What`s In A Cigarettes
A cigarette (French “small cigar”, from cigar + -ette) is a small roll of finely-cut tobacco leaves wrapped in a cylinder of thin paper for smoking. The cigarette is ignited at one end and allowed to smoulder; its smoke is inhaled from the other end, which is held in or to the mouth. Most modern manufactured cigarettes are filtered and include reconstituted tobacco and other additives. Cigarettes are sometimes smoked with a cigarette holder.
The term cigarette, as commonly used, refers to a tobacco cigarette but can apply to similar devices containing other herbs, such as cannabis. A cigarette is distinguished from a cigar by its smaller size, use of processed leaf, and paper wrapping, which is normally white, though other colors are occasionally available. Cigars are typically composed entirely of whole-leaf tobacco.
Rates of cigarette smoking vary widely. While rates of smoking have leveled off or declined in the developed world, they continue to rise in developing nations. Nicotine, the primary psychoactive chemical in cigarettes, has been shown to be addictive. Statistically each cigarette smoked shortens the user’s lifespan by 11 minutes. About half of cigarette smokers die of tobacco-related disease and lose on average 14 years of life. Cigarette use by pregnant women has also been shown to cause birth defects, including mental and physical disabilities. Secondhand smoke from cigarettes has been shown to be injurious to bystanders, which has led to legislation that has banned their smoking in many workplaces and public areas.
Cigarettes are the most frequent source of fires in private homes, which has prompted the European Union and the United States to ban cigarettes that are not fire standard compliant by 2011.
A reproduction of a carving from the temple at Palenque, Mexico, depicting a Mayan priest smoking from a smoking tube.
The earliest forms of cigarettes have been attested in Central America around the 9th century in the form of reeds and smoking tubes. The Maya, and later the Aztecs, smoked tobacco and various psychoactive drugs in religious rituals and frequently depicted priests and deities smoking on pottery and temple engravings. The cigarette, and the cigar, were the most common method of smoking in the Caribbean, Mexico and Central and South America until recent times.
The South and Central American cigarette used various plant wrappers; when it was brought back to Spain, maize wrappers were introduced, and by the seventeenth century, fine paper. The resulting product was called papelate and is documented in Goya’s paintings La Cometa, La Merienda en el Manzanares, and El juego de la pelota a pala (18th century).
By 1830, the cigarette had crossed into France, where it received the name cigarette; and in 1845, the French state tobacco monopoly began manufacturing them.
In the Georges Bizet opera Carmen, which was set in Spain in the 1830s, the title character Carmen was at first a worker in a cigarette factory.
In the English-speaking world, the use of tobacco in cigarette form became increasingly popular during and after the Crimean War, when British soldiers began emulating their Ottoman Turkish comrades and Russian enemies. This was helped by the development of tobaccos that are suitable for cigarette use, and by the development of the Egyptian cigarette export industry.
The widespread smoking of cigarettes in the Western world is largely a 20th century phenomenon – at the start of the century the per capita annual consumption in the USA was 54 cigarettes (equivalent to less than 0.5% of the population smoking more than 100 cigarettes per year), and consumption there peaked at 4,259 per capita in 1965. At that time about 50% of men and 33% of women smoked (defined as smoking more than 100 cigarettes per year). By 2000, consumption had fallen to 2,092 per capita, corresponding to about 30% of men and 22% of women smoking more than 100 cigarettes per year, and by 2006 per capita consumption had declined to 1,691; implying that about 21% of the population smoked 100 cigarettes or more per year.
During World War I and World War II, cigarettes were rationed to soldiers. During the second half of the 20th century, the adverse health effects of cigarettes started to become widely known and text-only health warnings became commonplace on cigarette packets. The United States has not yet implemented graphical cigarette warning labels, which are considered a more effective method to communicate to the public the dangers of cigarette smoking. Canada, India, Australia, and New Zealand, however, have both textual warnings and graphic visual images displaying, among other things, the damaging effects tobacco use has on the human body.
The cigarette has evolved much since its conception; for example, the thin bands that travel transverse to the “axis of smoking” (thus forming circles along the length of the cigarette) are alternate sections of thin and thick paper to facilitate effective burning when being drawn, and retard burning when at rest. Synthetic particulate filters remove some of the tar before it reaches the smoker.
Diagram of a cigarette.
1. Filter made of 95% cellulose acetate.
2. Tipping paper to cover the filter.
3. Rolling paper to cover the tobacco.
4. Tobacco blend.
Commercially manufactured cigarettes are seemingly simple objects consisting mainly of a tobacco blend, paper, PVA glue to bond the outer layer of paper together, and often also a cellulose acetate–based filter. While the assembly of cigarettes is straightforward, much focus is given to the creation of each of the components, in particular the tobacco blend, which may contain over 600 ingredients, many of them flavourants for the tobacco. A key ingredient that makes cigarettes more addictive is the inclusion of reconstituted tobacco, which has additives to make nicotine more volatile as the cigarette burns.
The paper for holding the tobacco blend may vary in porosity to allow ventilation of the burning ember or contain materials that control the burning rate of the cigarette and stability of the produced ash. The papers used in tipping the cigarette (forming the mouthpiece) and surrounding the filter stabilise the mouthpiece from saliva and moderate the burning of the cigarette as well as the delivery of smoke with the presence of one or two rows of small laser-drilled air holes.
According to Simon Chapman, a professor of public health at the University of Sydney, the burning agents in cigarette paper are responsible for fires and reducing them would be a simple and effective means of dramatically reducing the ignition propensity of cigarettes. Since 1980s Philip Morris and R.J. Reynolds developed fire-safe cigarettes but did not market them.
The burn rate of cigarette paper is regulated through the application of different forms of microcrystalline cellulose to the paper. Cigarette paper has been specially engineered by creating bands of different porosity to create “fire-safe” cigarettes. These cigarettes have a reduced idle burning speed which allows them to self-extinguish. This fire-safe paper is manufactured by mechanically altering the setting of the paper slurry.
New York was the first U.S. state to mandate that all cigarettes manufactured or sold within the state comply with a fire-safe standard. Canada has passed a similar nation-wide mandate based on the same standard. All U.S. states have passed fire-safe mandates.
European union wishes to ban in 2011 cigarettes that are not fire-safe. According to a study made by European Union in 16 European countries, 11,000 fires were due to cigarettes between 2005 and 2007. They caused 520 deaths and 1600 people injured 
The tobacco end of a cigarette
The process of blending, like the blending of scotch and cognac, gives the end product a consistent taste from batches of tobacco grown in different areas of a country that may change in flavour profile from year to year due to different environmental conditions.
Modern cigarettes produced after the 1950s, although composed mainly of shredded tobacco leaf, use a significant quantity of tobacco processing by-products in the blend. Each cigarette’s tobacco blend is made mainly from the leaves of flue-cured brightleaf, burley tobacco, and oriental tobacco. These leaves are selected, processed, and aged prior to blending and filling. The processing of brightleaf and burley tobaccos for tobacco leaf “strips” produces several by-products such as leaf stems, tobacco dust, and tobacco leaf pieces (“small laminate”). To improve the economics of producing cigarettes, these by-products are processed separately into forms where they can then be possibly added back into the cigarette blend without an apparent or marked change in the cigarette’s quality. The most common tobacco by-products include:
- Blended leaf (BL) sheet: a thin, dry sheet cast from a paste made with tobacco dust collected from tobacco stemming, finely milled burley-leaf stem, and pectin.
