What if they have been barking up the wrong tree?Warning; Those easily insulted by non-politically correct views; please save your immortal soul, protect your offspring avoid other global calamities ending in the destruction of the universe and read no further.
Lets get radical for a bit. I am saying way out there in left field among the kooks and deranged individuals. Away from government, sensibilities decreeing the product needs no scrutiny, it is the victim that needs to be blamed. Taking the product off the shelf, until it could be proven safe for consumption solved tainted tuna. Dealing with the product missed a huge opportunity in taxing the hospital patients for costs to health care. How do we in our wisdom, define a cigarette? Medicinal benefits would define it as a drug requiring a drug classification. Environmental issues would require monitoring by the ministry of the environment. Cigarettes are believed to be, by the federal Government and the World Health Organization, best suited as a political issue now regulated by the political consensus driven Ministry Of Health in an apparent vacuum well insulated from the knowledge of other departments.. A ministry whose head scientist is limited by lack of training it appears his background has been dedicated to political study. He is not well equipped to handle the issues of public safety at hand outside of the political implications, which promote through slander and segregation special taxation in direct contravention of the Canada health act. Ad agency spin in “Social Marketing” describes through the ministry website directives; attempts to direct what Canadians think as opposed to understanding what we actually do think. Gomery touched on that line of thinking and the dangers to integrity of Government process through political party branding. The 47,000 preventable deaths of smokers are currently, and we believe wisely, being cured by protecting non-smokers from inhaling less than 1/100,000 the concentration inhaled by smokers. This would indicate the powers that be find those smokers deaths inevitable and acceptable. Further to use those deaths as an abstract for political expediency is also an acceptable act. Deaths of 1/2 of the current 6 million smokers are actually seen to be inconsequential The fact the figure describes smoker deaths not non-smokers deaths can also easily be dismissed in kind, as long as the product produces profit, taxation levels will be maintained, which serves quite well the majority of community. The arguments of science and common sensibilities would have us actually punishing the manufacturers. Contrary to public belief that has not yet happened. In fact tobacco settlements removing manufacturers from further future liability in the United States were marked up and passed on to consumers, as were all the special billing for universal health care in Canada known as tobacco taxes. Stated to be cost to healthcare yet amounts are consistent with WHO recommendations price increases as “5% above the inflation rate for the next 5 years” Elimination of advertising and sponsoring of public events goes straight to the manufacturers bottom line. Not much wonder the Federal government was investing pension funds in big tobacco; profits have never been higher and cost of production never lower. Allowing unrestricted cheaper imported products to flow into Canada to compete with domestic regulated products again increased the share equity position.
Leading us to the obvious question; who are the real “paid stooges to big Tobacco”?
Soon similar taxation of the Pan Canadian strategy will expand the plan into the grocery stores. Hardly an attempt to hold manufacturers responsible, if indeed they are creating a health risk, efforts are aimed at passing liability again to the victims. The proposed 75% taxation of hamburger and 300% rebates to healthy food advertisers will suit a public need for increased taxation and party branding among media groups profiting from the promotion. It can be assumed the damage to the cattle industry will be temporary as were the detrimental effects to the hospitality industry through the imposition of smoking bans.
If truth were known the only one, of all the 5000 ingredients in Tobacco smoke all with safe levels measured in milligrams per cubic meter of air is of course dioxin. Dioxin requires 3 ingredients Ammonia, Organic material and a low temperature flame. Recent research in Japan showed no Dioxin in the paper or the Tobacco however, Dioxin did exist in the smoke. At the world trade center Dioxin levels monitored at levels below .16 Nana grams per cubic meter of air were considered safe. Co-incidentally the same safe level referred to by James Repace as his known safe level in air water and food he states according to the US government. It could be suspected the no safe level is actually predicated on this level of harm as are predictions of 42% of the public will get cancer at some point. This percentage is very close to the known risk of persons with maximum accumulated state levels of Dioxin stored in their body fat. Even without smoking, we will all likely reach the maximum saturation or state level due to other sources.
Fat really is the new tobacco.
This would say the medical charities and the health departments have been a little short of entire honesty in what they know is likely the most predominant cancer risk in smoking. This would allow us a new radical thought lets say a government 40 years ago banned the use of chlorine in cigarettes how many of the 47,000 preventable deaths would have actually been prevented. By rough calculation 2/3 the same level smoking has been reduced in that time frame. In the same period smoking related diseases increased by the same 2/3 level. A simple examination of dioxin poisoning and medical outcomes in fact will show clearly a Dioxin parallel to everything they say about smoking and the related diseases. If in fact you take their numbers as gospel you will by examining the side of a cigarette package and a few calculations quickly see; The levels of dioxin produced by a single package are in excess of 2 milligrams 1 milligram of Dioxin inhaled by a smoker every day will ultimately lead to the punishment the Ontario health department spoke of in “quit or be punished”. We shut down an incinerator in Toronto with dioxin levels a million times lower. Yet the government in efforts of protecting 6 million smokers fails to announce the full harm or do anything to reduce it. One can only conclude the death penalty is alive and well and living in Ontario. Industry health and safety controls are in fact a fictional political euphemism.
