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davidmalmolevine

More radioactivity debate!

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Dear Patrick,

Thank you for your respectful and thoughtful letter.

"I was struck by a statement you made in CC 46, The Radioactivity Debate, in your reply to Noucetta Kehdi. You stated that "researchers have induced cancer in animal test subjects that inhaled polonium 210 but were unable to cause cancer through the inhalation of any of the non-radioactive chemical carcinogens found in tobacco . . ."

If this statement has been proven to be incorrect, a simple citation of the more recent study or studies that disprove it would help to correct the record. As far as I know, nobody has offered any specific study to disprove this. If you have such a study, please let me know.

"Presumably you are referring to the Yuille et al article in your original column? If so, you are making an exceedingly weak argument. First, that article is now 37 years old, and literally thousands of research papers of the chemical composition of tobacco smoke and tobacco-related carcinogenesis have appeared since then. Second, few of the chemical carcinogens in tobacco smoke had even been *identified* in 1967, much less adequately tested using animal models,"

What is true in animal models may not be true for humans. I only mentioned the "Yuille" study because it differentiated between skin and airborn tests, and that it backed-up what humans have been experiencing in terms of radioactive tobacco cancer - there were few tobacco-related lung cancers before the mass use of chemical ferts, and there seems to be a temporal connection between the increase in chem ferts and an increase in tobacco and lung cancer.

".... either orally or via inhalation. Cannabis enthusiasts rightly fault prohitionists when they seletively cite outdated or subsequently refuted research, yet this example is just as misleading."

Again, if you have studies that directly refute that, please post them to me.

"Third, contrary to what you argue, it is just plain false that none of the chemical carcinogens in tobacco smoke have been shown to be inhalational carcinogens in animal studies (most of the carcinogens in tobacco smoke are created by combustion). To take one example, the PAH (polycyclic aromatic hydrocarbon) benzo[a]pyrene, which is a chemical carcingon present in both tobacco and cannabis smoke, caused respiratory tract cancers in 35% of Syrian Golden Hamsters in long-term exposure studies (using doses far higher than that present in tobacco/cannabis smoke, as is normally the case with such rodent toxicological studies) (e.g. Pauluhn et al, 1985; Thyssen et al, 1981)."

Is this a study that took into account both radiation and "airborne" application? Is this study on-line or in a place where I could easily access it?

"What's more, benzo[a]pyrene has been shown to preferentially cause so-called G>T DNA base-pair transversions in the tumour suppressor gene P53, which are very common in human tobacco-related lung tumors but much more rare in other cancers (Yoon et al, 2001; Pfeifer et al, 2002). Thus there is good evidence linking particular carcinogens in tobacco smoke to mutational profile often observed in tobacco-associated cancers."

How did they differentiate between cancern caused by the radioactivity and cancer caused by the benzo[a]pyrene? Were these tests airborn smoke?

"And of course, PAH's and many other tobacco-smoke carcinogens have been shown to be carcinogenic in animal models when they have been directly applied to respiratory tract tissue or administered orally or by intraperitoneal injection."

I always tell everyone not to apply cannabis tars to their lungs using sticks, pills or needles. At this point I must fall back on human experience. Why has the "benzo[a]pyrene" not caused a single case of human cannabis-related lung cancer in 6000 years of use?

"IMHO, there should be little doubt that chemical carcinogens, rather than Po from apatite, play the major role in tobacco-associated cancers."

Little doubt? Explain the lack of cancer in non-laboratory humans, then. Remeber, some people smoke the stuff like it was going out of style, but not one "marijuana-only" smoker has ever, ever, ever gone on to get lung cancer. I don't understand how you can have "little doubt" and take that glaring statistic into account at the same time.

You seem to forget that the government has spent millions of dollars trying to tell us that cannabis is inherently bad for us, and yet has failed to find a single case of marijuana-only cancer. It's not supprising they shout "benzo[a]pyrene" as much as possible because out of all the things tested on animals from cannabis, it hurts the most. But only (I believe) when it is applied in the most unnatural of doses in the most unnatural of ways. Please prove me wrong.

"By all means, though, I am interested in contrary evidence, and if you are aware of any good evidence associating Po in tobacco with tobacco-associated cancers, please email the references to me."

Well, have you read the other articles I have written on the subject? The info regarding fertilizer use is in both:

http://www.cannabisculture.com/articles/2673.html

http://www.cannabisculture.com/articles/2221.html

Here is a neat show I did on PTV about how to test for radioactivity in ferts:

http://www.pot-tv.net/archive/shows/pottvshowse-1153.html

As far as I know, that's all the material published on the issue. I am always collecting more information, so if you can help in that department, I would be very happy.

"The evidence hitherto presented in the two CC columns is not terribly convincing, to me. For instance, are there animal studies showing that inhalation of Po produces cancers at all the tobacco-associated cancer sites?"

There are human studies, which I find more interesting.

http://nepenthes.lycaeum.org/Drugs/THC/Health/cancer.rad.html

Levels of Po-210 were measured in cigarette smoke by Radford and Hunt (2) and in the bronchial epithelium of smokers and nonsmokers by Little et al. (3) After inhalation, ciliary action causes the insoluble radioactive particles to accumulate at the bifurcation of segmental bronchi, a common site of origin of bronchogenic carcinomas.

"Can these tumours be produced at Po doses analogous to those recieved by human tobacco smokers? Are the mutational profiles produced in these animal or in vitro models consistent with the mutational profiles observed in tumours of human smokers (e.g. overrepresentation of G>T transversions in P53)?"

Sorry, I'm a layman, you'll have to translate into common english for me.

"Is the carcinogenicity of tobacco tar correlated with its radioactivity?"

That seems reasonable. Does the following answer your question?

In a person smoking 1 1/2 packs of cigarettes per day, the radiation dose to the bronchial epithelium in areas of bifurcation is 8000 mrem per year -- the equivalent of the dose to the skin from 300 x-ray films of the chest per year. This figure is comparable to total-body exposure to natural background radiation containing 80 mrem per year in someone living in the Boston area.

http://nepenthes.lycaeum.org/Drugs/THC/Health/cancer.rad.html

Read the above links fully - especially the last one which was published in the 1980's in the NEJM - and you tell me.

"Is the carcinogenicity of tobacco tar impacted by type of fertilizer used to grow the tobacco?"

Another reasonable guess. We know the radioactivity is impacted by the type of fert:

http://www.cannabisculture.com/articles/2673.html

"It should be relatively easy to design experiments that would reveal whether and to what extent Po contributes to the carcinogenicity of tobacco smoke and tar."

Please do so, and I can steer other interested parties in that direction.

"In passing, I should point out that I don't believe that cannabis use is a significant risk factor for lung cancer, since it is typically consumed at far lower doses than is tobacco."

Due to the fact that there are exceptions to that rule who STILL don't get lung cancer, I prefer to believe that it is the dose of radiation, not the dose of tar, which is the most important factor.

"Nevertheless, it is perfectly clear that while cannabis itself, and particularly THC, are not carcinogenic (in fact, THC has an anti-tumor effect at very high doses), combustion of cannabis results in production of some of the same carcinogens found in tobacco smoke, including benzo[a]pyrene. Cannabis smoke is mutagenic in in vitro tests, and cannabis tar is carcinogenic in mouse skin test (in which cannabis tar is painted onto the skin). There are case-control epidemiological studies linking cannabis use to increased lung and head-and-neck cancer risk, but these are inconsistent."

Most people do not realize, nor are the media told, that a pre-cancerous lesion is any tissue abnormality; abrasion, eruption, or redness. Unlike the radioactive lesions caused by tobacco, the THC-related lesions contain no radioactivity.

We asked Tashkin how many people had gone on to get lung cancer in these studies -- or any other studies on long-term smokers like Rastas, Coptics, etc.?

Dr. Tashkin, sitting his UCLA laboratory, looked at me and said, "Well, that's the strange part. So far no one we've studied has gone on to get lung cancer."

"Was this reported to the press in the article?"

"Well, it's in the article," Dr. Tashkin said in passing, "but no one in the press even asked. They just assumed the worst."

http://www.art.net/~hopkins/Don/hemp/prohibition/no-clothes.html

"I don't doubt though that if cannabis smokers smoked as much cannabis as tobacco smokers smoked tobacco, that cannabis smoking would then by significantly associated with lung and other cancers.

Respectfully,

Patrick Spears

Refs

Pauluhn et al, 1985. Long-term inhalation study with benzo[a]pyrene and SO2 in Syrian golden hamsters. Exp. Pathol., 28,31.

Pfeifer et al, 2002. Tobacco smoke carcinogens, DNA damage and p53 mutations in smoking-associated cancers. Oncogene, 21, 7435â?"7451.

Thyssen et al, 1981. Inhalation studies with benzo[a]pyrene in Syrian golden hamsters. J. Natl. Cancer Inst., 66, 575.