- Reconstituted leaf (RL) sheet: a paper-like material made from recycled tobacco fines, tobacco stems and “class tobacco”, which consists of tobacco particles less than 30 mesh in size (~0.599 mm) that are collected at any stage of tobacco processing. RL is made by extracting the soluble chemicals in the tobacco by-products, processing the leftover tobacco fibres from the extraction into a paper, and then reapplying the extracted materials in concentrated form onto the paper in a fashion similar to what is done in paper sizing. At this stage ammonium additives are applied to make reconstituted tobacco an effective nicotine delivery system.
- Expanded (ES) or improved stems (IS): ES are rolled, flattened, and shredded leaf stems that are expanded by being soaked in water and rapidly heated. Improved stems follow the same process but are simply steamed after shredding. Both products are then dried. These two products look similar in appearance but are different in taste.
Whole tobacco can also be processed into a product called expanded tobacco. The tobacco is “puffed”, or expanded, by saturating it with supercritical carbon dioxide and heating the CO2 saturated tobacco to quickly evaporate the CO2. This quick change of physical state by the CO2 causes the tobacco to expand in a similar fashion as polystyrene foam. This is used to produce light cigarettes (“Lights”) by reducing the density of the tobacco and thus maintain the size of a cigarette while reducing the amount of tobacco used in each cigarette.
A recipe-specified combination of brightleaf, burley-leaf and oriental-leaf tobacco will be mixed with humectants such as propylene glycol or glycerol, as well as flavouring products and enhancers such as cocoa solids, licorice, tobacco extracts, and various sugars, which are known collectively as “casings”. The leaf tobacco will then be shredded, along with a specified amount of small laminate, expanded tobacco, BL, RL, ES and IS. A perfume-like flavour/fragrance, called the “topping” or “toppings”, which is most often formulated by flavor companies, will then be blended into the tobacco mixture to improve the consistency in flavour and taste of the cigarettes associated with a certain brand name. As well, they replace lost flavours due to the repeated wetting and drying used in processing the tobacco. Finally the tobacco mixture will be filled into cigarettes tubes and packaged.
In recent years, the manufacturers’ pursuit of maximum profits has led to the practice of using not just the leaves, but also recycled tobacco offal and the plant stem. The stem is first crushed and cut to resemble the leaf before being merged or blended into the cut leaf.
Cigarettes are a significant source of tax revenue in many localities. This fact has historically been an impediment for health groups seeking to discourage cigarette smoking, since governments seek to maximize tax revenues. Furthermore, some countries have made cigarettes a state monopoly, which has the same effect on the attitude of government officials outside the health field. In the United States, cigarettes are taxed quite heavily, but the states are a primary determinant of the total tax rate. Generally, states that rely on tobacco as a significant farm product tend to tax cigarettes at a low rate. It has been shown that higher prices for cigarettes discourage smoking. Every 10 percent increase in the price of cigarettes reduced youth smoking by about seven percent and overall cigarette consumption by about four percent. Thus increased cigarette taxes are proposed as a means to reduce smoking. Cigarette taxes range from $0.17 per pack in Missouri to $5.85 per pack in New York City. The federal government charges $1.01 per pack, which levied in conjunction with state and local cigarette taxes. In addition, consumers pay a sales tax on cigarettes in most U.S. jurisdictions.
In the UK, many people now illegally import cigarettes, or buy those illegally imported, due to the increasing tax. A packet is less than half the price in some other countries, making illegal importers a large profit, while still providing comparatively very cheap cigarettes. The average price for 20 legal cigarettes is £5.20, while imported packs are sold for less than £3; this is due to the fact that the large majority of the sale price of a legitimate pack is tax.
A Woolworths supermarket cigarette counter in New South Wales, Australia. Other Australian states currently prohibit such large displays.
Before the Second World War many manufacturers gave away collectible cards, one in each packet of cigarettes. This practice was discontinued to save paper during the war and was never generally reintroduced, though for a number of years Natural American Spirit cigarettes included “vignette” cards depicting endangered animals and American historical events; this series was discontinued in 2003. On April 1, 1970 President Richard Nixon signed the Public Health Cigarette Smoking Act into law, banning cigarette advertisements on television in the United States starting on January 2, 1971. However, some tobacco companies attempted to circumvent the ban by marketing new brands of cigarettes as “little cigars”; examples included Tijuana Smalls, which came out almost immediately after the ban took effect, and Backwoods Smokes, which reached the market in the winter of 1973–1974 and whose ads used the slogan, “How can anything that looks so wild taste so mild.”
In many parts of the world tobacco advertising and even sponsorship of sporting events has been outlawed. The ban on tobacco advertising and sponsorship in the EU in 2005 has prompted Formula One Management to look for races in areas that allow the tobacco sponsored teams to display their livery. As of 2007, only the Scuderia Ferrari retains tobacco sponsorship, continuing their relationship with Marlboro until 2011. In the United States, bolder advertising restrictions took effect on June 22, 2010.
In some jurisdictions, such as the Canadian provinces of Saskatchewan and Alberta, the retail store display of cigarettes is completely prohibited if persons under the legal age of consumption have access to the premises. In Ontario, Manitoba, and Quebec, Canada, the display of tobacco is prohibited for everyone, regardless of age, as of 2008. This includes non-cigarette products such as cigars and blunt wraps.
Typical pictogram indicating that smoking is permitted
Beginning on April 1, 1998, the sale of cigarettes and other tobacco products to people under 18 has been prohibited by law in all fifty states of the United States. The legal age of purchase has been additionally raised to 19 in Alabama, Alaska, New Jersey, Utah, and Nassau, Suffolk, and Onondaga counties in New York. The intended effect of this is to prevent upper class high school students from purchasing cigarettes for their younger peers. Legislation was pending as of 2004 in some other states. In Massachusetts, parents and guardians are allowed to give cigarettes to minors, but sales to minors are prohibited.
Similar laws exist in many other countries. In Canada, most of the provinces require smokers to be 19 years of age to purchase cigarettes (except for Quebec, Saskatchewan, Manitoba and Alberta, where the age is 18). However, the minimum age only concerns the purchase of tobacco, not use. Alberta, however, does have a law which prohibits the possession or use of tobacco products by all persons under 18, punishable by a $100 fine. Australia, New Zealand and Pakistan have a nationwide ban on the selling of all tobacco products to people under the age of 18.
Tabak-Trafik in Vienna. Since 1 January 2007, all cigarette machines in Austria must attempt to verify a customer’s age by requiring the insertion of a debit card or mobile phone verification.
Since 1 October 2007, it has been illegal for retailers to sell tobacco in all forms to people under the age of 18 in three of the UK’s four constituent countries (England, Wales and Scotland) (rising from 16). It is also illegal to sell lighters, rolling papers and all other tobacco-associated items to people under 18. It is not illegal for people under 18 to buy or smoke tobacco, just as it was not previously for people under 16; it is only illegal for the said retailer to sell the item. The age increase from 16 to 18 came into force in Northern Ireland on 1 September 2008. In the Republic of Ireland, bans on the sale of the smaller ten-packs and confectionery that resembles tobacco products (Candy cigarettes) came into force on May 31, 2007 in a bid to cut underaged smoking. The UK Department of Health plans to follow suit with the ten-pack ban.
