Chemicals

With state-of-the-art techniques, human papillomaviruses are now found in virtually 100% of cervical cancers. NIH Consensus Statement 102 and the International Agency for Research on Cancer have both declared that HPV causes human cervical cancer. Although they would not admit this, the alleged risk from smoking (and passive smoking) was generated by residual confounding, due to the high odds ratio associated with HPV infection.

The role of human papillomaviruses in bladder cancer has been less well studied. However, there have been more than 27 clinical/laboratory studies, which have indicated a prevalence of high-risk HPV types varying from 2.5% to 81%. HPV-16, which causes most cervical cancer, was the most commonly found type. "In addition, molecular studies suggest that the HPV-related oncoproteins E6 and E7 play a role in bladder carcinogenesis via inactivation and/or degradation of p53 adn pRb suppressor gene-associated proteins" (A Lopez-Beltran, AL Escudero. Human papillomavirus and bladder cancer. Biomed & Pharmacother 1997;51(6-7):252-257).

Chemical carcinogens, both from environmental sources and from smoking, have been alleged to cause bladder cancer. Dietary bracken fern in cattle has been a classic real-life example in animals. There are high rates of both bladder and alimentary tract cancers among cattle which graze on bracken-infested land. Chemical carcinogenesis by substances in the bracken ferns has traditionally gotten the blame. However, there is evidence implicating a role for bovine papilloma viruses, brought on by immunosuppression caused by the toxicity of the bracken fern.

From: Cooperation between bovine papillomaviruses and dietary carcinogens in cancers of cattle. ME Jackson, MS Campo. In: DNA tumor viruses. Oncogenic mechanisms. G Barbanti-Brodano, M Bendinelli, H Friedman, eds. Plenum Press, 1995, Ch 7, pp 111-122.

"However, cattle that were fed bracken but not injected with BPV2 also developed urinary bladder cancers. Nevertheless, BPV2 was found in the bladder cancers from both groups (WFH Jarrett and MS Campo, unpublished data), strongly suggesting that latent asymptomatic virus had been activated by the bracken diet (MS Campo et al. Latent papillomavirus infection in cattle. Res Vet Sci 1994;56:151-157), possibly as a result of the chronic immunosuppression caused by bracken feeding (Evans WC et al. Acute bracken poisoning in homogastric and ruminant animals. Proc Royal Soc Edin 1982;81:29-64). This result was confirmed in an experiment designed to test for synergism between BPV4 and bracken in alimentary tract cancer (see below), in which none of the cattle were experimentally exposed to BPV2, but bladder cancers occurred only in bracken-fed animals, and in 60% of the animals these cancers were positive for BPV2 DNA (MS Campo, WFH Jarrett. CIBA Found Symp 1986;120:117-130; MS Campo, WFH Jarrett. Cancer Res 1992;52:6898-6904). Of the naturally occurring bladder cancers, 46% were also found to be positive for BPV2 DNA. A group of cattle that were kept on a hay diet but immunosuppressed with azathioprine developed BPV2-positive hemangiomas of the bladder, again suggesting that immunosuppression leads to activation of latent virus."

Animal models of papillomavirus carcinogenesis. MS Campo. Virus Res 2002 Nov;89(2)249-261. "Tumorigenesis due to papillomavirus (PV) infection was first demonstrated in rabbits and cattle early last century. Despite the evidence obtained in animals, the role of viruses in human cancer was dismissed as irrelevant. It took a paradigm shift in the late 1970s for some viruses to be recognized as 'tumour viruses' in humans, and in 1995, more than 60 years after Rous's first demonstration of CRPV oncogenicity, WHO officially declared that 'HPV-16 and HPV-18 are carcinogenic to humans.'"

