New research suggests that nicotine creates cellular drills, targeting and perforating smooth muscles over a period of six hours.

Contrary to popular belief, that carbon dioxide level exposure had to be extreme in order to deposit enough tar to permanently damage the lungs, it is now becoming clear that the cause of lung cancer and other smoking related problems is in fact nicotine. It was an old wives’ tale or counterargument from smokers that because people living in big cities inhaled half of a pack to a pack of cigarette in smoke from smog each day, but did not have high lung cancer rates like second hand smokers, there must be something wrong with the tobacco studies that were done. Living in a city with hundreds of thousands of cars cars was equivalent to “two packs of cigarettes a day” while any smoker will have a 24-35 in 100 chance of lung cancer (500-1000 times higher than simply being a city dweller). In Bejing today, this rate is 42 in 100,000. People who use candles or incense frequently only have 7 or 8, slightly more than regular marijuana smokers. This perhaps indicated that in fact smoking cessation products cause lung cancer; that it is not smoke, but nicotine that causes the lung cancer has only been proved this last year. Possible explanations at the time included contaminants to tobacco or asbestos, hence natural brands such as American Spirit advertised as such to me as a teenager.
However, in 2013, a new paper delivered at the American Society for Cell Biology managed to watch the molecules of nicotine fold into drills after being present in the blood stream for a continuous six hours. These target smooth muscles, such as those found in the heart, epidermis, lungs, and reproductive system as well as throughout the body. This helps to explain why a secondhand smoker in a house with a heavy smoker has a greater chance of lung cancer than a light smoker. It is conceivable that users of e-cigs or nicotine substitution products such as the patch or gum living in a big city could give themselves lung cancer as well by pollutant exposure as the body becomes unable to naturally clean itself.
Much credit is deserved for Brown professor Ching-Ming Hai, who discovered these cellular drills called podosome rosettes. By establishing the link between heart disease such as atherosclerosis and nicotine, the way has been opened to investigate the role of nicotine on other organs such as the lungs. Being able to observe this phenomenon suggests a veritable hypothesis that other smooth muscles in the body will and do respond in a similar way, eventually tearing and folding under continued nicotine exposure.
Some research has existed which supports this hypothesis that lung cancer is caused by nicotine, including studies which suggest that lung cancer is sped up by nicotine exposure (Dasgupta). For the first time, it can be assuredly said that in fact the cause is in nicotine. This supports the population data. In all of Mexico, for example the lung cancer rate is 5 in 100,000 (Lazcano). Introducing smoke increases this eight times, to as much as and over 40 in 100,000 with smog and air pollution (Wang). With nicotine exposure, this jumps to the 30,000 in 100,000 or thirty percent that indicates lung cancer is caused by tobacco.
This is affirmed by research using populations in Sweden and in California in which smokers of marijuana were not found to have increased cancer rates, or only slight and suggested links to cancer. Research along these lines were released in the 1990s and 2000s, though did not have at this time any scientific rationale for the phenomenon, which can now be attributed to nicotine. Continuing research along these lines should provide alternatives and safe products, once again, to combat use of sweets and bubblegum which were originally the targets of tobacco advertising.


Dasgupta, Piyali, et al. “Nicotine induces cell proliferation by β-arrestin–mediated activation of Src and Rb–Raf-1 pathways.” The Journal of clinical investigation 116.8 (2006): 2208-2217.

Lazcano, Ponce EC, et al. “Trends of lung cancer mortality in Mexico.”Archives of medical research 28.4 (1996): 565-570.

Wang, Q. “[An analysis of incidence mortality and survival rates of lung cancer in Beijing].” Zhonghua liu xing bing xue za zhi= Zhonghua liuxingbingxue zazhi12.4 (1991): 205-207.

Addendum: It should be noted that this does not indicate that nicotine or tobacco is responsible for cancer. Since the US cracked down on tobacco use, with success in white males, the overall cancer mortality rate has increased from 184 per 100,000 in 1950-69 to 209 per 100,000 from 1970-1994. Today that rate holds steady at 203 per 100,000. In white females and in other demographics cancer rates have been steady or changed in negligible amounts, but these demographics have had increasing tobacco use rates. Cancer is a painful and unnatural death that can often involve long battles with the disease and should be combated with all resources available, in treatment and in prevention. While lung cancer rates have fallen, technological advances have allowed earlier detection of lung cancer, which at stage 0 and 1 is among the least deadly forms of cancer, but at later stages is among the most deadly. Without adjustments for technological advances in medical care, no positive statement can be made in regards to success or negative results from anti-smoking campaigns. Meta-data from overall cancer mortality does show that the resources in the war on cancer have been squandered and had an overall detrimental effect on the national health of the country, and some policy change is necessitated, although it must be noted there is no current biological explanation for the lower cancer rates in countries and places with higher tobacco use, these have been correlative not causal links.

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