Most countries in the world have a legal smoking age of 18. Six exceptions are Austria, Belgium, Denmark, Portugal, Switzerland and the Netherlands, where the age is 16. Since January 1, 2007, all cigarette machines in public places in Germany must attempt to verify a customer’s age by requiring the insertion of a debit card. Turkey, which has one of the highest percentage of smokers in its population, has a legal age of 18. Another curiosity is Japan, one of the highest tobacco-consuming nations, which requires purchasers to be 20 years of age (suffrage in Japan is 20 years old). Beginning in July 2008, Japan will enforce this age limit at cigarette vending machines through use of the taspo smart card. In other countries, such as Egypt, it is legal to use and purchase tobacco products regardless of age. Germany raised the purchase age from 16 to 18 on the 1 September 2007.
Some police departments in the United States occasionally send an underaged teenager into a store where cigarettes are sold, and have the teen attempt to purchase cigarettes, with their own or no ID. If the vendor then completes the sale, the store is issued a fine. Similar enforcement practices are regularly performed by Trading Standards Officers in the UK and the Gardaí Siochana, the police force of the Republic of Ireland.
As of 2002, Approximately 5.5 trillion cigarettes are produced globally each year and are smoked by over 1.1 billion people or greater than one-sixth of the world population. While smoking rates have leveled off or declined in developed nations, they continue to rise in developing parts of the world. Smoking rates in the United States have dropped by half from 1965 to 2006 falling from 42% to 20.8% of adults. In the developing world, tobacco consumption is rising by 3.4% per year.
Source: World Health Organization estimates, 2000
Nicotine, the primary psychoactive chemical in cigarettes, is addictive. Cigarette use by pregnant women has also been shown to cause birth defects (which include mental and physical disability). On average, each cigarette smoked shortens lifespan by 11 minutes and half of smokers die early of tobacco-related disease and lose, on average, 14 years of life.
Graphics on cigarette packets
Some countries require cigarette packs to contain warnings about health. The United States was one of the first. Other countries include Canada, most of Europe, Australia and in Asia (e.g. Hong Kong and Singapore). Since 2000, many developed countries began requiring graphic pictorial warning labels on a large portion of the front and back of each pack. Canada is the first country to enforced graphic warning on cigarette packaging. Such labels will be mandated in the United States in 2012.
Many governments impose restrictions on smoking tobacco, especially in public areas. The primary justification has been the negative health effects of secondhand smoke. Laws vary by country and locality. See:
- Smoking age
- Smoking bans
- Smoking bans by country
- Smoking bans in private vehicles
A discarded cigarette butt, lying on dirty snow.
The common name for the remains of a cigarette after smoking is a “(cigarette) butt”. The butt typically comprises about 30% of the cigarette’s original length. It consists of a tissue tube which holds a filter and some remains of tobacco mixed with ash. In extreme cases the filter is slightly burned. Cigarette butts are one source of tobacco for minors and low income people. The shape of a butt hinges on the manner of stubbing out. The intensely pressed butt possesses irregular shape at the end and wrinkled tissue. Cigarette butts may be a subject of studies over popularity of brands producing cigarettes.
A cigarette disposal canister, encouraging the public to dispose of their cigarettes properly.
Cigarette filters are made from cellulose acetate and are biodegradable, however depending on environmental conditions they can be resistant to degradation. Accordingly, the duration of the degradation process is cited as taking as little as 1 month to 3 years to as long as 10–15 years. One campaign group has suggested they never fully biodegrade.
This variance in rate and resistance to biodegradation in many conditions is a factor in littering and environmental damage. It is estimated that 4.5 trillion cigarette butts become litter every year. In the 2006 International Coastal Cleanup, cigarettes and cigarette butts constituted 24.7% of the total collected pieces of garbage, over twice as many as any other category.
Cigarette butts contain the chemicals filtered from cigarettes and can leach into waterways and water supplies.
Cellulose acetate and carbon particles breathed in from cigarette filters is suspected of causing lung damage.
Smouldering cigarette butts have also been blamed for triggering fires from residential fires to major wildfires and bushfires which have caused major property damage and also death as well as disruption to services by triggering alarms and warning systems.
Many governments have sanctioned stiff penalties for littering of cigarette butts, Washington State imposes a penalty of $1024.
Cigarette butt is one of the most commonly found litters on the street. Most high-rise littering also relates to cigarette butts.
Electronic cigarettes are nicotine delivery devices that closely resemble cigarettes but produce no smoke. Due to the novelty of the devices, the health effects of electronic cigarettes are unknown. These devices are illegal in some countries, such as New Zealand, Australia, and Singapore. In other countries, these devices require government approval before these products can be sold, such as Canada and Denmark.
Selected cigarette brands
Cigarette Components :
|Systematic (IUPAC) name|
|ATC code||N07BA01 QP53AX13|
|Mol. mass||162.26 g/mol|
|SMILES||eMolecules & PubChem|
|Melt. point||-79 °C (-110 °F)|
|Boiling point||247 °C (477 °F)|
|Bioavailability||20 to 45% (oral)|
|Legal status||Unscheduled (AU) ? (UK) ? (US)|
|Dependence Liability||Medium to high|
|Routes||smoked (as smoking tobacco, mapacho, etc.), insufflated (as tobacco snuff or nicotine nasal spray), chewed (as nicotine gum, tobacco gum or chewing tobacco), transdermal (as nicotine patch, nicogel or topical tobacco paste), intrabuccal (as dipping tobacco, snuffs, dissolvable tobacco or creamy snuff), vaporized (as electronic cigarette, etc.), directly inhaled (as nicotine inhaler), oral (as nicotini)|
Nicotine is an alkaloid found in the nightshade family of plants (Solanaceae) that constitutes approximately 0.6–3.0% of dry weight of tobacco, with biosynthesis taking place in the roots and accumulation occurring in the leaves. It functions as an antiherbivore chemical with particular specificity to insects; therefore nicotine was widely used as an insecticide in the past, and currently nicotine analogs such as imidacloprid continue to be widely used.
In low concentrations (an average cigarette yields about 1 mg of absorbed nicotine), the substance acts as a stimulant in mammals and is the main factor responsible for the dependence-forming properties of tobacco smoking. According to the American Heart Association, the “nicotine addiction has historically been one of the hardest addictions to break.” The pharmacological and behavioral characteristics that determine tobacco addiction are similar to those that determine addiction to drugs such as heroin and cocaine. Nicotine content in cigarettes has slowly increased over the years, and one study found that there was an average increase of 1.6% per year between the years of 1998 and 2005. This was found for all major market categories of cigarettes.
History and name
Nicotine is named after the tobacco plant Nicotiana tabacum which in turn is named after Jean Nicot de Villemain, French ambassador in Portugal, who sent tobacco and seeds from Brazil to Paris in 1560 and promoted their medicinal use. Nicotine was first isolated from the tobacco plant in 1828 by German chemists Posselt & Reimann, who considered it a poison. Its chemical empirical formula was described by Melsens in 1843, its structure was discovered by Garry Pinner in 1893, and it was first synthesized by A. Pictet and Crepieux in 1904.