It has been claimed that smoking causes immunosuppression, which leads to HPV activation ultimately resulting in cervical cancer. However, the similar supposed risk of cervical cancer trumpeted for passive smokers as for active smokers militates against this. It is not biologically plausible that the effect of a small amount of secondhand smoke is so similar to that of a large amount of firsthand plus secondhand smoke. That active and passive smokers have similar rates of exposure to high-risk HPVs due to lifestyle is the only plausible explanation.

Smokers are said to have higher rates of bacterial vaginosis than nonsmokers, and this has been claimed to be evidence of immunosuppression. However, it is now known that bacterial vaginosis is caused by a virus that infects the normal bacteria of the vagina, and the human host's immune system is not involved. The differences, again, are due to differences in exposure due to lifestyle.

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Bruce Ames and the Bracken Fern

"If you mention the manifesto that started the environmental movement to Bruce Ames [Rachel Carson's book, Silent Spring], he cannot help pointing out a little problem with the opening fable. There was a blight on this town that even its author, Rachel Carson, didn't know about. 'Here's this nice sylvan view of ferns,' Ames says, 'and one of the most common ones, the bracken fern, is absolutely full of carcinogens.' In fact these chemicals, which can be passed on through cow's milk or enter the soil when the plants die, might even be deadlier than the DDT that so concerned Carson, Ames says." (Not to Worry: Bruce Ames Helped Launch the Cancer Scare of the 1960s and 1970s. Now He Says Mushrooms Are More Threatening Than PCBs. Hippocrates 1988 Jan-Feb, p 28). But this view is baloney as well - IT WAS REALLY THE PAPILLOMA VIRUSES THAT CAUSED THE CANCER.

Bruce Ames and Lois Gold continue to promote junk science

Ames and Gold pretend, among other things, that diet and stomach cancer studies which ignore the existence of Helicobacter pylori supposedly "prove" that fruits and vegetables will prevent stomach cancer -- ignoring the fact that rates of stomach cancer depend most on HP infection, not on how many magic fruits and vegetables people eat; and that the purported "protective" effects of fruits and vegetables is the product of confounding. Ames and Gold are pseudo-debunkers who please the pro-industrialists, while protecting the health fascists' core fraud of ignoring the role of infection. (Politicizing Science: The Alchemy of Policy-Making. By Bruce Ames and Lois Swirsky Gold. Michael Gough, editor. Hoover Institute Press, 2003.)

More Ames & Gold Articles

Be Most Wary of Nature's Own Pesticides. By Bruce N. Ames. Los Angeles Times, Feb. 27, 1989.

Too Many Rodent Carcinogens - Mitogenesis Increases Mutagenesis. B.N. Ames, L.S. Gold. Science 1990 Aug 31;249(4972):970-971.

Mutagenesis tests

Predicting Rodent Carcinogenicity From Mutagenic Potency Measured in the Ames Salmonella Assay. Bethel A. Fetterman, Byung Soo Kim, Barry H. Margolin, Jonathan S. Schildcrout, Melissa G. Smith, S. Michelle Wagner, Errol Zeigera. Environmental and Molecular Mutagenesis 1997;29:312- 322. "The somatic mutation theory of carcinogenesis holds that mutations are a common first step in the development of a cancer cell; consequently, interest in these STI's has been fueled by their ability to identify potential carcinogens. The test receiving by far the most use and attention has been the Salmonella (SAL) mutagenesis test developed by Ames and colleagues [1973, 1975]. The SAL test gets its most extensive use as a preliminary screen during chemical and drug development. The results of this test are often the only toxicology-related information used by industry to decide whether to proceed with development of the chemical and to more definitive toxicological tests, or to label it a potential carcinogen, and put it aside, with no further testing.... Our study firmly establishes that the predictive relationship between quantitative SAL mutagenicity and carcinogenicity is, at best, weak, regardless of the potency measure used. The lack of a strong predictive relationship between SAL mutagenicity and rodent carcinogenicity hardly seems surprising. Mutagenesis may be only the first step in some pathways that lead to cancer. The inference drawn here, however, is that this DNA damage as measured by mutations in SAL is not the rate-limiting consideration in the ultimate development of cancer in rodents. (Funded by the National Institute of Environmental Health Sciences.)