Yoon et al, 2001. Methylated CpG Dinucleotides Are the Preferential Targets for G-to-T Transversion Mutations Induced by Benzo[a]pyrene Diol Epoxide in Mammalian Cells. Cancer Research 61, 7110-7117.

Yuille et al, 1967. Lung cancer following Pb210 inhalation in rats.Radiation Res 31:760-774."

I feel you are wrong. I smoke more cannabis than many tobacco smokers smoke tobacco, I know many other morning-noon&night puffers, I even know some dealers who have to do quality-control testing all day long.....none of us are in the Cancer ward. If we did get cancer, the #1 suspect would be the radioactive ferts, not the benzo[a]pyrene. That's what the above evidence tells me.

Respectfully,

David Malmo-Levine

www.potshotzine.com

www.cannabisculture.com

Always take time out to stop and smoke the flowers!

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Patrick,

Further regarding how "out-dated" my material was in our last conversation ...

I found in my research:

Surprisingly, the US National Cancer Institute, with an annual budget of $500 million, has no active grants for research on radiation as a cause of lung cancer.1

Winters, TH and Franza, JR. 'Radioactivity in Cigarette Smoke,' New England Journal of Medicine, 1982. 306(6): 364-365

http://nepenthes.lycaeum.org/Drugs/THC/Health/cancer.rad.html

It's not like the information was done once, refuted and never done again (as is often the case with cannabis research). This research was done repeatedly, verified, and then the funding was cut off.

It's also not true that any of this research was refuted, nor is it true than nothing has been done since the 1980's. Gus Kilthau (refered to in my work and below) was active in the late 1990's doing similar research, despite not being funded by the National Cancer Institute.

Basically, it's all just a coverup by the Chemical, Agricultural and Nuclear corporations, who all wish to avoid being held liable for polluting the earth and the lungs of smokers.

For another contemporary example of phosphate ferts being blamed for lung cancer in smokers, see the info below.

Sincerely (and curious to know what you think),

David Malmo-Levine

Does Tobacco Cause Cancer? Yes and no.

How is it that such a powerful spiritual healing substance has become public enemy number one in the ongoing war against cancer? Certainly, there is a massive body of scientific research that shows the carcinogenic potential of tobacco. People who smoke cigarettes, cigars, and pipes have, respectively, 68 percent, 22 percent and 12 percent higher mortality rates than non-smokers.

The conventional wisdom blames nicotine, but the culprit may be the way tobacco is processed for commercial production and the attitude with which it is used rather than the tobacco itself. From the Native American viewpoint, there are three reasons why smoking tobacco MAY be hazardous to health:

1. Overuse and addiction: People who smoke tobacco moderately, with prayer and attentiveness, do not become addicts.

2. Absence of sacred intent: When you use tobacco or any plant according to the Creator's plan, you recieve a blessing; when you ignore the creators plan, you recieve a curse. Not praying when using this most sacred herb is a sacrilege equivalent to stomping on a Bible. The payback may be cancer. And as I said earlier, praying with tobacco is a good way to become conscious of unconscious, habitual smoking, making it easier to stop.

3. Adulterated crops: Traditional Native Americans smoked only organic tobacco According to the Surgeon General's 1992 report Smoking and Health in the Americas, the smoke-attributable lung cancer mortality rates throughout Latin America are consistently lower than those in North America. Mexico has about one-fifth the rate of the United States. Central and South American Indians, traditionally heavy smokers, have a lower incidence of cancer.

Commercial tobacco, grow with pesticides and chemical fertilizers, is carcinogenic. Cigarette tobacco contains approximately one hundred carcinogenic compounds, including phenol, a poisonous, caustic acid that gradually destroys the brochial tissue, and benzopyrene, an irritant found in both coal and tobacco tars. Though clearly harmful, scientists consider these substances to be relatively weak carcinogens and not the major cause of smoking-related lung cancer. Tars, for example, probably account for 1 percent of smoke-attributable cancers. The chemical carcinogens in tobacco do not CAUSE cancer, they ENCOURAGE it, making it more likely to occur by weakening the lungs, damaging tissue, and making the cells more vulnerable to infection. Instead, it is the unusually high levels of radioactivity found in North American commercial tobacco that are the direct link between smoking and cancer.

The amount of background radiation exposure from ordinary air, food and water is small, about two hundred millirads per year, or five rads (five thousand millirads) in twenty five years. By modest estimates, an average cigarette smoker is exposed to a minimum of twenty rads per twenty-five years, four times the normal background radiation.

John B. Little, M.D., et al., "Distribution of Polonium in Pulmonary Tissues of Cigarette Smokers," New England Journal of Medicine 273 (December 16, 1965): 1350, and John B. Little and Edward P Radford Jr., "Polonium 210 in Bronchial Epithelium of Cigarette Smokers," Science 155 (February 3, 1967): 606.

- Radioactive Cigarettes -

For a comprehensive understanding of the biological dangers of tobacco radioactivity, we need to take into account the combined effect of various radioactive isotopes found in tobacco, the inefficient gaseous exchange in smokers' lungs (causing smoke particles to linger in the tissues), and radioactive "hot spots", such as the bifurcation of the bronchial tree, where the concentration of radioactive elements may be one thousand times greater than in the lungs. Considering all these factors, a person who smokes one and a half packs of cigarettes daily may recieve as much as 60 millirads of radiation each day, 21.9 rads per year, and 547.5 rads in twenty-five years: the equivalent of 547,000 chest x rays.

Marie Brady, R.T., "Radioactive Technologist Examines Radioactivity from Cigarette Smoke," an interview with Gustave F. Kilthau, M.R.T., Nurse Week/Health Week, June 1, 1996, p.2

Scientists have documented several reasons why tobacco produces dangerous levels of radioactivity:

- The chemical fertilizers used to grow tobacco contain calcium. Naturally occuring radium 226 is structurally similar to calcium and may fill its chemical bond, making these fertilizers radioactive.

- Because of wind direction in the United States, the East Coast, where most tobacco is grown, has high levels of airborne contaminants, including radioactive isotopes. For instance, radon gas produced across the continent blows east and is concentrated in the East Cost. Air and soil radioactivity levels have also increased because of fallout from nuclear testing during the 1950's and 1960's.

- Lead 210, a decay product or "daughter" of radium 226, has a strong tendency to attach to the tips of the fine hairs on tobacco leaves. As the tobacco leaves burn, lead 210 ladges in the lung tissue. Because lead 210 is not water-soluble, it does not wash quickly out of the smoker's body. as it decays, it exposes the body to carcinogenic alpha particles.

-During its half life of 21.5 years, lead 210 further decays into another toxic isotope, polonium 210.

Tobaccos grown in less contaminated environments and without high-phosphate fertilizers have a much lower polonium concentration. Tobaccos grown in India, for example, have less than 20 percent the polonium of American tobaccos. This may help explain why some tobaccos cause less cancer.

Polonium 210 becomes volatile and dangerous at temperatures above 500 degrees centigrade, well below the temperature of a burning cigarette. It bonds strongly and rapidly to smoke particles. Polonium 210 has a half-life of 138 days, ample time to shoot cancer-causing alpha radiation bullets at and into the bronchi and lungs. Researchers have confirmed that low doses of alpha radiation from polonium 210 can induce lung cancer in animals.

John B. Little, Ann R. Kennedy, and Robert B McGandy, "Lung Cancer Induced in Hamsters by Low Doses of Alpha Radiation from Polonium 210," Science 188 (May 16, 1975): 737-38. Also see the same authors "Effect of Dose Distribution on the Induction of Experimental Lung Cancer by Alpha Radiation," Health Physics 35 (November 1978): 595-606.

- Not suprisingly, the lung tissue, lymph nodes, and tumors of smokers contain unusual concentrations of the 210 radioisotopes.

The lung tissues of chain smokers are continuously bombarded with highly carcinogenic alpha radiation particles. These particles are the most likely direct cause of cancer in smokers, working in synergy with chemical carcinogens, viruses, genetic susceptibility, and emotional/spiritual factors.

Given the extreme toxicity of radiation, if the radioisotopes found in tobacco were delivering highly concentrated radiation doses to the lung cells, they would kill the cells rather than cause cancer. Instead, levels of radiation distributed throughout the lungs over an extended period of time is far more harmful than short-term, concentrated doses. In other words, contrary to what we might assume, radioactivity that is merely "warm" is sometimes more dangerous than that which is "hot".

Scientists who have conducted research confirming the radioactive componets of tobacco smoke include Dr. Edward P Radford Jr., former chairman of the prestigious Biological Effects of Ionizing Radiation Committee (Beir) of the National Academy of Sciences; Dr. Vilma R. Hunt of the Environmental Protection Agency; Dr. Edward Martell, a senior radiochemist with the National Center for Atmospheric Research; and Dr. John B. Little, chair of cancer cell biology at Harvard School of Public Health. Their evidence, presented in the New England Journal of Medicine, Science, American Scientist, and other publications, has never been refuted.

