung cancer pathogenesis. EGFR TK domain mutations are the first molecular change known to occur specifically in never smokers.” (Underline, Italic added.)

 

c.) The March 2, 2005 issue of the Journal of the National Cancer Institute (Vol. 97, No. 5, 326-328) also published an editorial, “EGFR Gene Mutations: A Call for Global x Global Views of Cancer,”  about this study, which said, in part:

 

Shigematsu et al. (12) showed that EGFR gene mutations are more prevalent in females than in males and, importantly, that this association is independent of smoking status. Men and women might be differentially exposed to an environmental factor. However, one potentially important difference between females and males is their exposure to estrogenic versus androgenic sex steroids. . . . Thus, given its oncogenic role in breast cancer, the estrogen receptor (ER) would be a prime suspect for a nuclear receptor cooperating with EGFR activation and thereby accounting for the female preponderance found in lung adenocarcinomas bearing EGFR gene mutations. . . . Shigematsu et al. (12) also extended the observation that lung adenocarcinomas harboring EGFR gene mutations are more commonly associated with never having smoked (8,9). This association might simply be due to the fact that there are fewer smokers at risk for EGFR mutant lung cancers as a result of competing illness (e.g., cardiovascular disease or other cancers). Probing this association further will require studying the incidence of EGFR gene mutations in a population-based cohort. Such an approach would allow one to ascertain the true number of smokers and nonsmokers at risk for developing lung cancer (nonsmokers typically outnumber smokers) and to determine whether the incidence of EGFR gene mutations in smokers and nonsmokers is truly different

 

Based on the foregoing study recently reported by the National Cancer Institute exposure to Environmental Tobacco Smoke is not, and cannot be, associated with as the cause of all, perhaps any, lung cancers in nonsmokers and that another unknown carcinogen(s) apparently is. It becomes strikingly apparent from the preceding information that a gene mutation unique to nonsmokers is necessary for lung cancers as described to occur for persons who do not smoke and that such gene mutation is not associated with exposure to Environmental Tobacco Smoke.