Note; the diesel trucks hauling the Toronto garbage are producing Dioxins thousands of times higher than the original incinerator. Simply increasing the temperature of burning by as little as 300 degrees could, have eliminated the dioxin in the original incinerator. But hey that’s just the radical view. Your doctor does know best. Huge sums being paid in the trucking deals are simply a matter of public demand among a public who were largely unaware a problem existed, prior to ad agency media campaigns of yet unknown origin.
The Evidence File
Risk “3.17 Potential effects. Some industrial chemicals and pesticides in the environment have been linked to lung diseases, reproductive problems and birth defects, developmental disorders, allergic reactions, lowered resistance to disease in humans and cancer. In wildlife, eggshell thinning, deformities, reproductive dysfunction, tumors, embryo and adult mortality have been linked to toxic substances.
3.18 Toxicity and risk. Generally, toxicity refers to the capability of a substance to injure humans and ecosystems. In this sense, all substances - both natural and synthetic - are potentially toxic. But it is the dose that makes the poison: even highly toxic substances will not cause harm unless people or wildlife are exposed to them in air, water, soil or food.
3.19 The concept of risk is central to federal decision-making on toxic substances and, by extension, was central to this audit. In simple terms, risk refers to the probability of experiencing harm combined with the extent of that harm. It is a function of the hazard presented by a substance and of our exposure to it. Estimating risk is not simple, and risk assessment is almost a scientific discipline unto itself. In theory, scientific calculations of the risk posed by some industrial chemicals and pesticides can be compared with levels considered to be acceptable and with the risk posed by other activities or conditions. The relative priority of the substances can then be established, and the environmental, social and economic costs and benefits of reducing the associated risk can be evaluated.
3.20 We live in a world full of risk. Driving a car, taking medication, smoking, and sunbathing are all activities that have a risk associated with them. Some risks result from personal choices; others are imposed on us. The extent to which toxic substances in the environment pose significant risks to human health and ecosystems is not a matter of scientific consensus. Some believe that the risks posed are insignificant - or at least acceptable - especially compared with other risks encountered and tolerated every day. Others disagree.
3.21 We are often faced with choices involving trade-offs between risks and benefits. Modern chemicals provide important economic, health and social benefits. Therefore, actions to reduce risks by eliminating exposure can have significant economic and social implications. For this reason, stakeholders often debate whether the costs of reducing the risks, including lost uses of the substance, are worth the benefits.
3.22 The use of chlorine to disinfect drinking water is an example of the complexity of risk as it pertains to toxic substances. The use of chlorine has been heralded as one of the most successful public health initiatives ever and is believed to prevent thousands of potentially fatal infections each year. Recently, however, chlorination by-products in drinking water have been linked to cases of bladder cancer, illustrating that there are benefits and risks associated with the same activity.”
Environmental smoke types have never been clearly defined and are actually the products of burning many quite different substances some obviously much more harmful than others.
http://monographs.iarc.fr/htdocs/monographs/vol38/tobaccosmoke.htmlSales-weighted average tar and nicotine contents (as measured by standard laboratory methods) have declined significantly since the 1950s in some parts of the world. The chemical composition of smoke depends on (a) the type of tobacco; (b) cigarette design, including filtration, blend selection (e.g., reconstituted sheet, expanded tobacco), ventilation, paper and additives; and (c) the smoking pattern.
2). The following site-specific sections are for those sites for which we now believe there to be sufficient evidence, since the 1986 monograph (
3), to conclude that smoking is a cause of cancer. (Note: although much of the evidence is based on cigarette smoking, many of the papers also contained information on other forms of tobacco smoking. Consequently, we use the generic term "tobacco" to include all forms of smoking. In addition, the term "non-smokers" as used by the authors, usually means the more appropriate term "never smokers.")
Surprisingly there was another side to the debate although the public was not allowed to hear it
http://www.junkscience.com/news2/zion.htm
http://bmj.bmjjournals.com/cgi/content/full/317/7154/348#resp1 http://bmj.bmjjournals.com/cgi/content/full/317/7154/348#resp1
Perhaps more surprising are press reports that Neil Collingshaw, the acting chief of the World Health Organisation's tobacco and health unit in Geneva, apparently did not know that such a study was being undertaken.3
The hot air on passive smoking
Experts who evaluated studies seem not to have had relevant experience
Opinions depend on what sort of evidence is thought most convincing
BAT has not tried to discredit data on passive smoking
Perhaps more surprising are press reports that Neil Collingshaw, the acting chief of the World Health Organisation's tobacco and health unit in Geneva, apparently did not know that such a study was being undertaken.