"Mechanisms of tobacco carcinogenesis" ?????

The Centers for Disease Control

See the Centers for Disease Control weasel about the anti-smokers' continuing inability to identify any mechanism of tobacco carcinogenesis: "Because of the chemical complexity of tobacco smoke it is unlikely that there is a single measureable mechanism of tobacco carcinogenesis." (Toxic Chemicals in Tobacco Products. Centers for Disease Control, Jan. 26, 2005.) They expect us to be brainwashed to accept their spiel of "scary chemicals" as sufficient evidence that chemical carcinogens are to blame, despite their incapacity to identify even one. Meanwhile, depite the fact that mechainisms by which viruses cause cancer have been identified, these corrupt health fascist gangsters continue to systematically ignore them.

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Choking on a Gnat While Swallowing a Camel

A typical ignorant attitude which is encourage by the health establishment because it furthers their health fascist political agenda (as well as enabling insider trading networks to exploit the effects of public hysteria on stock prices): "If large doses of carcinogens will eventually lead to cancer, why would we want to unnecessarily add to the levels of carcinogens we are exposed to? Thus, why use large amounts of pesticides when less or none will work just fine? Why expose ourselves to the carcinogens found in air pollution, car exhaust, cigarette smoke, etc. if we don't have to? If the dose is the poison, and I'm already getting dosed without trying to, why should I increase my risk?"

For benzo[a]pyrene, which is one of the common polycyclic hydrocarbons produced by combustion, "[T]he food chain is the dominant pathway of human exposure, accounting for about 97% of the total daily intake of BaP. Inhalation and consumption of contaminated water are only minor pathways of human exposure [2% from air, and 1% from water]. The long-term average daily intake of BaP by the general population is estimated to be 2.2 micrograms (ug) per day. Cigarette smoking and indoor activities do not substantially increase human exposure to BaP relative to background levels of BaP present in the environment." And, "[A]verage smokers (i.e., individuals who smoke 20 cigarettes a day) are taking in an additional 780 ng of BaP daily, which means that smokers get an additional 16% BaP from smoking" [based on pre-1979 cigarettes, which contained about twice the quantity of BaP as newer low-tar cigarettes]. Also, the exposure from cooked beef (0.2 -24.1 ug/kg) is less than the exposure from leafy vegetables (7.0 - 48 ug/kg). And, this research was sponsored by the U.S. Environmental Protection Agency. (Benzo-a-pyrene: Environmental partitioning and human exposure. H.A. Hattemer-Frey, C.C. Travis. Toxicology and Industrial Health 1991;7(3):141-157.)

Smoke from cigarettes accounts for less than 0.007% of U.S. Bap emissions per year. (Submission by Philip Morris U.S.A. to The National Toxicology Program. Appendix 7, "Benzo[a]pyrene: Environmental Distribution and Human Exposure." March 20, 1998.

Risk Assessment of Chemical Carcinogens: Is It Time For A Change? By Robert J. Scheuplein, Director, Office of Toxicological Sciences, Center for Food Safety and Applied Nutrition, Food and Drug Administration. Presented at the Brookings Institution, June 17, 1991. "[D]espite well over 500 papers on cancer risk assessment, on the biassay, on cancer thresholds and numerous related subjects, since 1961 (the date of Mantel and Bryan's paper) -- cancer risk assessment is still more of a regulatory tool than a scientific discipline and rests more on regulatory need than scientific plausibility" "So far, for any carcinogenic or mutagenic response in any given situation, be it man, mouse, isolated organ or a Salmonella plate assay, there is a demonstrable threshold or 'no effect level.' In thousands of studies with hundreds of thousands of animals, not a single carcinogen has been found that has not demonstrated an experimental threshold."

