Fine Particulate Matter in Tobacco and Air Pollution, a Prospective Review of Mortality Rates

Fine Particulate Matter in Tobacco and Air Pollution, a Prospective Review of Mortality Rates

    Review of mortality rates among tobacco smokers and non-smokers has been inconclusive. While tobacco use is associated with between 1 and 3 years decline in life expectancy in humans (Ferrucci, et al.) after controlling for exercise (associated with a 10 year change in life expectancy), this does not associate positively with rat studies seen in earlier reviews in which rats smoking over 20 cigarettes a day outlived non-smokers by 5% and human smoking patterns which mostly match this group. Studies have also shown poverty to have a similar detrimental effect on life expectancy, but will not be counted in this study, as the assumption must be made (lacking proper surveys) that exercise and income are positively correlated.
There are two ways of approaching this quantitatively, and both will be pursued in this review to check for logical fallacy. Firstly, the assumption can be made that due to an unsupported difference in the pulmonary systems of rats and humans, that tobacco smoke has a detrimental effect on the lifespan of humans and investigation of how this occurs must happen. Secondly, it can be assumed that there are other confounding factors such as air pollution and radioactive exposure which account for greater levels of mortality in certain geographical areas, making tobacco data coincidental (which would be supported by female trends in the UK where lung cancer increased significantly as smoking declined by 50%, as shown in a previous article).

Fine Particulate Matter in Tobacco: enough to cause cancer, early mortality, neither or both?
The average cigarette delivers 1525 (+-193) (μg/m3) of fine particulate matter (or “tar” on some cigarette warnings) over a period of around 300 seconds (Gerber, et al.), and each puff contains 60 ml  or .00006 m3, and there are around 10-20 puffs on a cigarette (sizes vary from 60 mm to 100 mm in commercially sold products, the 60 mm will be used, as the most commonly used). This means that in a cigarette there is .0006-.0012 m3 of smoke exposure, multiplied by the average 1525 (μg/m3) parts fine particulate matter yielding .72 μg of exposure. This multiplied by an average of 18 (+-8, depending on the state/smoker) cigarettes per day, delivering into the lung between 7 and 25 μg fine particulate matter exposure over the course of a day. This is the equivalent of standing in a closed garage with ten cars running for 30 minutes (Invernizzi et al.) to put it in perspective.
Is this enough to significantly change the risk for lung cancer or mortality, according to modern studies on air pollution, and assuming all other factors constant? Every 10 μg elevation in atmospheric fine particulate matter is associated with a decrease in life expectancy of .6 years which does fall within the realm of possibility of the decline of one to three years associated with tobacco use after adjustment for exercise mentioned earlier, but fails to explain why rats smoking similar amounts of tobacco lived 5% longer. To understand this, further investigation will be necessary into a couple confounding factors which may explain why tobacco smoke has a greater deleterious effect on humans than rats, when physically the pulmonary systems should react in step with each other.

Ferrucci, Luigi, et al. “Smoking, physical activity, and active life expectancy.” American Journal of Epidemiology 149.7 (1999): 645-653.

Gerber, Alexander, et al. “Tobacco smoke particles and indoor air quality (ToPIQ-II)–a modified study protocol and first results.” Journal of Occupational Medicine and Toxicology 1 (2015): 5.

Invernizzi, Giovanni, et al. “Particulate matter from tobacco versus diesel car exhaust: an educational perspective.” Tobacco control 13.3 (2004): 219-221.

Pope III, C. Arden, Majid Ezzati, and Douglas W. Dockery. “Fine-particulate air pollution and life expectancy in the United States.” New England Journal of Medicine 360.4 (2009): 376-386.

Zacny, James P., et al. “Human cigarette smoking: effects of puff and inhalation parameters on smoke exposure.” Journal of Pharmacology and Experimental Therapeutics 240.2 (1987): 554-564.

Effect of nicotine, alcohol, and THC on vein diameter

Nicotine shown to have half the constrictive properties on veins as alcohol, and marijuana actually will make them bigger (with vasorelaxatory properties identified in THC)!

Nicotine and vein constriction:
“Smoking was associated with significant changes in the aortic pressure-diameter relation that denote deterioration of the elastic properties and were maintained during the whole study period: the slope of the pressure-diameter loop became steeper (baseline, 35.43±1.38; minute 1, 45.26±1.65; peak at minute 10, 46.36±1.69 mm Hg/mm; P<.001) and aortic distensibility decreased (baseline, 2.08±0.12; minute 1, 1.60±0.08; nadir at minute 5, 1.54±0.07×10−6 cm2·dyne−1P<.001). In contrast, no changes in aortic elasticity indexes were observed with sham smoking."

Alcohol and vein constriction:
“Blood ethanol levels achieved at 60, 120, and 180 minutes were 649+-48, 1,285±81, and 2,546+-130jug/ml, respectively. LAD cross-sectional area was reduced significantly from control at the end of each of the three dosing periods (-24± 5%, -40± 3%, and -53±.3%; p<0.004). a-Adrenergic blockade had no effecton LAD cross-sectional area, while nicardipine partially reversed the ethanol-induced vasoconstriction. No significant change in vessel cross-sectional area took place in control dogs."
Marijuana and vein relaxation:
“The present results provide strong evidence that THC is a PPARγ ligand, stimulation of which causes time-dependent vasorelaxation”
This results in a lower blood pressure and better athletic performance.

Desensitization, Fear, and the Promise of Courage in Ordinary Men

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