3 Also surprising are comments from Sir Richard Doll that the full study had been submitted to two journals and rejected by both (BBC News 24, 1998 Mar 15). I assume that we will never know whether the BMJ considered and rejected the study and, if it did, for what reason.
All scientists interested in this area of research await the full report, although Action on Smoking and Health's website carries what it describes as the "formal abstract of the WHO paper (unpublished)" (
http://www.ash.org.uk/). This abstract reconfirms that the overall findings of the study are of a small positive association for spousal and workplace exposure, neither association being significant. This finding is consistent with results of previous research on spousal exposure, which in general show small positive associations that are not significant, and data on workplace exposure, which provide little or no indication of an increase in risk.
The "formal abstract" also reports: "Childhood exposure to ETS [environmental tobacco smoke] and exposure in vehicles and in public settings were not associated with lung cancer risk." The IARC's biennial report also suggests that there is little or no increase in the overall risk of adenocarcinoma.
The interpretation of low risk epidemiology is a matter of serious debate. If large studies, whatever they are considering, fail to find significant increases in risk then one must question whether there is a real increase in risk and, if there is, if that risk is quantifiable. To lower the standard of scientific debate simply because it concerns tobacco is unjustified.
MP's Report Canada's Charities: A Need for Reform
http://www.forces.org/evidence/files/bryden1.htmWhat follows in this paper is one backbench Member of Parliament's attempt to identify some of the problems that have accumulated in Canada's not-for-profit sector. This has been done mainly by studying the annual financial information forms (T3010) of about 600 charities. As the information on these forms is often of very poor quality, the analysis is certainly not definitive.
World Health Organization ETS research; No significant harm in ETS
http://oem.bmjjournals.com/cgi/content/abstract/53/9/606?ijkey=b9027c1933f6d2ffbd83693ef0fc3ffd51e21887&keytype2=tf_ipsecsha
Cause specific mortality and cancer incidence among employees exposed to 2,3,7,8-TCDD after a 1953 reactor accident
RESULTS: The estimated dose of TCDD for 135 men was > or = 0.1 microgram/kg body weight and for 69 men > or = 1 microgram/kg body weight. Increased cancer risk ratios were found with higher doses of TCDD and longer interval since first exposure for all sites combined and digestive and respiratory cancers in particular. Within the high dose group (> or = 1 microgram/kg body weight), total cancer mortality was increased > or = 20 years after first exposure (13 cases, standardised mortality ratio (SMR) 1.97, 95% confidence interval (95% CI) 1.05-3.36) as was respiratory cancer (six cases, SMR 3.06; 95% CI 1.12-6.66). Among current cigarette smokers, 12 cancer deaths occurred in the high dose group (SMR 3.42, 95% CI 1.77-5.97) compared with seven deaths at lower doses of TCDD (SMR 1.29, 95% CI 0.52-2.66). Regression analyses based on the Cox's proportional hazards model provided further evidence of a relation between cumulative dose of TCDD and occurrence of both overall and digestive cancer. No evidence of an effect of TCDD on overall mortality or deaths due to circulatory disease was found and no cases of non-Hodgkin's lymphoma or soft tissue sarcoma have been found to date. CONCLUSIONS: Our findings are consistent with a carcinogenic effect induced by TCDD at doses > or = 1 microgram/kg body weight. With such a small cohort, the risk estimates are not very stable and could be affected by selection and confounding.
Dioxin effects explained
Apart from new epidemiologic data since 1997, there are also new experimental studies (some of them used in the recent WHO risk assessments) and advances in the understanding of mechanisms of action of dioxins, particularly concerning the AhR. The AhR is a nuclear receptor and transcription factor. In the presence of TCDD, it forms an active heterodimer with the aromatic hydrocarbon nuclear translocator (ARNT/HIF-1β) and induces (or suppresses) the transcription of numerous genes, including P4501A1 (CYP1A1) (Whitlock 1999). In the last few years, additional components of the AhR complex have been identified, including the AhR repressor, AhR-interacting protein (also known as XAP2), Rb protein, receptor-interacting protein 140, SRC-1, p23, and the RelA NF-κB subunit (Carlson and Perdew 2002; Kumar and Perdew 1999; Mimura et al. 1999; Petrulis and Perdew 2002). Molecular mechanisms occurring downstream of AhR and possibly associated with cancer development, such as changes in cytosolic signaling proteins, calcium mobilization, tumor suppressor proteins, growth factors, oncogenes, and cell cycle proteins, have been characterized (Carlson and Perdew 2002; Enan et al. 1998; Matsumura 2003).