Nicotine is a hygroscopic, oily liquid that is miscible with water in its base form. As a nitrogenous base, nicotine forms salts with acids that are usually solid and water soluble. Nicotine easily penetrates the skin. As shown by the physical data, free base nicotine will burn at a temperature below its boiling point, and its vapors will combust at 308 K (35 °C; 95 °F) in air despite a low vapor pressure. Because of this, most of the nicotine is burned when a cigarette is smoked; however, enough is inhaled to provide the desired effects. The amount of nicotine inhaled with tobacco smoke is a fraction of the amount contained in the tobacco leaves.
Nicotine is optically active, having two enantiomeric forms. The naturally occurring form of nicotine is levorotatory, with [α]D = –166.4°. The dextrorotatory form, (+)-nicotine, has only one-half the physiological activity of (–)-nicotine. It is therefore weaker in the sense that a higher dose is required to attain the same effects. The salts of (+)-nicotine are usually dextrorotatory.
As nicotine enters the body, it is distributed quickly through the bloodstream and can cross the blood-brain barrier. On average it takes about seven seconds for the substance to reach the brain when inhaled. The half life of nicotine in the body is around two hours.
The amount of nicotine absorbed by the body from smoking depends on many factors, including the type of tobacco, whether the smoke is inhaled, and whether a filter is used. For chewing tobacco, dipping tobacco, snus and snuff, which are held in the mouth between the lip and gum, or taken in the nose, the amount released into the body tends to be much greater than smoked tobacco. Nicotine is metabolized in the liver by cytochrome P450 enzymes (mostly CYP2A6, and also by CYP2B6). A major metabolite is cotinine.
Other primary metabolites include nicotine N’-oxide, nornicotine, nicotine isomethonium ion, 2-hydroxynicotine and nicotine glucuronide.
Glucuronidation and oxidative metabolism of nicotine to cotinine are both inhibited by menthol, an additive to mentholated cigarettes, thus increasing the half-life of nicotine in vivo.
Detection of use
Nicotine can be quantified in blood, plasma, or urine to confirm a diagnosis of poisoning or to facilitate a medicolegal death investigation. Urinary or salivary cotinine concentrations are frequently measured for the purposes of pre-employment and health insurance medical screening programs. Careful interpretation of results is important, since passive exposure to cigarette smoke can result in significant accumulation of nicotine, followed by the appearance of its metabolites in various body fluids. Interestingly, nicotine use is not regulated in competitive sports programs, yet the drug has been shown to have a significant beneficial effect on athletic performance.
A 21 mg patch applied to the left arm. The Cochrane Collaboration finds that NRT increases a quitter’s chance of success by 50 to 70%. But in 1990, researchers found that 93% of users returned to smoking within six months.
Nicotine acts on the nicotinic acetylcholine receptors, specifically the ganglion type nicotinic receptor and one CNS nicotinic receptor. The former is present in the adrenal medulla and elsewhere, while the latter is present in the central nervous system (CNS). In small concentrations, nicotine increases the activity of these receptors. Nicotine also has effects on a variety of other neurotransmitters through less direct mechanisms.
By binding to nicotinic acetylcholine receptors, nicotine increases the levels of several neurotransmitters – acting as a sort of “volume control”. It is thought that increased levels of dopamine in the reward circuits of the brain are responsible for the euphoria and relaxation and eventual addiction caused by nicotine consumption. Nicotine has a higher affinity for acetylcholine receptors in the brain than those in skeletal muscle, though at toxic doses it can induce contractions and respiratory paralysis. Nicotine’s selectivity is thought to be due to a particular amino acid difference on these receptor subtypes.
Tobacco smoke contains the monoamine oxidase inhibitors harman, norharman, anabasine, anatabine, and nornicotine. These compounds significantly decrease MAO activity in smokers. MAO enzymes break down monoaminergic neurotransmitters such as dopamine, norepinephrine, and serotonin.
Chronic nicotine exposure via tobacco smoking up-regulates alpha4beta2* nAChR in cerebellum and brainstem regions but not habenulopeduncular structures. Alpha4beta2 and alpha6beta2 receptors, present in the ventral tegmental area, play a crucial role in mediating the reinforcement effects of nicotine.
Nicotine also activates the sympathetic nervous system, acting via splanchnic nerves to the adrenal medulla, stimulates the release of epinephrine. Acetylcholine released by preganglionic sympathetic fibers of these nerves acts on nicotinic acetylcholine receptors, causing the release of epinephrine (and norepinephrine) into the bloodstream. Nicotine also has an affinity for melanin-containing tissues due to its precursor function in melanin synthesis or its irreversible binding of melanin and nicotine. This has been suggested to underlie the increased nicotine dependence and lower smoking cessation rates in darker pigmented individuals.
In adrenal medulla
By binding to ganglion type nicotinic receptors in the adrenal medulla nicotine increases flow of adrenaline (epinephrine), a stimulating hormone and neurotransmitter. By binding to the receptors, it causes cell depolarization and an influx of calcium through voltage-gated calcium channels. Calcium triggers the exocytosis of chromaffin granules and thus the release of epinephrine (and norepinephrine) into the bloodstream. The release of epinephrine (adrenaline) causes an increase in heart rate, blood pressure and respiration, as well as higher blood glucose levels.
Side effects of nicotine.
Cotinine is a byproduct of the metabolism of nicotine which remains in the blood for up to 48 hours. It can therefore be used as an indicator of a person’s exposure to nicotine.
Nicotine’s mood-altering effects are different by report: in particular it is both a stimulant and a relaxant. First causing a release of glucose from the liver and epinephrine (adrenaline) from the adrenal medulla, it causes stimulation. Users report feelings of relaxation, sharpness, calmness, and alertness. By reducing the appetite and raising the metabolism, some smokers may lose weight as a consequence.
When a cigarette is smoked, nicotine-rich blood passes from the lungs to the brain within seven seconds and immediately stimulates the release of many chemical messengers including acetylcholine, norepinephrine, epinephrine, vasopressin, arginine, dopamine, autocrine agents, and beta-endorphin. This release of neurotransmitters and hormones is responsible for most of nicotine’s effects. Nicotine appears to enhance concentration and memory due to the increase of acetylcholine. It also appears to enhance alertness due to the increases of acetylcholine and norepinephrine. Arousal is increased by the increase of norepinephrine. Pain is reduced by the increases of acetylcholine and beta-endorphin. Anxiety is reduced by the increase of beta-endorphin. Nicotine also extends the duration of positive effects of dopamine and increases sensitivity in brain reward systems. Most cigarettes (in the smoke inhaled) contain 1 to 3 milligrams of nicotine.
Research suggests that, when smokers wish to achieve a stimulating effect, they take short quick puffs, which produce a low level of blood nicotine. This stimulates nerve transmission. When they wish to relax, they take deep puffs, which produce a high level of blood nicotine, which depresses the passage of nerve impulses, producing a mild sedative effect. At low doses, nicotine potently enhances the actions of norepinephrine and dopamine in the brain, causing a drug effect typical of those of psychostimulants. At higher doses, nicotine enhances the effect of serotonin and opiate activity, producing a calming, pain-killing effect. Nicotine is unique in comparison to most drugs, as its profile changes from stimulant to sedative/pain killer in increasing dosages and use. (Another drug that behaves similarly is ethanol).
