Martin screams healthcare
His highness King Dithers and company have new Health care gospel for the adoring crowds
Research
“The right to health relevant information derives from the principles of autonomy and self direction and has been recognised in international declarations. Providing accurate health information is part of the basis for obtaining "informed consent" and is a recognised component of business ethics, safety communications, and case and product liability law. Remarkably, anti-tobacco and pro-tobacco sources alike have come to emphasise the message that there is "no safe cigarette" or "no safe tobacco product". We propose that the "no safe" message is so limited in its value that it represents a violation of the right to health relevant information. There is a need to go beyond saying, "there is no safe tobacco product" to indicate information on degree of risks. The "no safe tobacco" message does not contradict, for example, the mistaken belief that so called light or low tar cigarettes are safer choices than higher tar cigarettes. We encourage a kind of "rule utilitarian" ethical position in which the principle of truth telling is observed while trying to produce the greatest good for the greatest number of people. Although harm reduction approaches to easing the burden of tobacco related diseases are founded on science based comparative risk information, the right to health information is independently related to the need to promote health literacy. This right should be respected whether or not harm reduction policies are judged advisable.”
Proof of an unwillingness to act
This email exchange with representatives of the Canadian government attempts to make the government aware of a public health issue affecting 6 million smokers as reported,
“Thousands of people could die unnecessarily as a result.”
. Here is absolute proof they do not give a dam and the blinders are firmly in place.
The exchange reads bottom up quite shocking.
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Replies
Hello Kevin,
Call the number I suggested and they can advise you this is not under
Product Safety.
Thankyou Sue.
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2006-02-10 01:20 PM
Please respond to
To: Tor Prodsafe
cc:
Subject: Re: WWW Form Submission
Hello Sue;
I appreciate your quick response. The issues at the link I provided go
well beyond the capabilities of a Tobacco control advisory. The issues are
more properly issues of the federal Health and Environment Ministries. The
assessments made suggest nothing is being done regarding Dioxins in
Cigarettes and the environment, thousands of people could die
unnecessarily as a result.
Is the Government even aware of the Dioxin levels in cigarettes and how
easily they could be removed?
Regards; Kevin
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Hello Kevin,
For your inquiry you can call the Tobacco Branch at 416-954-9825.
Thankyou Sue
(Kevin Deleted)
2006-02-06 12:49 PM
To: Tor_Prodsafe@hc-sc.gc.ca
cc:
Subject: WWW Form Submission
Below is the result of your feedback form. It was submitted by
Kevin on Monday, February 06, 2006 at 12:49:12
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realname:
message:
I am trying to understand how the Government is positioned in the idea
Dioxins in smoking are actually the primary cause of most cancers
although not well reported in the popular media. I would like someone
to interpret the following research I found at a smokers rights
website.
Could you let me know if this is valid, and if so is the Government
planning to do something to stop it? If Dioxins are so dangerous it
does make sense they do not belong in Tobacco products.
Best Regards; Kevin
http://www.smokersclubinc.com/modules.php?name=News&file=article&sid=2732
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You say Tomato…This is Funny at ASH ASS expense
Lets get the language straight
“A typical cigarette is no more tobacco than a newspaper is a Pine Tree, though the newsprint may come from tree pulp. Most cigarettes are made from "reconstituted tobacco", a paper-like material concocted from tobacco waste---roots, stems, twigs, leaf veins, dust and sweepings. This "tobacco" may be made from (colored, flavored, scented, texturized and nicotine-doctored) recycled paper, timber products waste, paper manufacturing waste, food processing waste, agricultural waste, coffee bean hulls, peanut shells, and puffed oats, barley, millet, wheat, rice, milo and, for movie audiences, popped corn. To call this tobacco is either an error or a lie”
Smoking related diseases? ETS? Do cigarettes emit Diesel fuel exhaust?
Over 30 human epidemiological studies have investigated the potential carcinogenicity of
diesel exhaust. These studies, on average, found that long-term occupational exposures to
diesel exhaust were associated with a 40 percent increase in the relative risk of lung cancer.
The lung cancer findings are consistent and the association is unlikely to be due to chance.
These epidemiological studies strongly suggest a causal relationship between occupational
diesel exhaust exposure and lung cancer.