Recently, molecular epidemiology investigations have been conducted on random samples of the Seveso population highly exposed to TCDD (zones A and B) and from the reference noncontaminated area (non-ABR) to evaluate how TCDD exposure affects the AhR pathway in human subjects in vivo
(Baccarelli et al. 2004; Landi et al. 2003). Because of the extremely long biologic half-life of TCDD, plasma TCDD levels were still substantially elevated in the exposed subjects, particularly in females and older subjects (Landi et al. 1997). Experimental studies indicate that, after a transient increase, cellular levels of AhR decrease following TCDD binding (Pollenz 2002). Nearly 20 years after the Seveso accident, the levels of AhR transcripts (measured in uncultured peripheral blood lymphocytes) were decreased in the exposed subjects and negatively correlated with current plasma TCDD levels (Landi et al. 2003). These results show that TCDD exposure causes a persistent alteration of the AhR pathway in human subjects and are consistent with down-regulation of this receptor, comparable with that observed in several other receptor-mediated systems (Pollenz 2002). The impact on the health of exposed individuals of the persistent decrease of AhR transcripts, which in turn may affect any AhR-regulated biologic function, is to be clarified. Down-regulation tends to decrease the amount of receptor available for ligand binding and to attenuate the resulting biologic responses. Thus, the AhR, like most receptor systems, may have high initial sensitivity to the ligand, whereas in the presence of high amounts of TCDD, down-regulation would buffer against excessive ligand-induced responses. High initial levels of exposure, rather than low persisting exposures, may be associated with the highest effects. In the industrial cohorts, cumulative exposure predicts cancer excess. However, it is likely that cumulative and peak exposures are highly correlated among industrial workers. The new evidence from animal studies and on the AhR should be used to refine quantitative risk assessment of TCDD and could modify estimates on tolerable intake in humans. This evidence put together, supports the approach taken by IARC to consider the animal and mechanistic data in the evaluation of carcinogenicity of these compounds in humans.
Health Effects of Dioxins
“Everyone in industrialized countries has a potent mixture of dioxins, furans, co-planar PCBs, PCNs and other similar compounds stored and accumulated in their bodyfat. This chemical concoction of compounds in our bodies is likely to add together, making up a total dioxin-like toxicity: dioxins plus PCBs is equivalent to more dioxins.”
“ 2,3,7,8-TCDD (often known simply as TCDD) is known for its lethal effects at very low concentrations: a millionth of a gram will kill a guinea pig. However, the reasons for its potency are very subtle, and connected with its structural similarity to potent natural hormones. The power of hormones lies in their ability to act in trace amounts as chemical messengers controlling vital processes in the body. Thus, an accidentally produced contaminant, i.e. TCDD, from the chemical industry can act as a wrong key in the subtle system of trace chemical messengers in the body by mimicking the action of a hormone”.
Linear effects would substantiate dose response and establishing safe levels of exposure, which could be monitored. Non-linear effects would support no safe levels exist. The same arguments if applied to ETS would result in easily attainable safe levels in ventilation not possible under current inconsistent delegations.
Non Linear vs. Linear
Cancer, Heart Disease, and Diabetes in Workers
Exposed to 2,3,7,8-Tetrachlorodibenzo-p-dioxin
Cox regression, using an internal comparison group with low exposure, found a statistically significant positive trend between all cancers (after a 15-year lag time) and cumulative exposure. Similar trends were present both for smoking-related cancers and non-smoking-related cancers, suggesting that the cancer findings were not limited to an interaction between TCDD and smoking. The finding of stronger trends with the logarithm of cumulative exposure rather than cumulative exposure itself indicates that the exposure-response trend is sublinear at very high doses, which in our data was probably a reflection of the extreme skewness of the exposure data.
The finding that the best lag time was 15 years (marginally better than a 10-year lag time) is consistent with current views that TCDD acts as both an initiator and promoter (25). Were TCDD to act as an initiator only, one might expect a longer lag of 20 years or more before the development of most tumors. Were TCDD to act as a promoter only, one might expect little or no lag. Because 1) there is still uncertainty about the basic biology of TCDD carcinogenesis, 2) our epidemiologic estimates of exposure are crude approximations of biologically relevant dose, and 3) statistical evidence is weak for favoring one lag time over another, we suggest that not too much interpretative weight be given to a finding that one particular lag period versus another provides a slightly better model.
For ischemic heart disease, there was only a modest trend of increasing SMRs with increasing exposure; the SMR for the highest category was 1.28 (95% CI = 0.92-1.72). However, internal analyses using Cox regression found statistically significant exposure-response trends. No lag time for heart disease was indicated in the Cox regression analysis, suggesting that any possible mechanism (e.g., an alteration of lipid profiles) occurred simultaneously with exposure. Because TCDD persists for a long time in the tissues [half-life, 8.7 years (26)], TCDD would be present for many years after exposure ceased, possibly resulting in a long-term effect.