Scientists with whom I spoke at the National Academy of Sciences lamented that the important link among tobacco, radioactivity and cancer has been tragically "passed over". Some researchers suggested a cover-up that might be economically motivated. If the general public becomes aware of the risks of low-dose radiation, the safe radiation exposure threshold might have to be lowered. Smokers who have cancer would have concrete proof of the mechanism that causes cancer, further establishing the tobacco industry's culpability. In other words, both the nuclear and tobacco industies would be more clearly liable for the damage to American health.

Additional evidence can be found in:

Edward P. Radford Jr. and Vilma R. Hunt, "Polonium-210: A Volatile Radioelement in Cigarettes," Science 143 (Jan. 17, 1964): 247-49

Edward P. Radford Jr. and Vilma R. Hunt "Cigarettes and Polonium-210," Science 144 (April 24, 1964): 366-67

Edward P. Radford Jr. and Vilma R. Hunt and John B. Little, "Carcinogenicity of Tobacco-Smoke Constituents," Science 165 (July 18, 1969): 312

Edward A. Martell, "Tobacco Radioactivity and Cancer in Smokers", American Scientist 63 (July-August 1975): 404-12

Edward P. Radford and Edward A. Martell, "Polonium-210: Lead 210 Ratios as n Index of Residence Times of Insoluble Particles from Cigarette Smoke in Bronchial Epithelium," in Inhaled Particles, vol. 4, ed. W.H. Walton (Oxford, U.K.: Pergamon Press, 1977), 567-81.

Michael Castleman, "Are Cigarettes Radioactive?" Medical Self-Care 10 (fall 1980):20-23

Taken from: "Honoring the Medicine - the Essential Guide to Native American Healing", by Kennith Cohen, 2003, One World/Ballentine Books, NY, pp 276-279, 379

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Date: Thu, 11 Mar 2004 11:16:14 EST

From: <[email protected]>

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To: <[email protected]>

Subject: Re: Regarding the radioactive fertilizer thing

David,

"Interesting site. Who pays to put it up, and for all the things to be written on it?"

Why do you assume that anyone pays to put that site up? The site is hosted for free by Yahoo, and the articles are written by me purely out of personal interest. I also run a site on geology.

"Why is there so much respect for results from animal studies? ... aren't they completely useless to evaluate anthing other than researcher bias?"

No, absolutely not. Animal studies are enormousy useful in many ways, for instance where ethics or practical concerns make human experiments impossible (e.g. toxicity and carcinogenicity tests). And since physiologically most mammals are very similar, the results are far from 'useless.' Animal studies are enormously useful, for instance for testing the safety, efficacy and mechanism of action of drugs, for determining the causes and mechanisms underlying disease processes, and so on. For instance, a compound that reduces introcular pressure or inhibits emesis (vomiting) in rabbits or ferrets is likely to do so in humans as well, since the physiological structures that mediate these reponses are basically the same in all mammals.

Of course, as I point out repeatedly in my articles, you have to be careful about extrapolating from animal experiments to humans, since the experimental conditions often do not reflect the human environment. Besides, reading my articles you'll see that I do cite human data wherever it exists, experimental and epidemiological, so its not like I'm ignoring human data in favor of animal data. Rather I'm including all relevant data.

"No mention (that I could find in my first cursory overview) is made of the long term Costa Rican human studies (1982) which concluded that - if anything - cannabis had a benefitial effect on the lungs, perhaps acting as an expectorant."

Which study, specifically, are you referring to? PubMed searches for costa rica + 1982 do not turn up any studies of lung function in cannabis smoking costa ricans. I'll be happy to include it if you give me a reference. What measures of lung function/harm did they include in their study, and how large was the sample?

If you actually read what I wrote, you'll see that I cite data showing the cannabis smoking does not cause COPD (chronic obstructive pulmonary disease - emphysema), and argue that it is not a major risk factor for lung cancer, which are the major pulmonary harms associated with tobacco smoking. There is, on the other hand, plenty of evidence that cannabis smoking causes chronic coughing and wheezing, slightly increases risk of respiratory infections (based on a very large american sample), impairs alveolar macrophage activity in the lungs, and in rare cases can cause spontaneous pneumothorax (from holding the smoke too hard using what's called the valsalva's manoever, causing a breach of the lungs). And I do point out clearly that cannabis smokers have increased phlegm production, which is basically the same thing as saying that it is an expectorant. I also do clearly point out that THC is a bronchodilator.

"The problem with sub-lingual spray is that it takes minutes to work, when some of the problems that cannabis is used for (nausea, stroke, epilepsy etc) seconds can mean the difference between relief and extreme discomfort (or even life and death). Certain conditions require a more rapid delivery system."

You're telling me something I already know. And in any event, smoking is obviously not the only way to rapidly deliver a dose. An inhaler (if it were developed) would be as fast, and an intravenous injection would be much faster. In fact, if your patient is having a stroke or a siezure, smoking a bong is going to be a bit difficult compared to an inhaler or an iv injection. As for nausea, I think smoking is a good way to go, except of course for people (like my grandmother) who arent pot smokers and who don't particularly want to gag and cough if they dont have to.

"You neither come across as anti-tobacco or anti-cannabis, but the whole site has a "pro-sativex" flavor to it. Don't fall prey to smoke -a-phobia ... smoke is a preferred delivery system to most medical traditions on the planet. It's monopolistic and eurocentric and just plain innacurate that pills, sprays, tinctures, patches and suppositories are superior routes, when actually they all have a greater chance of overdose do to the lack of "titration" ability from the slower methods of injestion."

I won't fall prey to smoke-a-phobia if you don't fall prey to smoke-a-philia/nonsmoke-a-phobia. For many people, smoking clearly is NOT at all a preferred method of administration. Its just plain inaccurate to think that one method of delivery is the best for all people and all indications, or that the only reason to develop nonsmoke delivery is for intellectual property. That's nonsense. There are many people out there who can benefit from cannabinoids, but who do not want to smoke it. I have been close to two older medical users who clearly benefitted from cannabinoids (one for glaucoma and one for neck spasticity), but stopped because the smoking (even short puffs from a waterpipe with little or no breath-hold) made them cough and hack too much. Even if it were perfectly safe with no health risks, many people, including many very sick people, just dont want to smoke their cannabinoids. I see the development of these alternative delivery methods as entirely positive.

By the same token, opiates are some of the most useful tools in the human pharmacopea, but no one thinks that everyone should smoke opium rather than taking it some other way, and injections, pills (example - demoral), sprays (example -stadol), and patches (example - fentanyl) are a godsend for many people. My wish is to use cannabinoids to alleviate as much suffering as possible, and for many people who suffer, smoking is not at all the best option. What you say about dose titration is true, though there is no reason to think that a THC inhaler would be any harder to dose-titrate than a joint, since the time to plasma-THC-peak would be the same. I see the development of these alternative delivery methods as entirely positive.

"Many researchers argue that certain cannabinoids - THC among them - require heat to work properly"

"Many researchers"? Really? Now that's odd, David, because I've read dozens of papers on cannabinoid pharmacology, and can't recall a single researcher ever saying such a thing, much less many researchers. I have, however, seen old papers where humans were given i.v. doses of THC, very small doses too (1-5mg), and still reported being high, so obviousy THC was working. Could you tell me which researchers you have in mind?

"As well, the cigarette was first developed in the Crimean War, and continued to be promoted in the American civil war, so cancer rates should have shot up in the late 1800's, not in the 1930's as is reported."

What was the prevalence of cigarette smoking prior to 1900? How many people smoked these cigarettes daily, and on average how many per day did they smoke? Obviously, since you say that "cancer rates should have shot up in the late 1800's," you are implying not merely that cigarettes existed prior to 1900 (which no one disputes), but that they were being widely used and used at high rates during the 1800's, whereas the ALA statistics I just cited (and every other source I've read) indicate that cigarette smoking was fairly modest until the early 20th century, when rates of consumption shot up enormously. Further, I wonder how many people who died in the 1800's were autopsied to inspect for lung cancer? In other words, would it even have been possible to detect a modest increase in lung cancer incidence in the late 1800's if it did occur? Finally, you should keep in mind that lung cancer has a very long latency period, on average about 40 years. That is, when a group of people start smoking regularly, you don't see an immediate rise in lung cancer in that group, you see it about 40 years later (about 85% of lung cancers occur in people who have been smoking for 40 years or more).

"It is the introduction of chem ferts, not cigarettes, that goes hand in hand with the rise of cancer rates."

So, you say. However, the facts appear to disagree, as does every review I've read of the epidemiology of lung cancer. According to one of your own sources (Marmorstein, 1986- I went and got the paper), the use of artificial high-phosphate fertilizers did not become widespread until after 1940. Its very clear that the steep increase in lung cancer rates began before 1940. To quote from my article:

"Case reports and epidemiological studies based on data from the first half of the twentieth century and earlier make it clear that even before the widespread adoption of chemical fertilizers and synthetic pesticides, smoking tobacco was still a major risk factor for lung and other cancers. Probably the earliest reports of tobacco-associated cancers were written by english physician John Hill in 1761, who in his Cautions Against the Immoderate Use of Snuff described a case of nasal cancer in an individual with a long and immoderate history of snuff use. Other early observations that pipe smoking was associated with oral cancer were made in Germany by Sommering in 1795 and by Virchow in 1863. In 1836, Samuel Hill stated in the New England Almanac and Farmer's Friend that "thousands and tens of thousands die of diseases of the lungs generally brought on by tobacco smoking is a fact as well known in the whole history of disease."

