Tobacco smoke

Tobacco smoke is an aerosol produced by the incomplete combustion of tobacco during the smoking of cigarettes and other tobacco products. Temperatures in burning cigarettes range from about 400 °C between puffs to about 900 °C during a puff. During the burning of the cigarette tobacco (itself a complex mixture), thousands of chemical substances are generated by combustion, distillation, pyrolysis and pyrosynthesis.[1][2] Tobacco smoke is used as a fumigant and inhalant.


The particles in tobacco smoke are liquid aerosol droplets (~ 20% water), with a mass median aerodynamic diameter (MMAD) that is submicrometer (and thus, fairly "lung-respirable" by humans). The droplets are present in high concentrations (some estimates are as high as 1010 droplets per cm3). Most cigarettes today contain a cigarette filter, which can reduce "tar" and nicotine smoke yields up to 50% by several different mechanisms, with an even greater removal rate for other classes of compounds (e.g., phenols).[1]

Tobacco smoke may be grouped into a particulate phase (trapped on a glass-fiber pad, and termed "TPM" (total particulate matter)) and a gas/vapor phase (which passes through such a glass-fiber pad). "Tar" is mathematically determined by subtracting the weight of the nicotine and water from the TPM. However, several components of tobacco smoke (e.g., hydrogen cyanide, formaldehyde, phenanthrene, and pyrene) do not fit neatly into this rather arbitrary classification, because they are distributed among the solid, liquid and gaseous phases.[1]

Tobacco smoke contains a number of toxicologically significant chemicals and groups of chemicals, including polycyclic aromatic hydrocarbons (benzopyrene), tobacco-specific nitrosamines (NNK, NNN), aldehydes (acrolein, formaldehyde), carbon monoxide, hydrogen cyanide, nitrogen oxides, benzene, toluene, phenols (phenol, cresol), aromatic amines (nicotine, ABP (4-Aminobiphenyl)), and harmala alkaloids.[3] The radioactive element polonium-210 is also known to occur in tobacco smoke.[1] The chemical composition of smoke depends on puff frequency, intensity, volume, and duration at different stages of cigarette consumption.[4]

Between 1933 and the late 1940s, the yields from an average cigarette varied from 33 to 49 mg "tar" and from < 1 to 3 mg nicotine. However, in the 1960s and 1970s, the average yield from cigarettes in Western Europe and the USA was around 16 mg tar and 1.5 mg nicotine per cigarette. Current average levels are lower.[5] This has been achieved in a variety of ways including use of selected strains of tobacco plant, changes in agricultural and curing procedures, use of reconstituted sheets (reprocessed tobacco leaf wastes), incorporation of tobacco stalks, reduction of the amount of tobacco needed to fill a cigarette by expanding it (like puffed wheat) to increase its "filling power", and by the use of filters and high-porosity wrapping papers.[6] The development of lower "tar" and nicotine cigarettes has tended to yield products that lacked the taste components to which the smoker had become accustomed. In order to keep such products acceptable to the consumer, the manufacturers reconstitute aroma or flavor.[4]