Technically, nicotine is not significantly addictive, as nicotine administered alone does not produce significant reinforcing properties. However, only after coadministration with an MAOI, such as those found in tobacco, nicotine produces significant behavioral sensitization, a measure of addiction potential. This is similar in effect to amphetamine.
Nicotine gum, usually in 2-mg or 4-mg doses, and nicotine patches are available, as well as smokeless tobacco which do not have all the other ingredients in smoked tobacco.
Dependence and withdrawal
Modern research shows that nicotine acts on the brain to produce a number of effects. Specifically, its addictive nature has been found to show that nicotine activates reward pathways—the circuitry within the brain that regulates feelings of pleasure and euphoria.
Dopamine is one of the key neurotransmitters actively involved in the brain. Research shows that by increasing the levels of dopamine within the reward circuits in the brain, nicotine acts as a chemical with intense addictive qualities. In many studies it has been shown to be more addictive than cocaine and heroin, though chronic treatment has an opposite effect on reward thresholds. Like other physically addictive drugs, nicotine causes down-regulation of the production of dopamine and other stimulatory neurotransmitters as the brain attempts to compensate for artificial stimulation. In addition, the sensitivity of nicotinic acetylcholine receptors decreases. To compensate for this compensatory mechanism, the brain in turn upregulates the number of receptors, convoluting its regulatory effects with compensatory mechanisms meant to counteract other compensatory mechanisms. The net effect is an increase in reward pathway sensitivity, opposite of other drugs of abuse such as cocaine and heroin, which reduce reward pathway sensitivity. This neuronal brain alteration persists for months after administration ceases. Due to an increase in reward pathway sensitivity, nicotine withdrawal is relatively mild compared to alcohol or heroin withdrawal. Nicotine also has the potential to cause dependence in many animals other than humans. Mice have been administered nicotine and exhibit withdrawal reactions when its administration is stopped.
A study found that nicotine exposure in adolescent mice retards the growth of the dopamine system, thus increasing the risk of substance abuse during adolescence.
Because of the severe addictions and the harmful effects of smoking, vaccination protocols have been developed. The principle is under the premise that if an antibody is attached to a nicotine molecule, it will be prevented from diffusing through the capillaries, thus making it less likely that it ever affects the brain by binding to nicotinic acetylcholine receptors.
These include attaching the nicotine molecule to a hapten such as Keyhole limpet hemocyanin or a safe modified bacterial toxin to elicit an active immune response. Often it is added with bovine serum albumin.
Additionally, because of concerns with the unique immune systems of individuals being liable to produce antibodies against endogenous hormones and over the counter drugs, monoclonal antibodies have been developed for short term passive immune protection. They have half-lives varying from hours to weeks. Their half-lives depend on their ability to resist degradation from pinocytosis by epithelial cells.
The LD50 of nicotine is 50 mg/kg for rats and 3 mg/kg for mice. 40–60 mg (0.5-1.0 mg/kg) can be a lethal dosage for adult humans. Nicotine therefore has a high toxicity in comparison to many other alkaloids such as cocaine, which has an LD50 of 95.1 mg/kg when administered to mice. It is unlikely that a person would overdose on nicotine through smoking alone, although intoxication can occur through the excessive use of nicotine patches, gum, nasal sprays or oral inhalers intended as smoking cessation aids. Spilling a high concentration of nicotine onto the skin can cause intoxication or even death, since nicotine readily passes into the bloodstream following dermal contact.
The carcinogenic properties of nicotine in standalone form, separate from tobacco smoke, have not been evaluated by the IARC, and it has not been assigned to an official carcinogen group. The currently available literature indicates that nicotine, on its own, does not promote the development of cancer in healthy tissue and has no mutagenic properties. However, nicotine and the increased cholinergic activity it causes have been shown to impede apoptosis, which is one of the methods by which the body destroys unwanted cells (programmed cell death). Since apoptosis helps to remove mutated or damaged cells that may eventually become cancerous, the inhibitory actions of nicotine may create a more favourable environment for cancer to develop, though this also remains to be proven.
The teratogenic properties of nicotine have not yet been adequately researched, and while the likelihood of birth defects caused by nicotine is believed to be very small or nonexistent, nicotine replacement product manufacturers recommend consultation with a physician before using a nicotine patch or nicotine gum while pregnant or nursing.[unreliable source?]
Women who use nicotine gum and patches during the early stages of pregnancy face an increased risk of having babies with birth defects, says a study that looked at about 77,000 pregnant women in Denmark. The study found that women who use nicotine-replacement therapy in the first 12 weeks of pregnancy have a 60 percent greater risk of having babies with birth defects, compared to women who are non-smokers, the Daily Mail reported. The findings were published in the journal Obstetrics and Gynaecology.
Effective April 1, 1990, the Office of Environmental Health Hazard Assessment (OEHHA) of the California Environmental Protection Agency added nicotine to the list of chemicals known to the state to cause developmental toxicity, for the purposes of Proposition 65.
Nicotine has very powerful effects on arteries throughout the body. Nicotine is a stimulant, it raises blood pressure, and is a vasoconstrictor, making it harder for the heart to pump through the constricted arteries. It causes the body to release its stores of fat and cholesterol into the blood.
It has been speculated[who?] that nicotine increases the risk of blood clots by increasing plasminogen activator inhibitor-1, though this has not been proven. Plasma fibrinogen levels are elevated in smokers and are further elevated during acute COPD exacerbation. Also Factor XIII, which stabilizes fibrin clots, is increased in smokers. But neither of these two effects has been shown to be caused by nicotine  as of 2009[update]. If blood clots in an artery, blood flow is reduced or halted, and tissue loses its source of oxygen and nutrients and dies in minutes.
Peripheral circulation in arteries going to the extremities is also highly susceptible to the vasoconstrictor effects of nicotine and the increased risk of clots and clogging.
The primary therapeutic use of nicotine is in treating nicotine dependence in order to eliminate smoking with its risks to health. Controlled levels of nicotine are given to patients through gums, dermal patches, lozenges, electronic/substitute cigarettes or nasal sprays in an effort to wean them off their dependence.
However, in a few situations, smoking has been observed to apparently be of therapeutic value to patients. These are often referred to as “Smoker’s Paradoxes”. Although in most cases the actual mechanism is understood only poorly or not at all, it is generally believed that the principal beneficial action is due to the nicotine administered, and that administration of nicotine without smoking may be as beneficial as smoking, without the higher risk to health due to tar and other ingredients found in tobacco.
For instance, recent studies suggest that smokers require less frequent repeated revascularization after percutaneous coronary intervention (PCI). Risk of ulcerative colitis has been frequently shown to be reduced by smokers on a dose-dependent basis; the effect is eliminated if the individual stops smoking. Smoking also appears to interfere with development of Kaposi’s sarcoma, breast cancer among women carrying the very high risk BRCA gene, preeclampsia, and atopic disorders such as allergic asthma. A plausible mechanism of action in these cases may be nicotine acting as an anti-inflammatory agent, and interfering with the inflammation-related disease process, as nicotine has vasoconstrictive effects.
Tobacco smoke has been shown to contain compounds capable of inhibiting MAO. Monoamine oxidase is responsible for the degradation of dopamine in the human brain. When dopamine is broken down by MAO-B, neurotoxic by-products are formed, possibly contributing to Parkinson’s and Alzheimers disease. Many such papers regarding Alzheimer’s disease and Parkinson’s Disease have been published. Recent studies find no beneficial link between smoking and Alzheimer’s disease and in some cases, suggest it may actually result in an earlier onset of the disease. However, nicotine has been shown to delay the onset of Parkinson’s disease in studies involving monkeys and humans.