In the eary twentieth century, within a decade of two of the widespread adoption of cigarette smoking, evidence linking tobacco smoking to lung cancers began to accumulate. According to Davey-Smith et al (1994), even by the late 1920's doctor Fritz Lickint in Germany had gathered evidence implicating tobacco smoking as "a major cause" of lung cancer. A letter to the editor of the Lancet (July 30, 1927) by Tylecote stated that "almost in every case (of cancer) I have seen and known of, the patient has been a regular smoker, generally of cigarettes.â? A 1928 study in the New England Journal of Medicine found that in a group of 35 cancer cases of the mouth and lungs, all but one case occurred in heavy smokers (Lombard and Doering, 1928). In 1936, Arkin and Wagner wrote an article for the Journal of the American Medical Association noted an increase in lung cancer and found that 90% of the cases they observed occurred in heavy smokers. Muller (1939), in what was probably the first controlled study of smoking and lung cancer, found that of 86 male lung cancer cases, 56 were heavy smokers, and only 3 were nonsmokers, and concluded that the "extraordinary rise in tobacco use" was "the single most important cause of the rising incidence of lung cancer."

Schairer and Schoniger (1943) conducted a case-control study that found that very heavy smokers were over 16 times more likely to develop lung cancer, and established a highly statistically significant dose-response. Wynder and Graham (1950) noted a significant increase in lung cancers from 1928 to 1945, and showed that the vast majority of lung cancer cases were occurring in heavy smokers and very few in nonsmokers. Doll and Hill (1950) noted an enormous increase in lung cancer deaths between 1922 and 1945 in England and Wales, and conducted an epidemiological study between 1948 and 1949 that showed that virtually all lung cancers occurred in smokers, and that the risk increased with increasing consumption. They estimated that the risk of lung cancer among those who smoked 25 or more cigarettes a day was a whopping 50 times greater than the risk in nonsmokers. Several case-control studies appearing around 1950 were some of the first large studies to quantify the risk (Doll and Hill, 1950, 1952; Wynder and Graham, 1950; Levin et al, 1950; Mills and Porter, 1950)."

Another way to look at artificial fertilizers being the cause of smoking-associated lung cancers is to look at cancer rates in countries where the tobacco is not grown with artificial fertilizers. Several of your sources (Marmorstein, 1986; Kilthau, 1980; Harley et 1980) cite India as one of the countries not using artifical fertz and having the lowest tobacco 210Po, so I looked for information on tobacco related cancers in India. Quoting again from my article:

"According to several sources, Indian tobacco has some of the lowest levels of 210Po in the world. For instance, figure 1 from Harley et al (1980) shows 210Po content of tobacco by country, and India is ranked as the lowest. Kilthau (1996), which is one of Malmo-Levine's sources, says that Indian tobacco is on average 5.75 times lower in polonium than U.S. tobacco (0.516 vrs 0.09 pCi/g). Yet studies tobacco-related illness in India, where the majority of smokers smoke additive-free bidis, show that bidi smokers have just as high if not higher risks of lung, oral, laryngeal, esophogeal, and stomach cancers, and have increased risk of coronary heart disease just as conventional cigarette smokers do (Notani et al, 1977; Jussawalla et al, 1979; Sankaranarayanan et al, 1989, 1990, 1991; Pais et al, 1996; Dikshit and Kanhere, 2000; Gajalakshmi and Shanta, 1996; Gupta et al, 1995, 2001; Rahman and Fukai, 2000). A recent large study showed that the smoking-related increase in respiratory, vascular, and neoplastic (cancer) mortality is the same in areas where bidis are smoked as it is in areas where conventional cigarettes are smoked (Gajalakshmi et al, 2003). Based on a case-control study, Jussawalla et al (1979) for instance reported an almost 20-fold increased risk of lung cancer (relative risk=19.3) for bidi smokers, while the risk associated with cigarette smoking in the same study was nearly as high. The relative risks of lung cancer from smoking in India, the country which putatively has the lowest average tobacco 210Po, are thus as high as those seen amongst the very heaviest smokers in the U.S. Interesting also is a report by Bogden et al (1981) that 210Po concentrations in tobacco from countries with high lung cancer incidence did not differ from the 210Po concentrations in tobacco from countries with low lung cancer incidence."

Also, here is my section on inhalational carcinogens in tobacco smoke. The example I gave before was benzo[a]pyrene, but subsequently I found that numerous chemical carcinogens in tobacco smoke have been tested in animal models by inhalation and found to produce lung and other cancers. From the article:

"For instance, inhalational exposure to benzo[a]pyrene (BaP), one of approximately 15 polycyclic aromatic hydrocarbons in tobacco smoke, has produced respiratory tract and upper digestive tract tumors in hamsters, guinea pigs, and rats, according to the EPA IRIS entry for that substance. There is also an elevated incidence of lung cancer in humans occupationally exposed to high levels of BaP from roofing tar and coke oven emmisions, though it can not be said with certainty that BaP accounts for this increase incidence. 1,3-butadiene is a chemical carcinogen in tobacco smoke that increases cancers, including lung cancers, in animal inhalational studies of rats and mice carried out by the National Toxicology Program. The structurally-related compound isoprene is present in tobacco smoke, and is also an inhalational carcinogen. Formaldehyde is carcinogenic in inhalational animal models using hamsters, mice, rats and monkies, and acetylaldehyde is carcinogenic in some animals models as well. N-nitrosodimethylamine and N-Nitrosodiethylamine increases lung tumors in inhalational tests with mice and rats. Increases in cancer incidence at multiple sites due to benzene exposure are seen in both inhalational animal models and in occupationally exposed humans. Ethylene oxide causes lung and other tumors in inhalation animal tests, as does ethyl carbamate. Tobacco is also significant source of cadmium, which tobacco accumulates from soil. Both human and animal data show that cadmium is an inhalational carcinogen. Cadmium smelt workers for instance were found to have double the risk of lung cancer, and inhalational exposure experiments with Wistar rats showed increase incidence of lung tumors.

It is important to point out that most of the known carcinogens in tobacco smoke are only carcinogenic at very high doses, that is, they are weak carcinogens. There are toxins and weak carcinogens in every plant humans consume (e.g. Ames and Gold, 1990). In tobacco smoke, however, the PAH's and tobacco-specific nitrosamines (e.g. NNK) are relatively very potent carcinogens, and are thought to play major roles in tobacco related carcinogenesis (Hecht 1999, 2003). And of course, because tobacco smoke is inhaled, respiratory tract cells are exposed to much higher doses of carcinogens than they would be if an equal amount of carcinogens were consumed orally.Â

It is also important to point out that the above is an overwhelmingly incomplete list. Many of compounds found to be carcinogenic in feeding, injection or skin-painting assays have never tested in inhalational models, so it is unknown precisely how many inhalational carcinogens are present in tobacco smoke. For instance, the tobacco-specific nitrosamines NNK and NNN are clearly some of the most potent lung carcinogens in tobacco smoke, and cause lung tumors in all species tested, regardless of mode of administration, in some case with single doses of less than 1 mg. In tests with cultured human bronchial epithelial cells, which serves as model human system, NNK rapidly induces malignant transformation, and the transformed cells form tumors when innoculated into mice (Zhou et al, 2003). NNK also inhibits apoptosis of human airway cells by activating the AKT pathway via an nAchR (nicotinic acetycholine receptor) -dependent mechanism (West et al, 2003), which may also contribute to its carcinogenicity. As yet there are no inhalation studies as yet with these compounds. Once they are tested, they will almost certainly be found to be one of the most potent inhalational lung carcinogens so far identified in tobacco smoke. Also, though benzo[a]pyrene is the most well-known PAH carcinogen, it is not the only one. There are about 14 PAHs in tobacco smoke, and of these dibenz[a,h]anthracene and 5-methylchrysene are more effective at producing lung tumors in mice (Ross et al, 1995). Yet, there apparently are no inhalational studies with these compounds.

A final point is that tobacco smokers never inhale single carcinogens. They inhale dozens at once, along with numerous other substances that are not themselves carcinogens, but can act as cocarcinogens that dramatically increase the carcinogenic potency of another carcinogen when administered simultaneously. For instance, when catechol is administered simultaneously with benzo[a]pyrene in the mouse skin test, it increased the number of mice with skin papillomas by about 150%, the total number of papillomas by about 560%, and number of mice with skin carcinomas by 300% (Van Duuren and Goldschmidt, 1976). Thus, even if it were true that none of the individual chemical carcinogens in tobacco smoke were capable of inducing lung tumors when administered in isolation (it isn't), it would not follow that the chemical carcinogens in tobacco smoke are not capable of causing lung tumors when administered in combination with other carcinogens, cocarcinogens, and promoters. "

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"Interesting site. Who pays to put it up, and for all the things to be written on it?"