Four industrial cohorts that served as a basis for IARC (1997) TCDD determination.
Study originally available to IARC in 1997a
Cancer SMR (95% CI) and definition of subcohort
No. of cancer deaths
Estimated TCDD at end of exposureb
Exposure–response data for TCDD
Fingerhut et al. 1991
1.5 (1.2–1.8), > 1 year exposure, 20 years of latency (59% of cohort)
114
Mean 418 ppt (n = 119)
Positive significant trend (p < p =" 0.003)" href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1247514#b33-ehp0112-001265" target="mainwindow">Steenland et al. (1999, 2001),c based on JEM and serum levels
Becher et al. 1996
1.3 (1.0–1.5), workers in two plants with documented chloracne and high serum TCDD levels
105
Plant 1: mean, 141 ppt (n = 190). Plant 2: mean, 402 ppt (n = 20)
Positive significant trend (p < href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1247514#b14-ehp0112-001265" target="mainwindow">Flesch-Janys et al. (1995), in Flesch-Janys et al. (1998; p = 0.01),c and in Becher et al. (1998; p = 0.03),c based on JEM and serum levels
Hooiveld et al. 1996
1.5 (1.3–1.9), workers in the most highly exposed plant (n = 549)
51
Geometric mean, 286 ppt (n = 48)
Medium- and high-exposure groups elevated (RRs = 4.7 and 4.1) versus low (Hooiveld et al. 1998),c based on work history and serum levels
Ott and Zober 1996
1.9 (1.1–3.0), chloracne and ≥20 years’ latency (n = 113)
18
Geometric mean, 400 ppt (n = 138)
Positive significant trend (p = 0.05) in original 1996 publication, based on body burden
Abbreviations: CI, confidence interval; NIOSH, National Institute for Occupational Safety and Health; SMR, standardized mortality ratio.
aIARC (1997; Table 38).
bIARC (1997; Table 22).
cPost-1997 findings.
Environ Health Perspect. 2004 September; 112(13): 1265–1268.
Published online 2004 June 10. doi: 10.1289/ehp.7219.
Copyright This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original DOI.
Effects of Primary smoking 50 year study spanning over 100 years
Indications were the product became much more harmful over the years.
http://bmj.bmjjournals.com/cgi/content/short/bmj.38142.554479.AEv1
Participants 34 439 male British doctors. Information about their smoking habits was obtained in 1951, and periodically thereafter; cause specific mortality was monitored for 50 years.
Main outcome measures Overall mortality by smoking habit, considering separately men born in different periods.
Results The excess mortality associated with smoking chiefly involved vascular, neoplastic, and respiratory diseases that can be caused by smoking. Men born in 1900-1930 who smoked only cigarettes and continued smoking died on average about 10 years younger than lifelong non-smokers. Cessation at age 60, 50, 40, or 30 years gained, respectively, about 3, 6, 9, or 10 years of life expectancy. The excess mortality associated with cigarette smoking was less for men born in the 19th century and was greatest for men born in the 1920s. The cigarette smoker versus non-smoker probabilities of dying in middle age (35-69) were 42% v 24% (a twofold death rate ratio) for those born in 1900-1909, but were 43% v 15% (a threefold death rate ratio) for those born in the 1920s. At older ages, the cigarette smoker versus non-smoker probabilities of surviving from age 70 to 90 were 10% v 12% at the death rates of the 1950s (that is, among men born around the 1870s) but were 7% v 33% (again a threefold death rate ratio) at the death rates of the 1990s (that is, among men born around the 1910s).
Conclusion A substantial progressive decrease in the mortality rates among non-smokers over the past half-century (due to prevention and improved treatment of disease) has been wholly outweighed, among cigarette smokers, by a progressive increase in the smoker v non-smoker death rate ratio due to earlier and more intensive use of cigarettes. Among the men born around 1920, prolonged cigarette smoking from early adult life tripled age specific mortality rates, but cessation at age 50 halved the hazard, and cessation at age 30 avoided almost all of it.
James Repace’s political assessment of ETS harm
http://www.acosh.org/art/critical_evaluation.pdf
the combined lung cancer and heart disease mortality risk for office workers in a typical
smoking-permitted office as: ETSHI = 225 deaths per million exposed workers per year.
Assuming a 45-year working lifetime, this risk corresponds to a working lifetime risk of
(45)(225 deaths/million) = 10 deaths per 1000 persons at risk. Repace (2005) estimated
that the predicted respirable smoke particulate (RSP) concentration during work hours
corresponding to this risk is 211 Mg/m3. In fact, Repace (2004) measured an RSP
concentration of 205 Mg/m3 in the Delaware Park Casino in the U.S., with a
corresponding carcinogenic particulate polycyclic aromatic hydrocarbon (PPAH)
concentration of 163 nanograms per cubic meter (ng/m3) before a Statewide smoking
ban, and corresponding RSP and PPAH concentrations
**after the smoking ban of 9Mg/m3 and 4 ng/m3 respectively.
*Note
In a non-smoking environment, the measured levels of air would be 250 times the known safe level according to the USEPA.