Diesel exhaust Dioxins are extremely high
“The average emission factor obtained from this work was 0.029 nanograms (ng) international toxic equivalency (I-TEQ)/km. The upper limit of the 95% confidence interval provides an estimated emission factor of 0.106 ng I-TEQ/km. Based on these values and 1993 diesel truck travel estimates, the projected U.S. annual emissions from on-road diesel vehicles are 4.4 g I-TEQ/yr with a 95% confidence upper bound of 16.1 g I-TEQ/yr.”
exposure to chlorine in indoor pools might increase the risk of childhood asthma
“the researchers looked at data from a survey of 1,881 children (ages 7–14) that was conducted from 1996 to 1999. The survey included questions about the children’s health status, respiratory symptoms, and lifestyle variables, including exposure to pets, environmental tobacco smoke (ETS, or second-hand smoke), and pool attendance. The children were also screened for asthma. From this data, the researchers found that pool attendance was the only variable that was significantly correlated with screening positive for asthma.”
Multicenter case-control study of exposure to environmental tobacco smoke and lung cancer in Europe
RESULTS: ETS exposure during childhood was not associated with an increased risk of lung cancer (odds ratio [OR] for ever exposure = 0.78; 95% confidence interval [CI] = 0.64- 0.96). The OR for ever exposure to spousal ETS was 1.16 (95% CI = 0.93- 1.44). No clear dose-response relationship could be demonstrated for cumulative spousal ETS exposure. The OR for ever exposure to workplace ETS was 1.17 (95% CI = 0.94-1.45), with possible evidence of increasing risk for increasing duration of exposure. No increase in risk was detected in subjects whose exposure to spousal or workplace ETS ended more than 15 years earlier. Ever exposure to ETS from other sources was not associated with lung cancer risk. Risks from combined exposure to spousal and workplace ETS were higher for squamous cell carcinoma and small-cell carcinoma than for adenocarcinoma, but the differences were not statistically significant. CONCLUSIONS: Our results indicate no association between childhood exposure to ETS and lung cancer risk. We did find weak evidence of a dose-response relationship between risk of lung cancer and exposure to spousal and workplace ETS. There was no detectable risk after cessation of exposure.
Compare to actual Dioxin exposures.
Health Evaluation of Airborne Pollution from the World Trade Center Disaster
World Trade Center (WTC) Disaster
| |
The World Trade Center (WTC) disaster sparked enormous concern about the quality of the environment in the surrounding neighborhoods. One of the immediate concerns was the effect of dust from the collapse of the towers on breathing, especially in rescue workers and more susceptible individuals. Fine particulate matter (PM) associated with dust from the crushed building materials may have unusual chemical properties and health effects. These reports describe results of experiments conducted by the Environmental Protection Agency which evaluated the chemistry and respiratory toxicity of fine PM from WTC dust and contributed to the short-term health risk assessment of WTC PM.
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.
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”.
“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.”
Medical Debate; Non Linear vs. Linear
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.
The World Health Organization and others strongly support a non-linear dose-response relationship for TCDD and cancer, whereas USEPA characterizes the dose-response function as linear. This review critically summarizes the available information on TCDD dose-response relationship for cancer utilizing a weight-of-evidence approach. This assessment concludes that the available data support a non-linear dose-response relationship as being most likely and appropriate for human cancer risk assessment, i.e., the evidence suggests that a biological threshold exists in the dose-response. While proof of a threshold is not absolute, and never can be, the level of certainty for TCDD is substantial because of the concordance of many lines of evidence and the consistency of repeated observations pointing to non-linearity.
statistically significant positive linear trends in SMRs with increasing exposure for all cancers combined and for lung cancer. 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.
Effects of Primary smoking 50 year study of doctors who smoke, spanning over 100 years
It is without question the product appeared to become much more dangerous over time
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 Lobby assessment of ETS harm
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 smoke free environment, the measured level citing the Repace quoted reports substantiating his theories, is 250 times beyond the acceptable level of risk as he states according to the USEPA Perhaps as he recommends utilizing Hurricane force winds is the only solution short of evacuating all enclosed public spaces.
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
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?
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?
Dioxin Revisited: Developments Since the 1997 IARC Classification of Dioxin as a Human Carcinogen
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.
Mortality and cancer incidence among employees exposed to 2,3,7,8-TCDD
evaluation of carcinogenicity.The rating system
Swimming pool off gasses more significant linked to Asthma than ETS
the researchers looked at data from a survey of 1,881 children (ages 7–14) that was conducted from 1996 to 1999. The survey included questions about the children’s health status, respiratory symptoms, and lifestyle variables, including exposure to pets, environmental tobacco smoke (ETS, or second-hand smoke), and pool attendance. The children were also screened for asthma. From this data, the researchers found that pool attendance was the only variable that was significantly correlated with screening positive for asthma.
In outdoor air Dioxin levels are beyond dangerous levels as a bioaccumulation hazard we cannot avoid
NATIONAL DIOXIN AIR MONITORING NETWORK (NDAMN)
the long-range and transboundary transport of dioxin-like compounds in air over the United States.