Recent studies have indicated that nicotine can be used to help adults suffering from autosomal dominant nocturnal frontal lobe epilepsy. The same areas that cause seizures in that form of epilepsy are responsible for processing nicotine in the brain.
It has been noted that the majority of people diagnosed with schizophrenia smoke tobacco. Estimates for the proportion of schizophrenics who smoke range from 75% to 90%. It was recently argued that the increased level of smoking in schizophrenia may be due to a desire to self-medicate with nicotine. More recent research has found that mildly dependent users got some benefit from nicotine, but not those who were highly dependent. All of these studies are based only on observation, and no interventional (randomized) studies have been done. Research on nicotine as administered through a patch or gum is ongoing.
Nicotine appears to improve ADHD symptoms. Some studies are focusing on benefits of nicotine therapy in adults with ADHD.
Research as a potential basis for an antipsychotic agent
When the metabolites of nicotine were isolated and their effect on first the animal brain and then the human brain in people with schizophrenia were studied, it was shown that the effects helped with cognitive and negative symptoms of schizophrenia. Therefore, the nicotinergic agents, as antipsychotics which do not contain nicotine but act on the same receptors in the brain are showing promise as adjunct antipsychotics in early stages of FDA studies on schizophrenia. The prepulse inhibition (PPI) is a phenomenon in which a weak prepulse attenuates the response to a subsequent startling stimulus. Therefore, PPI is believed to have face, construct, and predictive validity for the PPI disruption in schizophrenia, and it is widely used as a model to study the neurobiology of this disorder and for screening antipsychotics. Additionally, studies have shown that there are genes predisposing people with schizophrenia to nicotine use.
Therefore with these factors taken together the heavy usage of cigarettes and other nicotine related products among people with schizophrenia may be explained and novel antipsychotic agents developed that have these effects in a manner that is not harmful and controlled and is a promising arena of research for schizophrenia.
List of cigarette smoke carcinogens
According to the U.S. Department of Health and Human Services, the following are known human carcinogens found in cigarette smoke:
|Chemical||Amount (per cigarette)|
|Acetaldehyde||980 micrograms to 1.37 milligrams|
|Acrylonitrile||formerly 1 to 2 milligrams. This product was used as a fumigant in tobacco. Its use has since been discontinued.|
|4-Aminobiphenyl||0.2 to 23 nanograms per cigarette|
|Benzene||5.9 to 75 micrograms|
|1,3-Butadiene||152 to 400 micrograms|
|2-Naphthylamine||1.5 to 35 nanograms|
|N-Nitrosodiethanolamine||24 to 36 nanograms|
|N-Nitrosodiethylamine||up to 8.3 nanograms|
|N-Nitrosodimethylamine||5.7 to 43 nanograms|
|4-(N-Nitrosomethylamino)-1-(3-Pyridyl)-1-Butanone||up to 4.2 micrograms|
|N-Nitrososarcosine||22 to 460 nanograms|
|Polonium-210Citation needed||variable, depending on soil and fertilizer used to grow tobacco|
|Polycyclic aromatic hydrocarbons||28 to 100 milligrams|
|Vinyl chloride||5.6 to 27 nanograms|
The health effects of tobacco
|The health effects of tobacco are the circumstances, mechanisms, and factors of tobacco consumption on human health. Epidemiological research have been focused primarily on tobacco smoking, which has been studied more extensively than any other form of consumption.|
The health effects of tobacco are the circumstances, mechanisms, and factors of tobacco consumption on human health. Epidemiological research have been focused primarily on tobacco smoking, which has been studied more extensively than any other form of consumption.
Tobacco is the single greatest cause of preventable death in the United States and worldwide. Tobacco use leads most commonly to diseases affecting the heart and lungs, with smoking being a major risk factor for heart attacks, strokes, chronic obstructive pulmonary disease (COPD), emphysema, and cancer (particularly lung cancer, cancers of the larynx and mouth, and pancreatic cancer). It also causes peripheral vascular disease and hypertension, all developed due to the exposure time and the level of dosage of tobacco. Furthermore, the earlier and the higher level of tar content in the tobacco filled cigarettes causes the greater risk of these diseases. Cigarettes sold in developing nations tend to have higher tar content, and are less likely to be filtered, potentially increasing vulnerability to tobacco-related disease in these regions.
The World Health Organization (WHO) estimate that tobacco caused 5.4 million deaths in 2004 and 100 million deaths over the course of the 20th century. Similarly, the United States Centers for Disease Control and Prevention describes tobacco use as “the single most important preventable risk to human health in developed countries and an important cause of premature death worldwide.”
Smoke contains several carcinogenic pyrolytic products that bind to DNA and cause many genetic mutations. There are over 19 known chemical carcinogens in cigarette smoke. Tobacco also contains nicotine, which is a highly addictive psychoactive chemical. When tobacco is smoked, nicotine causes physical and psychological dependency. Tobacco use is a significant factor in miscarriages among pregnant smokers, it contributes to a number of other threats to the health of the fetus such as premature births and low birth weight and increases by 1.4 to 3 times the chance for Sudden Infant Death Syndrome (SIDS). The result of scientific studies done in neonatal rats seems to indicate that exposure to cigarette smoke in the womb may reduce the fetal brain’s ability to recognize hypoxic conditions, thus increasing the chance of accidental asphyxiation. Incidence of impotence is approximately 85 percent higher in male smokers compared to non-smokers, and is a key factor causing erectile dysfunction (ED).
Although tobacco may be consumed by either smoking or other smokeless methods such as chewing, the World Health Organization (WHO) only collect data on smoked tobacco. Smoking has therefore been studied more extensively than any other form of consumption.
In 2000, smoking was practiced by 1.22 billion people, predicted to rise to 1.45 billion people in 2010 and 1.5 to 1.9 billion by 2025. If prevalence had decreased by 2% a year since 2000 this figure would have been 1.3 billion in 2010 and 2025.
Smoking is generally five times more prevalent among males than females, however the gender gap declines with younger age. In developed countries smoking rates for men have peaked and have begun to decline, however for women they continue to climb.
As of 2002, about twenty percent of young teens (13–15) smoke worldwide, with 80,000 to 100,000 children taking up the habit every day—roughly half of whom live in Asia. Half of those who begin smoking in adolescent years are projected to go on to smoke for 15 to 20 years.
The WHO states that “Much of the disease burden and premature mortality attributable to tobacco use disproportionately affect the poor”. Of the 1.22 billion smokers, 1 billion of them live in developing or transitional nations. Rates of smoking have leveled off or declined in the developed world. In the developing world, however, tobacco consumption is rising by 3.4% per year as of 2002.
The WHO in 2004 projected 58.8 million deaths to occur globally, from which 5.4 million are tobacco-attributed, and 4.9 million as of 2007. As of 2002, 70% of the deaths are in developing countries.