Tumorigenic agents

Tumorigenic agents in tobacco and tobacco smoke
Compounds In processed tobacco, per gram In mainstream smoke, per cigarette IARC evaluation of evidence of carcinogenicity
In laboratory animals In humans
Polycyclic aromatic hydrocarbons
Benz(a)anthracene   20–70 ng sufficient  
Benzo(b)fluoranthene   4–22 ng sufficient  
Benzo(j)fluoranthene   6–21 ng sufficient  
Benzo(k)fluoranthene   6–12 ng sufficient  
Benzo(a)pyrene 0.1–90 ng 20–40 ng sufficient probable
Chrysene   40–60 ng sufficient  
Dibenz(a,h)anthracene   4 ng sufficient  
Dibenzo(a,i)pyrene   1.7–3.2 ng sufficient  
Dibenzo(a,l)pyrene   present sufficient  
Indeno(1,2,3-c,d)pyrene   4–20 ng sufficient  
5-Methylchrysene   0.6 ng sufficient  
Quinoline 1–2 μg      
Dibenz(a,h)acridine   0.1 ng sufficient  
Dibenz(a,j)acridine   3–10 ng sufficient  
7H-Dibenzo(c,g)carbazole   0.7 ng sufficient  
N-Nitrosodimethylamine 0–215 ng 0.1–180 ng sufficient  
N-Nitrosoethylmethylamine   3–13 ng sufficient  
N-Nitrosodiethylamine   0–25 ng sufficient  
N-Nitrosonornicotine 0.3–89 μg 0.12–3.7 μg sufficient  
4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone 0.2–7 μg 0.08–0.77 μg sufficient  
N-Nitrosoanabasine 0.01–1.9 μg 0.14–4.6 μg limited  
N-Nitrosomorpholine 0–690 ng   sufficient  
Aromatic amines
2-Toluidine   30–200 ng sufficient inadequate
2-Naphthylamine   1–22 ng sufficient sufficient
4-Aminobiphenyl   2–5 ng sufficient sufficient
Formaldehyde 1.6–7.4 μg 70–100 μg sufficient  
Acetaldehyde 1.4–7.4 μg 18–1400 μg sufficient  
Crotonaldehyde 0.2–2.4 μg 10–20 μg    
Miscellaneous organic compounds
Benzene   12–48 μg sufficient sufficient
Acrylonitrile   3.2–15 μg sufficient limited
1,1-Dimethylhydrazine 60–147 μg   sufficient  
2-Nitropropane   0.73–1.21 μg sufficient  
Ethyl carbamate 310–375 ng 20–38 ng sufficient  
Vinyl chloride   1–16 ng sufficient sufficient
Inorganic compounds
Hydrazine 14–51 ng 24–43 ng sufficient inadequate
Arsenic 500–900 ng 40–120 ng inadequate sufficient
Nickel 2000–6000 ng 0–600 ng sufficient limited
Chromium 1000–2000 ng 4–70 ng sufficient sufficient
Cadmium 1300–1600 ng 41–62 ng sufficient limited
Lead 8–10 μg 35–85 ng sufficient inadequate
Polonium-210 0.2–1.2 pCi 0.03–1.0 pCi sufficient sufficient


Tobacco smoke, besides being an irritant and significant indoor air pollutant, is known to cause lung cancer, heart disease, chronic obstructive pulmonary disease (COPD), emphysema, and other serious diseases in smokers ( and in non-smokers as well). The actual mechanisms by which smoking can cause so many diseases remain largely unknown. Many attempts have been made to produce lung cancer in animals exposed to tobacco smoke by the inhalation route, without success. It is only by collecting the "tar" and repeatedly painting this on to mice that tumors are produced, and these tumors are very different from those tumors exhibited by smokers.[1] Tobacco smoke is associated with an increased risk of developing respiratory conditions such as bronchitis, pneumonia, and asthma. Tobacco smoke aerosols generated at temperatures below 400 ℃ did not test positive in the Ames assay.[7]

In spite of all changes in cigarette design and manufacturing over the last 50 years, the use of filters and "light" cigarettes has neither decreased the nicotine intake per cigarette, nor has it lowered the incidence of lung cancers (NCI, 2001; IARC 83, 2004; U.S. Surgeon General, 2004).[8] The shift over the years from higher- to lower-yield cigarettes may explain the change in the pathology of lung cancer. That is, the percentage of lung cancers that are adenocarcinomas has increased, while the percentage of squamous cell cancers has decreased. The change in tumor type is believed to reflect the higher nitrosamine delivery of lower-yield cigarettes and the increased depth or volume of inhalation of lower-yield cigarettes to compensate for lower level concentrations of nicotine in the smoke.[9]