"Why do you assume that anyone pays to put that site up? The site is hosted for free by Yahoo, and the articles are written by me purely out of personal interest. I also run a site on geology."

Then the non-offended answer would have been "I do the research voluntarily, and Yahoo puts it up for free."

I just want to know how you make a living so I can properly assess the bias - don't take it personally, but this debate is so money-warped already I think everyone should have their cards on the table.

DML:

"Why is there so much respect for results from animal studies? ... aren't they completely useless to evaluate anthing other than researcher bias?"

Patrick:

"No, absolutely not. Animal studies are enormousy useful in many ways, for instance where ethics or practical concerns make human experiments impossible (e.g. toxicity and carcinogenicity tests). And since physiologically most mammals are very similar, the results are far from 'useless.' Animal studies are enormously useful, for instance for testing the safety, efficacy and mechanism of action of drugs, for determining the causes and mechanisms underlying disease processes, and so on. For instance, a compound that reduces introcular pressure or inhibits emesis (vomiting) in rabbits or ferrets is likely to do so in humans as well, since the physiological structures that mediate these reponses are basically the same in all mammals."

Isn't it true that Thalidomide doesn't cause birth defects in rats, but DOES in humans? Isn't it true that saftey and efficacy tests were only instituted after what synthetic medicine did to people? Isn't it true that herbal medicine has an advantage over synthetic medicine in that it's practitioners are more likely to encounter human examples to study and also more likely to test medicines on themselves (and thus know even more about what they do to others)?

"Of course, as I point out repeatedly in my articles, you have to be careful about extrapolating from animal experiments to humans, since the experimental conditions often do not reflect the human environment."

I think it goes beyond "being careful" - human studies are in every way superior, and since the Thalidomide scandal could not have been prevented through animal testing, the risk-to-benefit ratio of synthetics is in every way inferior to natural herbal medicine. What, exactly, can pills do that herbs can't do?

"Besides, reading my articles you'll see that I do cite human data wherever it exists, experimental and epidemiological, so its not like I'm ignoring human data in favor of animal data. Rather I'm including all relevant data."

Sorry, but I have yet to see a mouse study that helps explain how cannabis helps humans - you're likely to get different results if you study lab mice vs. wild mice using cannabis naturally in their own habitat (if they do at all)....so you still haven't addressed the worthlessness of studying researcher bias - you haven't even mentioned researcher bias as a negative factor in the entire equation - you haven't addressed how researcher bias doesn't skew every laboratory study ... at least with human non-lab studies you are studying the bias of the subject instead of the bias of those who write the protocol.

"No mention (that I could find in my first cursory overview) is made of the long term Costa Rican human studies (1982) which concluded that - if anything - cannabis had a benefitial effect on the lungs, perhaps acting as an expectorant."

Which study, specifically, are you referring to? PubMed searches for costa rica + 1982 do not turn up any studies of lung function in cannabis smoking costa ricans. I'll be happy to include it if you give me a reference. What measures of lung function/harm did they include in their study, and how large was the sample?"

Interesting date that you begin your search - by that time the Reagan White House cut all funding to such studies, never to return. Here are the three largest long-term studies, still well within the age of scientific respectability:

Carter, W.E. (ed), Cannabis in Costa Rica: A Study of Chronic Marijuana Use, Philadelphia: Institute for Study of Human Issues (1980); Rubin, V. and Comitas, L., Ganja in Jamaica, The Hague: Mouton (1975); Stefanis, C. et al, Hashish: Studies of Long Term Use, New York: Raven Press (1977).

http://www.erowid.org/plants/cannabis/cannabis_myth5.shtml

819132-CostaRica.gif

"Users in our matched-pair sample smoked marihuana in addition to as many tobacco cigarettes as did their matched non-using pairs. Yet their small airways were, if anything, a bit healthier than their matches. We must tentatively conclude either that marihuana has no harmful effect on such passages or that it actually offers some slight protection against the harmful effects of tobacco smoke. "

- Costa Rican Study, 1980, William Carter, Institute for Study of Human Issues. (ISHI, 3401 Science Center, Philadelphia)

... 82 people studied - 41 users and 41 non-users. The users were longterm users (average 9 joints per day for 17 years) - "Understanding Marijuana", Mitch Earleywine, 2002, Oxford Uni press, p.80

"If you actually read what I wrote, you'll see that I cite data showing the cannabis smoking does not cause COPD (chronic obstructive pulmonary disease - emphysema), and argue that it is not a major risk factor for lung cancer, which are the major pulmonary harms associated with tobacco smoking. There is, on the other hand, plenty of evidence that cannabis smoking causes chronic coughing and wheezing, slightly increases risk of respiratory infections (based on a very large american sample), impairs alveolar macrophage activity in the lungs, and in rare cases can cause spontaneous pneumothorax (from holding the smoke too hard using what's called the valsalva's manoever, causing a breach of the lungs)."

Those are the effects of prohibited cannabis, not legal cannabis. The use of a thing cannot be disserned from it's abuse. If cannabis were legal, I'm sure using organic bubblehash through a water pipe would not result in the same harsh side-effects as the current chemmy-bunk shwag smoked in an aluminum can or worse.

"And I do point out clearly that cannabis smokers have increased phlegm production, which is basically the same thing as saying that it is an expectorant. I also do clearly point out that THC is a bronchodilator."

Expectorant sounds like a positive thing, but "increased phlegm production" sounds negative.

DML

"The problem with sub-lingual spray is that it takes minutes to work, when some of the problems that cannabis is used for (nausea, stroke, epilepsy etc) seconds can mean the difference between relief and extreme discomfort (or even life and death). Certain conditions require a more rapid delivery system."

P:"You're telling me something I already know."

It isn't reflected in your work.

"And in any event, smoking is obviously not the only way to rapidly deliver a dose. An inhaler (if it were developed) would be as fast, and an intravenous injection would be much faster."

They are working on a spray but it's not as fast. Smoke is fine, if you know about organics and bubblehash and water-filters and vaporizers and magnifying glasses on a sunny day..... - none of which can be monopolized by the pharmasuits.

"In fact, if your patient is having a stroke or a siezure, smoking a bong is going to be a bit difficult compared to an inhaler or an iv injection."

I would rather have a joint and give no money to "Bayer: the uberwarprofitters" - it works faster, is twenty times cheaper and you will probably need a friend to help you with whatever you decide to use anyway.

"As for nausea, I think smoking is a good way to go, except of course for people (like my grandmother) who arent pot smokers and who don't particularly want to gag and cough if they dont have to."

A bit of heated bubble hash in a glass bong or with a vaporizer, and she doesn't need to support the evil pharma-nazi's. See my research on Bayer at www.cannabisculture.com/news/gwbayer

DML

"You neither come across as anti-tobacco or anti-cannabis, but the whole site has a "pro-sativex" flavor to it. Don't fall prey to smoke -a-phobia ... smoke is a preferred delivery system to most medical traditions on the planet. It's monopolistic and eurocentric and just plain innacurate that pills, sprays, tinctures, patches and suppositories are superior routes, when actually they all have a greater chance of overdose do to the lack of "titration" ability from the slower methods of injestion."

P:"I won't fall prey to smoke-a-phobia if you don't fall prey to smoke-a-philia/nonsmoke-a-phobia. For many people, smoking clearly is NOT at all a preferred method of administration. Its just plain inaccurate to think that one method of delivery is the best for all people and all indications, or that the only reason to develop nonsmoke delivery is for intellectual property."

Um, no. The only reason that smoked-cannabis is not being allowed on anything other than compassionate grounds and there are no legal distributors other than GW pharmaceutical is PRECISELY because of the intellectual property rights. If you read the IOM report on Cannabis (1999) they state very plainly that they plan to institute a monopoly on distribution of medical cannabinoids using non-smoked delivery systems. It is the main focus of GW pharmaceutical selling it's stock on the market - intellectual property rights - featured heavily on their website.

"That's nonsense. There are many people out there who can benefit from cannabinoids, but who do not want to smoke it."

They should have the choice. But let's not pretend spray is superior to smoke because it's just as safe (when done properly) and much cheaper and quite faster. People's hesitation to use smoke is more stigma than anything else - it is not a cross-cultural phenomena.

"I have been close to two older medical users who clearly benefitted from cannabinoids (one for glaucoma and one for neck spasticity), but stopped because the smoking (even short puffs from a waterpipe with little or no breath-hold) made them cough and hack too much."

They were probably not using bubblehash, probably smoking stale smoke, probably wasn't organic. The vaporizer works good too. They should have the choice of any delivery system ... but the fact is smoking is the preferred method for most people.

"Even if it were perfectly safe with no health risks, many people, including many very sick people, just dont want to smoke their cannabinoids. I see the development of these alternative delivery methods as entirely positive."