Perhaps hurricane force winds in all enclosed public spaces could be the only solution short of massive evacuations.
at 80 Mg/m3, the risk would be (80/211)(10 per 1000) =
~ 4 per 1000 (rounded). Thus the estimated range in risk is between 4 and 15 per 1000,
with the most likely value, based on measured data in Table 1 above, about 10 combined
deaths from heart disease and lung cancer per 1000 workers per working lifetime of 45
years. This risk range is (10 per 1000)/(1 per 1,000,000) = 10,000 times the de minimis
or “acceptable” risk level. Therefore I find the LS proposal to be without merit
Compare the one in a million acceptable level of risk Repace references, a risk of; TCDD Dioxin or Radiation
http://www.gascape.org/index%20/Health%20effects%20of%20Dioxins.html
In limit has remained at 0.006-pg/kg bw/day until the present. It was based on the assumption that dioxin caused cancer in the same way as radioactivity: i.e. just one molecule on the DNA could have an effect, leaving no safe level, only a level which can be predicted to cause a certain risk of cancer. The US EPA has a standard risk, deemed tolerable, of one in a million over a 70 year lifetime, and this was used to set the limit. Since most people take in far more than 0.006 pg/kg bw/day, enforcement of this limit would have huge implications for the industries producing dioxins. So, scientists have been employed to produce arguments against the EPA. A committee re-examined the Kociba slides and reclassified some of the tumours as benign. Millions of dollars were poured into investigations into the mechanism of dioxin. These have increased our knowledge but they have not established definitely whether or not dioxin causes severe health problems in human beings.the USA, a very low minimum risk intake was set for 2,3,7,8-TCDD, on the basis of cancer incidence in a large experiment on rats (Kociba, 1978).
Are TCDD results reflective of confounding, or simply increased accumulation from alternate sources?
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1247514
The IARC classification of TCDD as a group 1 carcinogen (IARC 1997) has stirred some controversy. For example, Cole et al. (2003) argue that the original IARC classification of epidemiologic evidence for TCDD as “limited” (IARC 1997) was incorrect, claiming that “inadequate” would have been more appropriate (i.e., a causal interpretation was not “credible”). However, these authors ignored the original IARC focus on high-exposure subcohorts, ignored the positive exposure–response analyses, and raised the issue of possible confounding by smoking and other chemical carcinogens without any serious consideration of whether such possible confounding is likely, or whether it could account for the observed elevation of all-cancer mortality in those with higher TCDD exposure.
With normal levels beyond the levels of maximum harm risk, can ETS or other minor sources of Dioxins be seriously considered potential hazards in an environment where major Dioxin hazards cannot be avoided?
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1247514#b19-ehp0112-001265
In our view, the epidemiologic and toxicologic evidence since the IARC (1997) classification of TCDD as a human carcinogen has strengthened the case for IARC’s decision. Furthermore, the dose–response assessments for TCDD and cancer indicate that TCDD exposure levels close to those in the general population may be carcinogenic and argue for caution in setting the upper ranges of long-term permissible exposure to dioxins.
Real physical testing for Dioxins in primary smoking.
http://www.mindfully.org/Pesticide/Dioxins-Cigarette-Smoke.htm
Dioxins in cigarettes, smoke, and ash were determined using gas chromatography/mass spectrometry. The total concentration of polychlorinated dibenzo-p-dioxins (PCDDs) in cigarette smoke was approximately 5.0 µ/m3 at the maximum level, whereas various cogeners from tetra-octa-chlorodibenzo-p-dioxin (-CDD) were detected. Particularly, the total concentration of hepta-CDD cogeners was the highest among these cogeners. Mass fragmentograms of various PCDD cogeners were similar to those in flue gas samples collected from a municipal waste incinerator. The PCDD cogeners that were not present in the cigarettes were found in the smoke samples. The 2, 3, 7, 8-TCDD toxic equivalent value---an index for effects on humans—for total PCDDs in smoke was 1.81 nng/m3 using the toxic factor of the United States Environmental Protection Agency. Daily intake of PCDDs by smoking 20 cigarettes was estimated to be approximately 4.3 pg. kg body/weight/day. This value was close to that of the ADIs: 1-5 pg. kg body/weight/day reported in several countries. A heretofore-unrecognized health risk was represented by the presence of PCDDs in cigarette smoke.