In the United States, lung cancer incidence and mortality rates are particularly high among African American men. Lung cancer tends to be most common in developed countries, particularly in North America and Europe, and less common in developing countries, particularly in Africa and South America.[8] Over 85% of all lung cancers are attributed to cigarette smoking; however, only a fraction of long-term cigarette smokers develop lung cancer. Cancer of the lung is occasionally observed among nonsmokers, indicating a genetic susceptibility in lung tumorigenesis. The incidence of lung cancer seems to have increased in dogs as well as in humans and cigarette smoking can hardly be incriminated.[10]

Tobacco polyphenols (e. g., caffeic acid, chlorogenic acid, scopoletin, rutin) determine the taste and quality of the smoke. Freshly cured tobacco leaf is unfit for use because of its pungent and irritating smoke. After fermentation and aging, the leaf delivers mild and aromatic smoke.[11]

Plant smoke in general has a bacteriostatic effect and is one of the oldest methods of preserving meat (along with salting, adding sugar, and drying).

Nicotine hypothesis

According to the mainstream "nicotine hypothesis", nicotine is the main biochemical reason for tobacco smoking. Nicotine is similar to acetylcholine, an important neurotransmitter. The uptake of nicotine may be facilitated by other chemicals present in tobacco smoke. However, the nicotine theory cannot explain the following contradictions:[12]

  • Nicotine alone does not seem capable of totally substituting for cigarette smoke.
  • Lettuce cigarettes reinforced with nicotine were not accepted more readily than non-nicotine cigarettes (however, marijuana cigarettes are an exception).
  • Nicotine given either by ingestion or intravenously was incapable of completely suppressing smoking in humans.
  • Animals will not self-inject nicotine or do so only indifferently, whereas they will self-inject cocaine and amphetamine very readily.
  • If nicotine were a reinforcer for smoking, smokers would not be expected to like low-nicotine cigarettes.

Other possibilities are various neurotransmitter-like psychoactive aromatic amines (amphetamines, indole-based synthetic cannabinoids, ergine-type alkaloids), synthesized randomly by pyrolysis and pyrosynthesis during smoking and found in various plant smoke condensates. Nicotine itself may serve as a template for further psychoactive compounds.

Peak plasma levels of nicotine occur 2–10 min after smoking tobacco. Nicotine undergoes a large first-pass effect during which the liver metabolizes 80–90%. Protein binding ranges from 4.9% to 20%. The apparent volume of distribution varies between 1 and 3 l/kg. The metabolites include isomethylnicotinium ion, nornicotine, cotinine, and nicotine-1-N-oxide. Nicotine passes into breast milk in small quantities.[7] In addition to nicotine, tobacco smoke contains small amounts of the alkaloids anatabine, anabasine, nornicotine, N-methylanabasine, anabaseine, nicotine N'-oxide, myosmine, β-nicotyrine, cotinine, and 2,3'-bipyridyl.[13]

The nicotine molecule contains two nitrogen atoms with basic properties. The nicotine molecule can thus add one proton to form a monoprotonated species or two protons to form the diprotonated species. Nicotine in tobacco smoke exists in either a protonated or unprotonated form, depending on the presence of natural acids and bases, the tobacco blend, tip ventilation, and the use of additives. Whereas protonated nicotine is positively charged and not volatile, unprotonated nicotine ("free-base nicotine") from tobacco smoke is volatile and readily passes into lipid cell membranes. More unprotonated nicotine in a puff delivers more nicotine to the brain. The same holds true for other (tobacco and non-tobacco) alkaloids. The approximate dividing line between dominance by protonated forms or by the unprotonated form is a pH of 8. At pH 8, the two fractions are present in equal parts. At any lower pH, the fraction of protonated nicotine is greater.[13]