You don't know or don't agknowledge the history of medicine as a history of monopoly .... but if you care to research the subject, that is what you will find:

www.cannabisculture.com/news/potpatent

"By the same token, opiates are some of the most useful tools in the human pharmacopea, but no one thinks that everyone should smoke opium rather than taking it some other way"

I disagree. I'm someone, and if you can get pain relief without giving money to nazi-bayer, why not?

"... and injections, pills (example - demoral), sprays (example -stadol), and patches (example - fentanyl) are a godsend for many people."

That's fine, but I don't use them, and currently their producers enjoy a monopoly on effective stimulants, relaxants, analgesics and euphorics that they could be supplying themselves in their back yard and then smoking the resins of. That is the future of medicine, IMHO.

"My wish is to use cannabinoids to alleviate as much suffering as possible, and for many people who suffer, smoking is not at all the best option. What you say about dose titration is true, though there is no reason to think that a THC inhaler would be any harder to dose-titrate than a joint,"

Except for the fact that GW refuses to do comparitive studies....doesn't give you much faith in the product .... it would be like refusing to test aspirin against white willow bark..... what are they afraid of?

" since the time to plasma-THC-peak would be the same."

Onset is faster with smoke. The spray has to be "digested" - the smoke is instant. Onset is important if you're wretching or spastic or having a heart attack.

"I see the development of these alternative delivery methods as entirely positive."

If it was in a non-monopoly situation, I would agree. But the producers of pharmaceutical products enjoy a medical monopoly, their safety and efficacy tests provide an economic barrier to medicine that (unjustly) prevents the herbs from competing with pills.

"Many researchers argue that certain cannabinoids - THC among them - require heat to work properly"

"Many researchers"? Really? Now that's odd, David, because I've read dozens of papers on cannabinoid pharmacology, and can't recall a single researcher ever saying such a thing, much less many researchers.

I will quote the people who should know:

"We are producing an extract from the whole plant, which is a bit like syrup. It will be delivered to the patient in the form of a heated vapor because cannabis needs heat to work" - Mark Rogerson, GW Pharmaceutical spokesman, "Hunt for Cannabis Cure", Daily Mail (UK), Jan. 19, 1999.

I also talked to Dr. Paul Hornby of Hedron Analytical, who says that cannabis needs heat to work properly. I can supply you with the names of other researchers who say the same thing, if you require further citations before you look into the matter yourself.

DML:

"As well, the cigarette was first developed in the Crimean War, and continued to be promoted in the American civil war, so cancer rates should have shot up in the late 1800's, not in the 1930's as is reported."

P:"What was the prevalence of cigarette smoking prior to 1900? How many people smoked these cigarettes daily, and on average how many per day did they smoke? Obviously, since you say that "cancer rates should have shot up in the late 1800's," you are implying not merely that cigarettes existed prior to 1900 (which no one disputes), but that they were being widely used and used at high rates during the 1800's, whereas the ALA statistics I just cited (and every other source I've read) indicate that cigarette smoking was fairly modest until the early 20th century, when rates of consumption shot up enormously. Further, I wonder how many people who died in the 1800's were autopsied to inspect for lung cancer? In other words, would it even have been possible to detect a modest increase in lung cancer incidence in the late 1800's if it did occur?"

I maintain that if cigarettes, not phosphate fertilizer, is the main cause of tobacco-related lung cancer, there should be a connetion between cigarette consumption and cancer rates. I don't have that information .... but I gather that you don't either.

"Finally, you should keep in mind that lung cancer has a very long latency period, on average about 40 years. That is, when a group of people start smoking regularly, you don't see an immediate rise in lung cancer in that group, you see it about 40 years later (about 85% of lung cancers occur in people who have been smoking for 40 years or more)."

I believe you, but I want the source to that information anyway.

DML:

"It is the introduction of chem ferts, not cigarettes, that goes hand in hand with the rise of cancer rates."

P:"So, you say. However, the facts appear to disagree, as does every review I've read of the epidemiology of lung cancer. According to one of your own sources (Marmorstein, 1986- I went and got the paper), the use of artificial high-phosphate fertilizers did not become widespread until after 1940."

Please write out exactly what he said on the subject and please also provide sources. I have sources that disagree with that:

By the 1860's, however, Britian used more soil nutrients than all the European countries combined. In the hearings before an Imperial French commission (1865), British consumption of fertilizers was estimated at half a million tons, including 250,000 tons of prepared bones and superphosphate and about 150,000 tons of guano.

Britsh Imports of Guano and Sodium Nitrate:

Year Guano Sodium Nitrate

1845 283,300 tons 7,700 tons

1850 116,000 12,000

1855 305,000 15,000

1860 141,000 37,300

1865 237,000 51,000

World Production of Phosphatic Rock

1847 500 tons

1850 1,000 tons

1854 10,000 tons

1857 30,000 tons

1860 65,000 tons

1863 93,000 tons

1866 135,000 tons

1869 240,000 tons

1872 307,000 tons

World Production of Phosphate Rock and Superphosphate

Year phosphate rock superphosphate

1875 500,000 tons n.a.

1880 500,000 tons 900,000 tons

1885 1,200,000 tons 1,600,000 tons

1890 1,600,000 tons 2,000,000 tons

1895 2,200,000 tons 3,500,000 tons

1900 3,100,000 tons 4,800,000 tons

1905 3,800,000 tons 6,100,000 tons

The discovery of large deposits of phosphate rock in South Carolina in 1868 and in Florida nineteen years later led to the formation of an American superphosphate industry which developed quickly. Output rose from 28,000 tons in 1868 to 161,000 in 1879 and to 410,000 tons in 1883. United States production passed the million-ton mark in 1898.

-The Chemical Industry during the Nineteenth Century

L.F. Haber, Oxford, 1958, pp. 60- 62, 106-107

Estimated World Production of fertilizers:

1900 = 1,000,000 tons of Phosphatic fertilizer

1913 = 2,500,000 tons of Phosphatic fertilizer

A the beginning of the century three nitrogenous fertilizers were articles of commerce: guano, sodium nitrate, and sulphate of ammonia. Guano was the least important.... World production, once large, had declined owing to the gradual exhaustion of the richest deposits on the island of Peru. In the years before the Great War output fluctuated between a low point of about 40,000 tons and a peak of 133,000 tons. ... From the second half of the nineteenth century onwards sodium nitrate replaced guano."- The Chemical Industry, 1900-1930, L.F. Haber, Clarendon Press, 1971, pp. 98-99

"Its very clear that the steep increase in lung cancer rates began before 1940."

Your cancer research seems solid - it's your fertilizer research that's lacking.

"Case reports and epidemiological studies based on data from the first half of the twentieth century and earlier make it clear that even before the widespread adoption of chemical fertilizers and synthetic pesticides, smoking tobacco was still a major risk factor for lung and other cancers. Probably the earliest reports of tobacco-associated cancers were written by english physician John Hill in 1761, who in his Cautions Against the Immoderate Use of Snuff described a case of nasal cancer in an individual with a long and immoderate history of snuff use."

One case. It seems like it is still accurate to call pre-1900 tobacco related cancer a "rarity" or "seldom seen". This information does nothing to refute the argument that radiation from chemical phosphate ferts is the MAIN reason why people get lung/nose/throat cancer from tobacco smoking TODAY.

"Other early observations that pipe smoking was associated with oral cancer were made in Germany by Sommering in 1795 and by Virchow in 1863. In 1836, Samuel Hill stated in the New England Almanac and Farmer's Friend that "thousands and tens of thousands die of diseases of the lungs generally brought on by tobacco smoking is a fact as well known in the whole history of disease." In the eary twentieth century, within a decade of two of the widespread adoption of cigarette smoking, evidence linking tobacco smoking to lung cancers began to accumulate. According to Davey-Smith et al (1994), even by the late 1920's doctor Fritz Lickint in Germany had gathered evidence implicating tobacco smoking as "a major cause" of lung cancer. A letter to the editor of the Lancet (July 30, 1927) by Tylecote stated that "almost in every case (of cancer) I have seen and known of, the patient has been a regular smoker, generally of cigarettes.â? A 1928 study in the New England Journal of Medicine found that in a group of 35 cancer cases of the mouth and lungs, all but one case occurred in heavy smokers (Lombard and Doering, 1928). In 1936, Arkin and Wagner wrote an article for the Journal of the American Medical Association noted an increase in lung cancer and found that 90% of the cases they observed occurred in heavy smokers. Muller (1939), in what was probably the first controlled study of smoking and lung cancer, found that of 86 male lung cancer cases, 56 were heavy smokers, and only 3 were nonsmokers, and concluded that the "extraordinary rise in tobacco use" was "the single most important cause of the rising incidence of lung cancer."