Actual measured levels in Cigarette smoke; Dioxins were found in the smoke although not in the cigarettes. Dioxins are produced by mixing Chlorine with organic materials and burning at low temperatures. This would indicate Dioxins are a significant harm in smoking. The 8.7-year half-life of Dioxins corresponds to the risk elevations with use, and identical timeframe predictable reductions in risk after cessation, of both products.
The Dioxin risk is not necessary as no Dioxins would be present if chlorine additives were prohibited.
Every smoking related disease is also significantly related to Dioxin poisoning.
Governments have somehow assessed the added mortality is an acceptable risk factor in allowing the Dioxin poisonings to continue. Quite hypocritical in relation to ETS being described, as no safe level exists citing 47,000 preventable deaths yet none of the 47,000 preventable deaths will be prevented with smoking bans. Primary smoke consumed in thousands of times higher concentrations is ignored. Convenient political positions allowing punishments and taxing of consumers and designed ignorance in respect to a harmful product, preventable deaths and deliberate failures in regulating product safety. This gives a new meaning to the term right honorable in respect to politicians and sheds a new light on the institutions who advise them and dole out the awards.
British Columbia Provincial Ministry of Health ”Radon is a naturally occurring, radioactive gas, which is given off by traces of uranium in soil and rock. It is found at varying levels all over the world…. The Ministry of Health estimates that about 100 people a year die of radon induced lung cancer in the Province of British Columbia. Radon likely causes more lung cancers than second hand tobacco smoke.”
ETS lung Cancer risk is shown here to be below 100 in BC total population at levels averaging 163 NG/M3 air PPAH or 205 MG/m3 air RSP. 2/3 of Lung cancer patients are stated to be smokers. The risk is understandably much higher among smokers.
The smoke produced by the product can be banned for health reasons, yet the product is protected and remains on the shelf.
Calculations
Repace calculations are purely political and have absolutely no merit as demonstrated herein. Repace is either deliberately deceptive in his presentations or completely ignorant in assessing a multitude of proven information. The volumes of Dioxin like content in tobacco smoke is not sustainable in comparison to actual amounts found in real scientific testing nothing short of 100,000 chain smokers in an unventilated smoking area could produce the levels he contends.
The proportions of PPAH assumed to be equal or more dangerous than dioxins risk can be calculated by ratio et al Repace submissions
[Brook v. Burswood Casino (1999); Badillo v. American Tobacco et al. (1998); Avallone v. American Tobacco et al. (1998); Mullen et al. v. Treasure Chest (1999); Dunn v. Napoleon’s Casino (2003)]
The existence of 163 Nanograms per cubic meter of air would exceed the known safe level in air water and food by 10,000 times this would establish the known safe level at or below 16.3 Pico grams per cubic meter of air. 1/10 the safe level of Dioxins established as safe et al The WTC monitoring. 160NG/M3 air quality was allowed flexibility in acceptable air standards as exposures would be as stated be one year in duration. Dioxin risk drops with cessation of exposure. We can therefore equate the risk of PPAH to the risk of Dioxins as shown to be Repaces intent. The Parroting of his assessments at the WHO and many Health departments around the planet confirms the consensus view is in total agreement with his submissions. No safe level exists and Designated smoking rooms can afford no protection. The existence of 4 NG/M3 of air as found in non-smoking environments should indicate a need to evacuate those buildings until a safe level can be established.
An average of RSP 205 MG/M3 contains PPAH 163 NG/M3 By calculation .08%
A single package of 25 cigarettes each producing 100 Mg RSP can produce 2500 MG total RSPs This would indicate by .08% calculation each package produces 2500 x .0008 = 2 milligrams PPAH with a risk to human health greater or equal to Dioxin with a known safe level not exceeding .16 NG/M3 determined from monitoring of the World Trade Center monitoring program in New York. The level of acceptable risk inhaling smoke produced by a single package of cigarettes; in PPAH, exposure is shown to be exceeded by 123 million times 2x 10-3 vs. .0163 x 10-12
Conclusions Assuming a smoker inhales 1/3 to 1/2 of total 2 Milligrams Dioxin like toxins produced this would establish an extreme health risk exists in the use of this product, which should prove fatal for all users. Regardless of the fact this has not been seen to be the case the established risk of second hand smoke, as the basis for smoking bans should remain consistent where a much larger harm is seen to exist Neil Coleslaw in his book exhibits a willingness to participate in efforts to in effect kill more smokers as the Industry is nationalized while destroying the industry from within. This of course would allow a new opportunity in new startup companies and illegal black market trade, which will grow market share as the national brands decline. Others in Anti ETS advocacy claim there is no proof Canadian Tobacco is any safer than other tobacco. We always had good reason to believe the control of additives Flue curing and regulated growing conditions would result in a safer product. Michael Hurley publicly stated recently there is absolutely no evidence to prove Canadian tobacco is any safer than products produced elsewhere. Good science is dismissed as are smokeless tobacco products known to reduce respiratory health risks enormously. Nicotine delivery products much more expensive in smoking patches are allowed advertising are promoted by government ministries despite potentially harmful side effects making them not an option for many. The product is protected and the victims are attacked decided by consensus view as best practices, pleasing all stakeholders, in, for all intents and purposes; a gold rush mentality constructing a huge health regime. Cigarettes should be immediately banned from use until such time as harmful ingredients can be removed in the interest of public safety. Monetary concerns have to remain secondary when public safety and the imminent deaths of millions of Canadian citizens hang in the balance. To err on the side of safety should be the dominant principle in a caring and just society. Not just a term recited when convenient for highroad positioning.