Determination of polycyclic aromatic hydrocarbons in the lung. H Seto, T Ohkubo, T Kanoh, M Koike, K Nakamura, Y Kawahara. Arch Environ Contam Toxicol 1993 May;24(4):498-503. "Polycyclic aromatic hydrocarbons (PAHs) accumulated in human lung samples from men (n = 236) and women (n = 128) were determined by high-performance liquid chromatography (HPLC) to examine their association with lung cancer. The mean values for benzo[a]pyrene (BaP), benzo[k]fluoranthene (BkF), and benzo[g,h,i]perylene (BghiP) in lungs (ng/g dry lung) of Japanese autopsied patients were 0.54, 0.44, and 0.87, respectively. The modal values were 0.3, 0.3 and 0.5, respectively. Each of the PAH concentrations was highly correlated with the others (r > 0.83). PAH concentrations in the lungs showed age-related increases with low correlation-coefficient values. BaP, BkF and BghiP concentrations in lungs of various subgroups were in the following order: male > female; and lung cancer > all cancers > non-cancer among male not female group. Only BghiP concentration in the lungs of the male smoker group is significantly higher (P < 0.10) than that of the male non-smoker group. Even among non-smoker groups, PAH concentrations in the lungs of male group were significantly higher than those of female group."

Benzo[a]pyrene 7,8-diol-9,10-epoxide

Benzo[a]pyrene 7,8-diol-9,10-epoxide is metabolized from benzo[a]pyrene

"Benzo[a]pyrene is metabolized to approximately 20 primary and secondary oxidized metabolites and to a variety of conjugates (see HSDB [366] information immediately below). Several metabolites can induce mutations, transform cells and/or bind to cellular macromolecules; however, only a 7,8-diol-9,10-epoxide is presently considered to be an ultimate carcinogenic metabolite [847]." {Environmental Contaminants Encyclopedia. Benzo[a]pyrene (BAP) Entry. July 1, 1997. Compilers/Editors Roy J. Irwin, National Park Service.)

Anti-smokers falsely blame benzo[a]pyrene 7,8-diol-9,10-epoxide for "tobacco-induced" lung cancer

High DNA damage by benzo[a]pyrene 7,8-diol-9,10-epoxide in bronchial epithelial cells from patients with lung cancer: comparison with lung parenchyma. Rojas M, Marie B, Vignaud JM, Martinet N, Siat J, Grosdidier G, Cascorbi I, Alexandrov K.Cancer Lett. 2004 Apr 30;207(2):157-63. They claim that "The high formation of BDPE-N(2)-dG adducts in bronchial epithelial cells and investigations showing that the profile of mutations induced by BPDE in these cells is similar to that seen in the p53 gene isolated from human lung tumors implicates benzo[a]pyrene as important carcinogen in tobacco-induced lung cancer in human beings." However, the levels found in smokers and non-smokers overlapped, with "4-fold interindividual differences in the DNA adduct levels in the range of 36.5-175.4 BPDE-N(2)-dG adducts/10(8) nucleotides in smokers (mean: 84.7+/-38.4; n = 13) and 3-fold differences in the range of 19.7-62.4 in non-smokers (mean: 37.6+/-22.2; n = 3," which is not consistent with the vastly greater difference in exposure to tobacco smoke between smokers and non-smokers. Their conclusion also ignores the key fact that, among both smokers and non-smokers, food is the largest source of BaP from which benzo[a]pyrene 7,8-diol-9,10-epoxide is metabolized. In the "Discussion," they employ the typical anti-smoker evasive technique of raising this issue and then dropping it, without examining its implications! They also completely ignore the possibility that infection could influence adduct formation. (And, note that they invoke FORCES's friends, Ernst L. Wynder and S.S. Hecht of the American Health Foundation, as authority for their claim that BAP and BPDE are "involved in the aetiology of lung cancer.")