If you adjust your information to recieve the correct information regarding the use of chemical phosphate ferts extensively in the latter half of the 1800's, then the cancer could also be a result of the fertilizers. You have done nothing to establish that tobacco consumption has increased during this time - you only point to cigarette comsuption increases. Tobacco was consumed in enough quantity before the introduction of cigarettes to account for many, many cancer deaths starting in the 1700's (when immoderate use of tobacco began) - but there is little evidence of these deaths before the 1920's - far less than one would expect if tobacco by itself was the cause of cancer. You cannot dismiss the possibility of radiation being the #1 reason for tobacco related cancer with the information you have provided so far.

Here is my latest research on fertilizers:

How radioactive is your fertilizer?

By David Malmo-Levine

Perhaps the worst thing about chemical fertilizers is the radiation. A growing number of scientists believe that it is the radioactivity in high-phosphate fertilizer that leads to lung cancer in tobacco smokers. Given the testing done so far, it is relatively safe to assume that most chemical fertilizers will be unnecessarily high in radioactivity. However, not all organic fertilizers are low in radioactivity. There may be natural or human-related radiation that can find it?s way into the food cycle of quality-guano-producing animals.

The following test for the relative radioactivity of various fertilizers was done at SRC Analytical in Saskatoon, Saskatchewan (1-800-240-8808) ? an accredited laboratory. The tests were conducted with a EG&G Berthold (for alpha and beta) and a APTEC gamma detector (for gamma). A previous test ? the results of which are printed on the next page - was done using a Beckman Coulter counter in scintillation fluid ? which may account for the variation in readings on both tests of the ?control? ? the ?DML seabird guano?.

For the beginners, ?N? means ?Nitrogen? (for vegetative growth), ?P? means ?Phosphorus? (for budding) and ?K? means Potassium (for budding and cold-weather protection).

As well, it is good to keep in mind that alpha radiation is only dangerous when ingested because it doesn?t penetrate through skin. Basically, none of it is good for you, but alpha has the reputation for being the most cancer-causing of the three. It is interesting that the alpha count appears low in the liquid fertilizers ? until you compare alpha count per amount of nutrient ? then some of the solids appear to rate lower over-all.

SCR Analytical - radioactivity test of various fertilizers - 2003-2004

Fertilizer Type of fertilizer N-P-K Alpha Beta Gamma Total Counts per minute

Way To Grow Organic Solid 9-27-0 11.4 10.8 6.0 28.2

South East Asian

Seabird Guano

Way To Grow Organic Solid 13-1-3 15.0 45.0 24.0 84.0

Texas Insect-Eating

Bat Guano

General Hydroponics Chemical Liquid 0-5-4 3.2 56.2 36.2 95.6

Flora Bloom

DML Seabird Guano Organic Solid unknown 15.6 42.0 60.0 117.6

Advanced Nutrients

Mother Earth ?Bloom? Organic Liquid 0.5-1.5-2 2.6 84.6 52.2 139.4

Advanced Nutrients Chemical Liquid 1.5-4.6-5.7 3.5 105.2 70.0 178.7

Sensi Bloom

Way To Grow Organic Solid 0-32-0 60.0 78.0 126.0 264.0

Philippine Fruit-Eating

Bat Guano

Miracle Grow Chemical Liquid 10-52-10 15.6 180.0 84.0 279.6

Ultra Bloom

Hedron Analytical Inc. - radioactivity test of various fertilizers ? 2002

Fertilizer Type of fertilizer N-P-K Counts Per Minute

Evergro Specialty Organic 12-0-0 90

Blood Meal

Green Valley Organic 12-0-0 96

Blood Meal

RainGrow Organic 0-12-0 102

Boom-A-Long

Sea Spray Organic 0.5-1-0.5 125

Green Vally Organic 7-11-0 154

Blood & Bone

RainGrow Organic 4-2-3 160

Homestead Organic 4-14-0 174

Bone Meal

DML Seabird Guano Organic Unknown 178

Miracid Chemical 30-10-10 248

Soil Acidifier

Shultz All Purpose Chemical 10-15-10 258

Miracle Grow Chemical 18-24-16 285

For Roses

Green Valley Chemical 10-8-6 326

Rhododendron

Shultz Chemical 8-14-9 393

African Violet Plus

General Hydroponics Chemical 2-1-6 400

Flora Grow

Miracle Grow Chemical 15-30-15 409

Water soluble

Greenleaf Evergreen, Chemical 13-6-7 437

Tree and Hedge Feeder

Stern?s Miracle Grow Chemical 18-18-21 538

For Tomatoes

Miracle-Gro Chemical 15-30-15 547

Plant Food Engrais

Greenleaf shur gro Chemical 20-20-20 672

Greenleaf shur gro Chemical 20-20-20 693

Shultz instant orchard Chemical 19-31-17 740

Shultz tomato plus Chemical 18-19-30 874

Evergro Fruit Tree Chemical 4-20-20 1037

And Berry Food

Osmocote Chemical 18-6-12 2021

Time-Release

Green Valley Chemical 5-20-20 2384

Berry Food

Hopefully, the effect of this pamphlet will be to 1) get all fertilizer companies to care about how much radiation goes into their products, and 2) to explain better to consumers and farmers why chemical fertilizers are destructive and why everyone should switch over to low-radiation organic fertilizers.

Please vote with your consumer dollar and help restore and improve our living soil ? mother nature is depending on you.

More information

To get a hold of some good bat and bird guano, try ?We?re The Shit? ? dealers in fine guanos: 604-842-7790.

For more information on organic cannabis growing, (or cannabis growing in general) check out the growers forum at www.cannabisculture.com. Just click on ?forums? when you get to the home page, and follow the simple instructions.

Anyway, I hope this information was helpful to you.

I can't wait to read your final version.

David

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I haven't sent these off to Patrick yet, but here are some more links to help steer researchers into the direction of phosphate ferts as the major source of danger in tobacco and cannabis.

photos:

http://www.fluoridealert.org/phosphate/photographs.htm

fertilizer analysis:

http://www.orau.org/ptp/collection/consumer%20products/fertilizer.htm

http://www.greenpeace.to/pdfs/LCC_2002.pdf

chemical fertilizers demineralize farm soil...plants grown in low mineral soil absorb radionuclides much more efficiently:

http://www.championtrees.org/topsoil/nukedust.htm

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Debate? Looks more like trolling with spam, four times, to an unresponsive audience by a man desperate for attention.

But hey thanks for showing how another person knows what a goof you are. Keep up the good work ruining your imaginary reputation!

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40 years ago, there was a large phosphorus plant in the tiny community of long harbour, newfoundland...i don't know why they would set up a large plant out in the middle of nowhere...maybe they knew they were doing something that was going too hazardous to be located near a larger population OR maybe the government bribed them to build it in a small community as political payback...here is the order to shut down the mill from 30 years ago:

http://www.canlii.org/nl/laws/regu/c1996r.2/20040817/whole.html

the company (albright & wilson americas) still exists as part of the largest multinational phosphate corporation in the world:

http://www.1800miti.com/Companies/US/profit/page84awaf.html

and the company is still leaving hazardous waste lying around (they have been fined many times and the largest fine i could find on them was $900,000):

http://www.epa.state.oh.us/pic/nr/1998/april/nhs8albr.html

the former president of albright & wilson americas is now the chairman of the synthetic organic chemical manufacterers association (and vegetarian comedian kevin nealon is going to perform at their annual dinner):

http://www.socma.org/about/board.htm#

according to the report on tv, that phosphate plant in newfoundland would recieve raw ore from a "uranium mine" in florida by ship, process it, and dump the radioactive near the waterfront next to the the tiny community of long harbour (about 800 people at the time)...i think the report may be mistaken about the uranium mine (should have been apatite mine?) unless the plant was covertly extracting uranium for the weapons industry or some other sinister radioactive purpose

anyhoo, the slag waste heap looks like its over a hundred feet high and a kilometre long...its a known radiation hazard...a documentary done several years after it closed showed deformity in the animal population...apparently, albright & wilson made a deal with the idiot newfie government that protects them from having to clean up their radioactive waste *AND* they can't be held liable for any harm caused by that waste...wow...they must have been excellent negotiators

recently, a multinational corporation has expressed interest in purchasing the slag heap...they want to ship it all to their processing plant and sift through the radioactive remains to get radioactive phosphate solids to spread on vast sugarcane and other tropical agriculture 'holdings'...its estimated that the job of removing the massive slag heap at a rate that will supply their phosphorus plants will take 10 years...the people in the town would love the jobs and they don't want the slag heap but they also don't want to have radioactive dust blown all over them for a decade...i haven't been able to find out who the multinational corporation is but i'll bet they're linked to rhodsia corp. which recently bought albright & wilson and is now squeezing every last penny out of them

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DML could you please use the god dam quote box.Its a little hard and very frustrating to figure out who is saying what.

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The quote characters themselves aren't good enough?

My responses are usually right after their statements, and my responses are in quotes and theirs are not. This allows me to carry on a conversation and identify that it was me who was doing it. I also leave a little space between each statement ... it's not THAT hard to follow, is it?