As we already know from multiple research findings of DSR technologies and if those findings are valid, it is indisputable “no safe level exists”. If in fact, dioxin is the predominant risk, as research would indicate. The banning of chlorine in cigarettes is a minimal action which could reduce the risk and eliminate virtually all substantial risk in second hand smoke {ETS} this of course would lower greatly the perceived necessity to impose smoking bans or smoking restrictions when scientific product safety evaluations could allay all fears in the public. This strategy of course would necessitate a re-evaluation of healthcare costs and smoker’s ultimate liability for those costs. Government; which through failure to remain consistent with environmental process and other lapses in good judgment, would have to shoulder a great deal of the blame and misdirected expense liability. Tobacco taxes collected should be returned to those who paid them unnecessarily in contravention of the Canada health act as special fees for health care.
Tobacco companies although largely responsible for distributing an unsafe product, did act to within a tightly monitored regulatory environment and were not directed to change operational standards in the absence of restrictions of the ingredients of their products. The Government and stakeholders in anti environmental tobacco smoke advocacy by ignoring the larger harm which is shown here to exist, are potential defendants in future class actions or as individual actions seeking damages will no doubt show; The presentations have consistently stated ETS is potentially more dangerous than primary smoke this is totally without merit. They knew of a higher risk to smokers yet took no action in the public interest to regulate ingredients or to remove the products from the shelf as has been the case in other products seen to be much less dangerous. Public trust in the largest charity and government organizations were deliberately franchised in false and misleading promotions decrying smoking directly as safer than the smoke produced. Prohibiting the sale and distribution of smokeless tobacco products has compounded the problem, this would give a false sense of security to the users believing anti side stream smoke campaigns to be purely political in nature benefiting those who do not like the smell. Convenient lack of knowledge of the stakeholders would be little defense considering the impact of those decisions. Perhaps in an effort to maintain credibility and expenditures of public money in exchange for best value a more balanced approach in assessing the validity of industry lobbies and media spin should be considered prior to future international embarrassments and poor managerial decisions. If excess funds are available within the charity organizations to finance the huge media promotions we have seen in Canada perhaps it is time to scrutinize those organizations and direct where goodwill donations actually go in organizations accepting funds stating funds will be used to find cures. If an organization promotes political mood it should be law they advertise purpose before accepting funds obviously intended to go elsewhere.
All participating stakeholders have deliberately been deceptive in descriptions of tobacco smoke and mortality outcomes. The proof can be found at Health Canada in Sammec research, which demonstrates a timeline dose response relationship not corresponding to smoking habits 20-30 years previously nearly as predominant as the exposures to environmental dioxins. The smoking patterns in 1976 were reduced significantly while dioxin levels were on the rise corresponding with the increases of mortality more obviously mirroring dioxin poisoning. The increases of many other related diseases more significantly attributed to dioxins have been increasing as smoking decreases. The existence of trace amounts of dioxins in cigarettes is ignored when assessing smokers exposed; painting a picture smoking has a more significant unrelated danger than dioxins although significant associations are evident consistently.
By reducing dioxin potentials in cigarettes we cannot help but reduce mortality in smoking, apparently not much interest is seen in reducing potential harm, more so collection of taxes and protecting industry positions is more predominant in stakeholders concerns. 47,000 preventable deaths are largely being ignored for self-important motivating factors in absence of civic responsibility, which could limit the mortality figures significantly with simplistic regulation removing chlorine and chlorine derivatives from tobacco products. Additionally Import regulations need to be significantly adjusted to conform to domestic growing and curing guidelines. Allowing the advertising and sale of smokeless tobacco products will significantly reduce disease and mortality of respiratory tract risks. If 47,000 preventable deaths are to be reduced, the focus should shift to the product and away from punishing the consumers.
Here is another laughable time waster, see if you can spot just the first 50 flaws in the long list of spin-doctored foolishness.
This one was cited around the planet if you can believe it. Right up there with global warming hype, claiming Polar Bears are dropping like flies from hypothermia no less.
http://www.acosh.org/art/critical_evaluation.pdf