The shift in prevalence of tobacco smoking to a younger demographic, mainly in the developing world, can be attributed to several factors. The tobacco industry spends up to $12.5 billion dollars annually on advertising, which is increasingly geared towards adolescents in the third world because they are a very vulnerable audience for the marketing campaigns. Adolescents have more difficulty understanding the long term health risks that are associated with smoking and are also more easily influenced by “images of romance, success, sophistication, popularity, and adventure which advertising suggests they could achieve through the consumption of cigarettes”. This shift in marketing towards adolescents and even children in the tobacco industry is debilitating to organizations’ and countries’ efforts to improve child health and mortality in the developing world. It reverses or halts the effects of the work that has been done to improve health care in these countries, and although smoking is deemed as a “voluntary” health risk, the marketing of tobacco towards very impressionable adolescents in the developing world makes it less of a voluntary action and more of an inevitable shift.
In the 1930s German scientists showed that cigarette smoking caused lung cancer. In 1938 a study by a Johns Hopkins University scientist suggested a strongly negative correlation between smoking and lifespan. In 1950 five studies were published in which “smoking was powerfully implicated in the causation of lung cancer”. These included the now classic paper “Smoking and Carcinoma of the Lung” which appeared in the British Medical Journal. This paper reported that “heavy smokers were fifty times as likely as non-smokers to contract lung cancer”.
In 1953 scientists at the Sloan-Kettering Institute in New York City demonstrated that cigarette tar painted on the skin of mice caused fatal cancers. This work attracted much media attention and the New York Times and Life both covered the issue. The Reader’s Digest published an article entitled “Cancer by the Carton”.
A team of British scientists headed by Richard Doll carried out a longitudinal study of 34,439 medical specialists from 1951 to 2001, generally called the “British Doctors Study.” The study demonstrated that that about half of the persistent cigarette smokers born in 1900–1909 were eventually killed by their habit (calculated from the logarithms of the probabilities of surviving from 35–70, 70–80, and 80–90) and about two thirds of the persistent cigarette smokers born in the 1920s would eventually be killed by their habit. After a ban on smoking in all enclosed public places was introduced in Scotland in March 2006, there was a 17 percent reduction in hospital admissions for acute coronary syndrome. 67% of the decrease occurred in non-smokers.
The health effects of tobacco have been significant for the development of the science of epidemiology. As the mechanism of carcinogenicity is radiomimetic or radiological, the effects are stochastic. Definite statements can be made only on the relative increased or decreased probabilities of contracting a given disease; Philosophically and theoretically speaking, it is impossible to definitively prove a direct causative link between exposure to a radiomimetic poison such as tobacco smoke and the cancer that follows. Tobacco companies have capitalized on this philosophical objection and exploited the doubts of clinicians, who consider only individual cases, on the causal link in the stochastic expression of the toxicity as actual disease.
There have been multiple court cases on the issue that tobacco companies have researched the health effects of tobacco, but suppressed the findings or formatted them to imply lessened or no hazard.
A study published in the journal Pediatrics refers to the danger posed by what the authors call “third-hand smoke” — toxic substances that remain in areas where smoking has recently occurred. The study was reviewed in an story broadcast by the Voice of America.
The term “smoker” is used to mean a person who habitually smokes tobacco on a daily basis. This category has been the focus of the vast majority of tobacco studies. However, the health effects of less-than-daily smoking are far less well understood. Studies have often taken the data of “occasional smokers” (those who have never smoked daily) and grouped them with those who have never smoked.[
A recent European study on occasional smoking published findings that the risk of the major smoking-related cancers was 1.24 times higher for occasional smokers than for those who have never smoked at all. (For a confidence interval of 95%, this data showed an incidence rate ratio of 0.80 to 1.94.) This compares to studies showing that habitual heavy smokers have greater than 50 times the incidence of smoking-related cancers.
Smoke, or any partially burnt organic matter, contains carcinogens (cancer-causing agents). The potential effects of smoking, such as lung cancer, can take up to 20 years to manifest themselves. Historically, women began smoking en masse later than men, so an increased death rate caused by smoking amongst women did not appear until later. The male lung cancer death rate decreased in 1975 — roughly 20 years after the initial decline in cigarette consumption in men. A fall in consumption in women also began in 1975 but by 1991 had not manifested in a decrease in lung cancer related mortalities amongst women.
Smoke contains several carcinogenic pyrolytic products that bind to DNA and cause genetic mutations. Particularly potent carcinogens are polynuclear aromatic hydrocarbons (PAH), which are toxicated to mutagenic epoxides. The first PAH to be identified as a carcinogen in tobacco smoke was benzopyrene, which has been shown to toxicate into an epoxide that irreversibly attaches to a cell’s nuclear DNA, which may either kill the cell or cause a genetic mutation. If the mutation inhibits programmed cell death, the cell can survive to become a cancer cell. Similarly, acrolein, which is abundant in tobacco smoke, also irreversibly binds to DNA, causes mutations and thus also cancer. However, it needs no activation to become carcinogenic.
There are over 19 known carcinogen in cigarette smoke. The following are some of the most potent carcinogens:
- Polynuclear aromatic hydrocarbons are tar components produced by pyrolysis in smoldering organic matter and emitted into smoke. Many of them are highly carcinogenic and mutagenic, because they are toxicated to mutagenic epoxides, which are electrophilic alkylating agents. The first PAH to be identified as a carcinogen in tobacco smoke was benzopyrene, which been shown to toxicate into a diol epoxide and then permanently attach to nuclear DNA, which may either kill the cell or cause a genetic mutation. The DNA contains the information on how the cell function; in practice, it contains the recipes for protein synthesis. If the mutation inhibits programmed cell death, the cell can survive to become a cancer cell, a cell that does not function like a normal cell. The carcinogenity is radiomimetic, i.e. similar to that produced by ionizing nuclear radiation. Tobacco manufacturers have experimented with combustionless vaporizer technology to allow cigarettes to be consumed without the formation of carcinogenic benzopyrenes. However, such products have not become popular.
- Acrolein is a pyrolysis product that is abundant in cigarette smoke. It gives smoke an acrid smell and an irritating, lachromatory effect and is a major contributor to its carcinogenity. Like PAH metabolites, acrolein is also an electrophilic alkylating agent and permanently binds to the DNA base guanine, by a conjugate addition followed by cyclization into a hemiaminal. The acrolein-guanine adduct induces mutations during DNA copying and thus causes cancers in a manner similar to PAHs. However, acrolein is 1000 times more abundant than PAHs in cigarette smoke, and is able to react as is, without metabolic activation. Acrolein has been shown to be a mutagen and carcinogen in human cells. The carcinogenity of acrolein has been difficult to study by animal experimentation, because it has such a toxicity that it tends to kill the animals before they develop cancer. Generally, compounds able to react by conjugate addition as electrophiles (so-called Michael acceptors after Michael reaction) are toxic and carcinogenic, because they can permanently alkylate DNA, similarly to mustard gas or aflatoxin. Acrolein is only one of them present in cigarette smoke; for example, crotonaldehyde has been found in cigarette smoke. Michael acceptors also contribute to the chronic inflammation present in tobacco disease.
- Nitrosamines are a group of carcinogenic compounds found in cigarette smoke but not in uncured tobacco leaves. Nitrosamines form on flue-cured tobacco leaves during the curing process through a chemical reaction between nicotine and other compounds contained in the uncured leaf and various oxides of nitrogen found in all combustion gases. Switching to Indirect fire curing has been shown to reduce nitrosamine levels to less than 0.1 parts per million.