More unprotonated nicotine in tobacco smoke increases smoke "strength", "impact", or "kick". However, the irritation and harshness of smoke at higher pH makes it harder for smokers to inhale it. Cigarette design ensures that the smoke has enough unprotonated nicotine to rapidly transfer nicotine into the brain but not so much of it as to be too harsh for the smoker. Variability in the acid-base nature of tobacco leaf is considerable. Flue-cured ("bright") tobacco typically produces acidic smoke, whereas air-cured ("burley") tobacco typically produces basic smoke. The natural acids in tobacco smoke (e.g., formic acid, acetic acid, and propionic acid) can protonate nicotine, while the natural bases (e.g., ammonia) tend to neutralize the acids and keep more nicotine in the unprotonated form. Acidic tobacco additives such as levulinic acid are used as "smoothing" agents to reduce smoke harshness.[13]

See also


  1. Robert Kapp (2005), "Tobacco Smoke", Encyclopedia of Toxicology, Volume 4 (2nd ed.), Elsevier, pp. 200–202, ISBN 978-0-12-745354-5
  2. Ken Podraza (29–30 October 2001), Basic Principles of Cigarette Design and Function (PDF), Philip Morris USA
  3. "Harmala Alkaloid". Science Direct. Elsevier B.V. Retrieved 26 November 2017.
  4. The Health Consequences of Smoking: The Changing Cigarette (PDF), U.S. Dept. of Health and Human Services, p. 49
  5. K. Rothwell; et al. (1999), Health effects of interactions between tobacco use and exposure to other agents, Environmental Health Criteria, World Health Organization
  6. Michael A. H. Russell (1977), "Smoking Problems: An Overview", in Murray E. Jarvik; Joseph W. Cullen; Ellen R. Gritz; Thomas M. Vogt; Louis Jolyon West (eds.), Research on Smoking Behavior (PDF), NIDA Research Monograph, pp. 13–34, archived from the original (PDF) on 2015-07-23
  7. C Lynn Humbertson (2005), "Tobacco", in Philip Wexler (ed.), Encyclopedia of Toxicology, 4 (2nd ed.), Elsevier, pp. 197–200, ISBN 978-0-12-745354-5
  8. Anthony J. Alberg; Jonathan M. Samet (2010), "Epidemiology of Lung Cancer", in Robert J. Mason; V. Courtney Broaddus; Thomas R. Martin; Talmadge E. King, Jr.; Dean E. Schraufnagel; John F. Murray; Jay A. Nadel (eds.), Murray and Nadel's Textbook of Respiratory Medicine, 1 (5th ed.), Saunders, ISBN 978-1-4160-4710-0
  9. Neal L. Benowitz; Paul G. Brunetta (2010), "Smoking Hazards and Cessation", in Robert J. Mason; V. Courtney Broaddus; Thomas R. Martin; Talmadge E. King, Jr.; Dean E. Schraufnagel; John F. Murray; Jay A. Nadel (eds.), Murray and Nadel's Textbook of Respiratory Medicine, 1 (5th ed.), Saunders, ISBN 978-1-4160-4710-0
  10. Julien L. Van Lancker (1977), "Smoking and Disease", in Murray E. Jarvik; Joseph W. Cullen; Ellen R. Gritz; Thomas M. Vogt; Louis Jolyon West (eds.), Research on Smoking Behavior (PDF), NIDA Research Monograph, 17, pp. 230–280, archived from the original (PDF) on 2015-07-23
  11. T. C. Tso (2007), "Tobacco", Ullmann's Encyclopedia of Industrial Chemistry (7th ed.), Wiley, pp. 1–26, doi:10.1002/14356007.a27_123, ISBN 978-3527306732
  12. Murray E. Jarvik (1977), "Biological Factors Underlying the Smoking Habit", in Murray E. Jarvik; Joseph W. Cullen; Ellen R. Gritz; Thomas M. Vogt; Louis Jolyon West (eds.), Research on Smoking Behavior (PDF), NIDA Research Monograph, pp. 122–148, archived from the original (PDF) on 2015-07-23
  13. "Chemistry and Toxicology of Cigarette Smoke and Biomarkers of Exposure and Harm" (PDF), How Tobacco Smoke Causes Disease, U.S. Department of Health and Human Services, 2010, pp. 27–102, ISBN 978-0-16-084078-4
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