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Dude, what you and others are doing here is very important and many would like you to keep it up. Never mind the dweeb who slammed you on this several months ago...

I can add that I work in the radiation industry and there are many places where the Gov't regulators have looked the other way. One such place is Port Hope, Ontario. The Cameco plant (formerly Eldorado Nuclear) was used to process Uranium for reactors and whatever else I'm sure. We drove by the plant a while ago and there was an area filled with many 45 gal. drums in dis-array. I had a geiger counter in the car and the readings went through the roof, even though we were on a public street outside the fence.

Later we drove to an area nearby, down by the lake where there was no buildings, just a dirt road and an empty field. Again the geiger showed indications, for some mystery reason there was something, possibly underground. These are things most people don't know, happening right in their back yard.

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During the height of Peru's golden age of guano, around 1840 to 1880, it has been estimated that the Peruvians excavated over 20,000,000 tons of guano for export, creating around $2 billion in profits. However, by 1909-10, Peru's guano reserves were severely depleted and could only yield around 48,000 tons of guano a year.

http://www.american.edu/TED/ice/guano.htm

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05.tobacco.jpg

http://www.cnn.com/interactive/world/0008/farm.history/05.tobacco.jpg

http://www.cnn.com/interactive/world/0008/farm.history/content5.html

"It is quite certain that tobacco is exclusively an American plant and that half a hundred varieties have been found here. It is also certain that eight or possibly nine types were used by the aborigines of this country at the time of the Discovery, and that in some localities the Indians cultivated tobacco for centuries before that great historic event.

The essential methods of using tobacco have not changed since the first visit of Columbus. Not only did the Indian smoke tobacco in the pipe at that time but he also smoked cigars, made by rolling tobacco in dry leaves, and cigarettes, made smaller but in the same manner. Tobacco was also chewed and snuffed. It was used as a great curative remedy and in a myriad ways ceremonially. ... It was prized for its narcotic effect. It was his medicine, and a remedy for many of his ills. ... The American Indian was not a lover of strong tobacco and often added to it various barks and plants for the purpose of producing a milder mixture."

From "Tobacco, Pipes and Smoking Customs of the American Indians", George A. West, out of the Bulletin of the Public Museum of the City of Milwaukee, Vol. XVII, June 11, 1934 (reprinted 1970 by Greenwood Press), pp. 379-380

"In early Colonial days tobacco was actually used as money. At one time it is said every available space, even the streets, the gardens, and yards of Jamestown were planted with tobacco, so valuable was it as a crop." p. 84

...

"Most of the tobacco consumed in the United States up to the seventies of the nineteenth century was in the form of cigars and smoking tobacco. .... by 1920 consumption had practically jumped 500 percent, or from eight billion to over fourty-eight billion (cigarettes). Within another five years ... consumption had reached 82 and 1/4 billions." p. 85

"According to a statement in TOBACCOLAND, published by the Liggett and Myers Tobacco Company in 1941, a good tobacco farmer puts about 800 pounds of fertilizer to the acre." p. 99

From "Smoke Over America", Dr. Jesse Mercer Gehman, 1943, The Roycrofters,

U. S. Census Data

1790 3,929,214 1870 39,818,449 1950 151,325,798

1800 5,308,483 1880 50,155,783 1960 179,323,175

1810 7,239,881 1890 62,947,714 1970 203,302,031

1820 9,638,453 1900 75,994,575 1980 226,545,805

1830 12,866,020 1910 91,972,266 1990 248,709,873

1840 17,069,453 1920 105,710,620 2000 281,421,906

1850 23,191,876 1930 122,775,046

1860 31,433,321 1940 131,669,275

http://www-rohan.sdsu.edu/~jmahaffy/courses/s00/math121/lectures/

discrete_dyn_sys/discrete.html

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DML can you clear a few things up for me.

The radioativity and cancer didn't make a serious increase till the introduction of chemical ferts, correct?

Do the chemical ferts also contribute to the addictive factor ciggs have on us tabbaccoo smokers?

with ther underhandedness of the tabbaccoo industry is thre a way to dissconnect ourselves from it while stil ebing smokers.

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"DML can you clear a few things up for me."

I'll give it a shot - but I'm only half-way done my research.

"The radioativity and cancer didn't make a serious increase till the introduction of chemical ferts, correct?"

Yes and no. There were several factors to take into consideration. Virginia tobacco was milder than most of the other types - easier to draw into the lungs. The smoke from dark leaf tobacco (the kind used most for cigars and pipe tobacco) was more often inhaled just into the mouth or nose.

The most telling bit of evidence thus far is that there was virtually no cases of lung cancer and few cases of other cancer at the turn of the century - and more than one researcher has dismissed the "we didn't know how to identify cancer" or "we didn't look into it back then" or even "people didn't live that long back then".

Then you must take into account the introduction of cigarettes (they have been around from the beginning, but were only mass produced in the 1850's and only machine produced in the 1880's) and their effect on the smoking practices. Most (but not all) of the standard research blames cigarettes - not chem ferts - for the increase in lung cancer, as they were both introduced at about the same time ... but the hole in that theory was that overall tobacco use didn't increase - people just smoked less cigars and pipe tobacco. As I mentioned before, cancer was rare back then compared to now, and if it was just the tobacco that caused cancer you would have seen a HUGE death rate from head and neck and nose cancer from the dark-leaf cigars and pipes - it's nowhere to be found (at around the turn of the century).

"Do the chemical ferts also contribute to the addictive factor ciggs have on us tabbaccoo smokers?"

I can't see the chemicals contributing to taste or effect of the nicotine. I did notice, however, that people do not really smoke tobacco when they smoke the modern cigarette - they smoke PAPER - cellulose - that has been soaked in (chemically fertilized) tobacco juice. There's lots of other things added, too ... to improve shelf life, burning consistancy and - if it's in their power to do so - attractiveness or mildness or other "addictive qualities" ... I'm pritty sure.

"...with ther underhandedness of the tabbaccoo industry is thre a way to dissconnect ourselves from it while stil ebing smokers."

Grow yer own and keep it organic ... practice rituals of respect and moderation ... and find some dark leaf varities and add them to other smokeable plants like mullien and coltsfoot.

Or else quit and just smoke the kind herb.

I hope that all helps. I'll expand on this argument and organize/source everything soon.

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it takes about 20 years for cancer to develop from exposure to carcinogens...people lived long enough to develop cancer in the 1800's...in 1850, average life expectancy was only 38 but that includes the high infant mortality rate which dragged the average life expectancy down (the figures measure life expectancy AT BIRTH)...here's an interesting life expectancy chart:

http://www.infoplease.com/ipa/A0005140.html

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Quote:

I hope that all helps. I'll expand on this argument and organize/source everything soon.


looking forward to it.

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haha yer pulling my leg with that page-o-links...here's some more links that might interest you

this doc wrote a book (not peer reviewed research) linking medical radiation to heart disease and the majority of cancer cases in the usa...if he's right, cancer can be caused by lower levels of radiation than originally thought

http://www.ratical.org/radiation/CNR/RMP/index.html

this guy says that exposure to low levels of ionizing radiation is 20 times more dangerous than previously thought:

http://www.foe.arc.net.au/kohnlein/kohnpaper.html

conventional wisdumb says that the LD50 for whole body radiation exposure is 400,000 mrems (the lethal dose required to kill 50% of human subjects)...since radiation exposure is accumulative, it doesn't matter how long a period over which the exposure takes place...daily tobacco use exposes smokers to 8,000 - 16,000 mrems per year so it should take somewhere between 25 - 50 years of smoking to kill half the smokers...tobacco does kill half of all long term smokers so the LD50 for radiation matches the mortality profile for smokers but it would be incorrect to say that they died of radiation poisoning

ionizing radiation causes cancer:

http://web.ccr.jussieu.fr/curie.100/fulltext/lewis.html

researchers are mystified as to why smoking tobacco multiplies the risk of radon induced lung cancer (but we know its because radon progeny are concentrated in tobacco)...oddly, japanese smokers have less lung cancer despite the widespread popularity of tobacco in that country...its likely that japan didn't use much chemical fertilizer prior to world war 2...the tobacco industry in japan is dominated by japan tobacco inc which is the third largest tobacco corporation in the world:

http://www.rerf.or.jp/eigo/rerfupda/death/radiat.htm

japan used to grow its own tobacco but globalization has sharply reduced the amount of domestic tobacco farming...fukushima prefecture had tens of thousands of acres of tobacco farms but 75% of the tobacco acreage has been abandoned since 1975...i think the japanese used traditional methods of farming before they subcontracted the job out to chemmy killing fields:

http://www.newfarm.org/international/gleanings/2003/november/jp_future.shtml

the lung cancer rate in japan is increasing but its still less than 2/3 the rate in the usa...some researchers think its because of the sushi:

lung cancer and sushi

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reading over this again reminds me of the radioactive buds article a while back that CC did. it listed a bunch of commonly used ferts with there perspective radioactive proporties.

in both tabbaccoo and the herbs "you are what you eat" holds true.

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