Anti-smokers try to blame BaP for breast cancer

Chemically induced DNA hypomethylation in breast carcinoma cells detected by the amplification of intermethylated sites. B Sadikovic, TR Haines, DT Butcher, DI Rodenhiser. Breast Cancer Res. 2004; 6(4): R329–R337. As usual, the anti-smoker charlatans ignore key facts including vastly higher exposure to BaP from food versus smoking, and the possible role of infection. Epstein-Barr virus has been implicated as a possible cause of breast cancer.

Sadikovic - Breast Cancer Res 2004 full article / PubMed Central

CpG Methylation of Human Papillomavirus Type 16 DNA in Cervical Cancer Cell Lines and in Clinical Specimens: Genomic Hypomethylation Correlates with Carcinogenic Progression. V Badal, LS Chuang, EH Tan, S Badal, LL Villa, CM Wheeler, BF Li, HU Bernard. J Virol 2003 Jun;77(11):6227-6234. "In 81 patients from two different cohorts, the LCR and the E6 gene of HPV-16 DNA were found to be hypermethylated in 52% of asymptomatic smears, 21.7% of precursor lesions, and 6.1% of invasive carcinomas. This suggests that neoplastic transformation may be suppressed by CpG methylation, while demethylation occurs as the cause of or concomitant with neoplastic progression.... Two speculative and opposing views might explain this observation. The cell may have an antiviral defense that senses viral DNA as foreign and targets it for transcriptional repression. Alternatively, DNA methylation may be yet another example of the numerous strategies developed by HPVs that favor a subclinical, long-term maintenance of the viral infection. Such a model would be reminiscent of the life cycle of Epstein-Barr virus, which includes DNA methylation-dependent silencing of a specific promoter during one form of latency."

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Formaldehyde

Reevaluation of mortality risks from nasopharyngeal cancer in the formaldehyde cohort study of the National Cancer Institute. GM Marsh, OA Youk. Regul Toxicol Pharmacol 2005 Aug;42(3):275-283. "CONCLUSIONS: Overall, our reanalysis provided little evidence to support NCI's suggestion of a causal association between formaldehyde exposure and mortality from NPC. NCI's conclusion of a possible causal association was driven heavily by anomalous findings in one study plant (Plant 1). An independent and larger study of Plant 1 by the current authors concluded the NPC excess was not associated with formaldehyde exposure. Our findings cast considerable additional uncertainty regarding the validity of NCI's suggested causal association."

Epstein-Barr virus is by far the main cause of nasopharyngeal cancer. And studies which ignore it are defective and will falsely blame irrelevant, non-causal associations.

Official OSHA Policy on Secondhand Smoke

"Because the organic material in tobacco doesn't burn completely, cigarette smoke contains more than 4,700 chemical compounds. Although OSHA has no regulation that addresses tobacco smoke as a whole, 29 CFR 1910.1000 Air contaminants, limits employee exposure to several of the main chemical components found in tobacco smoke. In normal situations, exposures would not exceed these permissible exposure limits (PELs), and, as a matter of prosecutorial discretion, OSHA will not apply the General Duty Clause to ETS." (02/24/2003 - Reiteration of Existing OSHA Policy on Indoor Air Quality: Office Temperature/Humidity and Environmental Tobacco Smoke. Standard Number: 1910.1000.)

"Tobacco-Specific" [sic] Nitrosamines

N'-Nitrosonornicotine. CAS No. 16543-55-8. Report on Carcinogens, Eleventh Edition. U.S. Department of Health and Human Services, Public Health Service, National Toxicology Program. Announcement of the draft in the Federal Register was on Nov. 13, 2007. For NNN: "No adequate human studies of the relationship between exposure to N-nitrosonornicotine and human cancer have been reported (IARC 1978, 1985, 1987)." NNK and N′-nitrosoanatabine (NAT), N′-nitrosoanabasine (NAB), 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), 4-(Methylnitrosamino)-4-(3-pyridyl)-1-butanol (iso-NNAL) are not listed among the carcinogens.

cast 05-01-08