Figure 1 shows the locations of NDAMN sites. Previously EPA has reported on the
preliminary results of monitoring at 9 rural locations from June1998 through December
1991, and calendar year 2002. The year 1999 measurement at the 9 rural stations indicated
an annual mean TEQDF–WHO98 air concentration of about 11.3 fg m-3. In the year 2000, the
mean of 18 rural stations and 8 remote areas were 14.6 fg m-3 and 2.0 fg m-3, respectively.
The truth cigarettes cause cancer but they never had to
Link to Borg central, George Bush Senior an active participant
Tobacco settlements; more punishment for the victims
EPA post Sept 11 Dioxin monitoring stations
Carcinogenicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin
Multicenter case-control study of exposure to environmental tobacco smoke and lung cancer in Europe
Radioactive Polonium in Tobacco
Agent Orange and Cancer: An Overview for Clinicians
Uncertainty in Estimating Exposure
Dioxin Concentrations in women with endometriosis
Overarching (Exaggeration) Concerns
IARC Monographs on the Evaluation of Carcinogenic Risks
Lifetime probability of developing [41.2] and dying [27.4] from cancer
Carcinogenicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin
Dioixins; Uncertainty in Estimating Exposure Using a Toxicokinetic Model
Dioxin concentrations in women with endometriosis
Canada; The Federal Infrastructure for Understanding Risks
IARC Monographs Understanding Risk
Repace Associates Inc., Secondhand Smoke Consultants evaluation of risk in DSRs
Lifetime probability of developing and dying from cancer
If smoking death is preventable, why is no one interested in preventing it?
Conventional wisdom revisits past mistakes
Is James Repace a stooge for big Tobacco?
Just one credible journalist could change the plan
Yes, I saved the best for last
Environmental Dioxin reductions in North America began in 1986, with 8.7-year half-life, reductions in disease should be predicted to occur in 2003. No major decrease in smoking occurred in 1983 to reflect the assumed 20-year dose response. With 2/3 reduction in smoking since 1960 smoking related diseases continued to climb as reductions in smoking occurred no significant reductions in Cancers or smoking related diseases was seen, yet we read today.
Right on target Cancers decline, no smoking bans required
“ATLANTA (AP) - For the first time in more than 70 years, annual cancer deaths in the United States have fallen, a turning point in the war on cancer likely achieved by declines in smoking and better tumour detection and treatment.
The number of cancer deaths dropped to 556,902 in 2003, down from 557,271 the year before, according to a recently completed review of U.S. death certificates by the National Center for Health Statistics. “
"Even though it's a small amount, it's an important milestone," said Dr. Michael Thun, who directs epidemiological research for the American Cancer Society.
It's the first annual decrease in total cancer deaths since 1930, according to a cancer society analysis of federal death data.
For more than a decade, health statisticians have charted annual drops of about one per cent in the cancer death rate - the calculated number of deaths per 100,000 people. But the actual number of cancer deaths still rose each year because the growth in total population outpaced the falling death rates.
"Finally, the declining rates have surpassed the increasing size of the population," said Rebecca Siegel, a Cancer Society epidemiologist.
In Canada, there has also been a downward trend in mortality rates from cancer in recent years, said Kerstin Ring, a spokeswoman for the Canadian Cancer Society. Incidence rates have been relatively stable since about the mid-1990s, she added. In 2005, there were an estimated 69,500 cancer deaths in Canada.
In the U.S., experts are attributing the success to declines in smoking and the earlier detection and more effective treatment of tumours. Death rates have fallen for lung, breast, prostate and colorectal cancer, according to American Cancer Society officials, who analyzed the federal death data.
"This number shows that, perhaps, a corner has been turned," Caplan said.
Also from the Canadian Cancer Society???
Cancer is on the rise despite the consistent declines
Canada is facing a cancer crisis and we need your help to stop it
Sign our petition urging the federal government to implement the solution to the cancer crisis – the Canadian Strategy for Cancer Control.
Why do we need a national strategy to fight cancer?
Unless action is taken now, Canada will be facing a cancer crisis in a few years. With the aging of the baby boomers and the overall increase in population, cancer will become the single greatest cause of death by 2010. It is already the leading cause of premature death.
In 2005, it is estimated that:
149,000 Canadians will be diagnosed with cancer – 3,500 more than last year
69,500 Canadians will die from cancer – 1,200 more than last year
And these numbers will continue to increase unless the federal government does something about it.
In addition to the significant personal toll, cancer will also have devastating effects on the economic health of our country.
The Heart research information disagrees.
“There are few outward symptoms of atherosclerosis, or cardiovascular disease,
Which is the leading cause of death in the developed world.”
The downward trend continues credibility wise.
Incredible new revelation could destroy smoking ban mentality
The real problem we should be concerned with
posted by FXR @ 11:14 PM
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