In addition to chemical, nonradioactive carcinogens, tobacco and tobacco smoke contain small amounts of lead-210 (210Pb) and polonium-210 (210Po) both of which are radioactive carcinogens. The presence of polonium-210 in mainstream cigarette smoke has been experimentally measured at levels of 0.0263–0.036 pCi (0.97–1.33 mBq), which is equivalent to about 0.1 pCi per milligram of smoke (4 mBq/mg); or about 0.81 pCi of lead 210 per gram of dry condensed smoke (30 Bq/kg).
Research by NCAR radiochemist Ed Martell determined that radioactive compounds in cigarette smoke are deposited in “hot spots” where bronchial tubes branch. Since tar from cigarette smoke is resistant to dissolving in lung fluid, the radioactive compounds have a great deal of time to undergo radioactive decay before being cleared by natural processes. Indoors, these radioactive compounds linger in secondhand smoke, and therefore greater exposure occurs when these radioactive compounds are inhaled during normal breathing, which is deeper and longer than when inhaling cigarettes. Damage to the protective epithelial tissue from smoking only increases the prolonged retention of insoluble polonium 210 compounds produced from burning tobacco. Martell estimated that a carcinogenic radiation dose of 80–100 rads is delivered to the lung tissue of most smokers who die of lung cancer.
The view that polonium 210 is responsible for many cases of cancer in tobacco smokers is disputed by at least one researcher.
Nicotine that is contained in cigarettes and other smoked tobacco products is a stimulant and is one of the main factors leading to continued tobacco smoking. Although the amount of nicotine inhaled with tobacco smoke is quite small (most of the substance is destroyed by the heat) it is still sufficient to cause physical and/or psychological dependence. The amount of nicotine absorbed by the body from smoking depends on many factors, including the type of tobacco, whether the smoke is inhaled, and whether a filter is used. Despite the design of various cigarettes advertised and even tested on machines to deliver less of the toxic tar, studies show that when smoked by humans instead of machines, they deliver the same net amount of smoke. Ingesting a compound by smoking is one of the most rapid and efficient methods of introducing it into the bloodstream, second only to injection, which allows for the rapid feedback which supports the smokers’ ability to titrate their dosage. On average it takes about ten seconds for the substance to reach the brain. As a result of the efficiency of this delivery system, many smokers feel as though they are unable to cease. Of those who attempt cessation and last three months without succumbing to nicotine, most are able to remain smoke free for the rest of their lives. There exists a possibility of depression in some who attempt cessation, as with other psychoactive substances. Depression is also common in teenage smokers; teens who smoke are four times as likely to develop depressive symptoms as their nonsmoking peers.
Although nicotine does play a role in acute episodes of some diseases (including stroke, impotence, and heart disease) by its stimulation of adrenaline release, which raises blood pressure, heart rate, and free fatty acids, the most serious longer term effects are more the result of the products of the smouldering combustion process. This has enabled development of various nicotine delivery systems, such as the nicotine patch or nicotine gum, that can satisfy the addictive craving by delivering nicotine without the harmful combustion by-products. This can help the heavily dependent smoker to quit gradually, while discontinuing further damage to health.
Nicotine is a highly addictive psychoactive chemical. When tobacco is smoked, most of the nicotine is pyrolyzed; a dose sufficient to cause mild somatic dependency and mild to strong psychological dependency remains. There is also a formation of harmane (a MAO inhibitor) from the acetaldehyde in cigarette smoke, which seems to play an important role in nicotine addiction probably by facilitating dopamine release in the nucleus accumbens in response to nicotine stimuli. According to studies by Henningfield and Benowitz, nicotine is more addictive than cannabis, caffeine, ethanol, cocaine, and heroin when considering both somatic and psychological dependence. However, due to the stronger withdrawal effects of ethanol, cocaine and heroin, nicotine may have a lower potential for somatic dependence than these substances. About half of Canadians who currently smoke have tried to quit. McGill University health professor Jennifer O’Loughlin stated that nicotine addiction can occur as soon as five months after the start of smoking.
Recent evidence has shown that smoking tobacco increases the release of dopamine in the brain, specifically in the mesolimbic pathway, the same neuro-reward circuit activated by drugs of abuse such as heroin and cocaine. This suggests nicotine use has a pleasurable effect that triggers positive reinforcement. One study found that smokers exhibit better reaction-time and memory performance compared to non-smokers, which is consistent with increased activation of dopamine receptors. Neurologically, rodent studies have found that nicotine self-administration causes lowering of reward thresholds—a finding opposite that of most other drugs of abuse (e.g. cocaine and heroin). This increase in reward circuit sensitivity persisted months after the self-administration ended, suggesting that nicotine’s alteration of brain reward function is either long lasting or permanent. Furthermore, it has been found that nicotine can activate long term potentiation in vivo and in vitro. These studies suggest nicotine’s “trace memory” may contribute to difficulties in nicotine abstinence.[original research?]
The carcinogenity of tobacco smoke is not explained by nicotine per se, which is not carcinogenic or mutagenic. However, it inhibits apoptosis, therefore accelerating existing cancers. Also, NNK, a nicotine derivative converted from nicotine, can be carcinogenic.
It is worth noting that nicotine, although frequently implicated in producing tobacco addiction, is not significantly addictive when administered alone. The addictive potential manifests itself after co-administration of an MAOI, which specifically causes sensitization of the locomotor response in rats, a measure of addictive potential.
According to three separate studies commissioned by governments in the US and Europe, scientists have identified a genetic link that makes people more likely to become addicted to tobacco. This genetic variation causes individuals to smoke more cigarettes, makes it harder for them to quit and increases their likelihood of developing lung cancer by up to 80%.
Genetic markers of more than 35,000 people (mostly smokers and ex-smokers) were surveyed by scientists in three separate studies, and all three found lung cancer to be associated with similar sets of genetic differences. The genetic variations of note encode nicotine receptors on cells and were identified on a region of chromosome 15. Possessing a single copy of the mutation raises an individual’s risk of lung cancer by approximately 30%; for two copies the increase is about 80%. The gene was found to be attributable to 14% of lung cancer cases, and it was found to confer similar lung cancer risks irrespective of smoking status or quantity smoked.
Another study related to genetic changes in smokers was conducted by Wan L Lam and Stephen Lam from the BC Cancer Agency, in 2007. The study revealed that cigarette smoke can turn on or off some of the genes, which otherwise would remain inactive. Some changes on genetic level could be reversed after the smoking was quit, yet others could not. Examples of reversible genes involved the so-called xenofobic functions, nucleotide metabolism and mucus secretion. Smoking turns off some DNA repair genes that cannot be reversed. It also switches off some genes responsible from protection from cancer growth in the body.
||This article may require copy editing for grammar, style, cohesion, tone or spelling. You can assist by editing it. (December 2008)|
Nicotine stains on primarily the 2nd and 3rd fingers in a heavy smoker.
Summary of tobacco related diseases. Click to enlarge
A person’s increased risk of contracting disease is directly proportional to the length of time that a person continues to smoke as well as the amount smoked. However, if someone stops smoking, then these chances gradually decrease as the damage to their body is repaired. A year after quitting, the risk of contracting heart disease is half that of a continuing smoker. The health risks of smoking are not uniform across all smokers. Risks vary according to amount of tobacco smoked, with those who smoke more at greater risk. Light smoking is still a health risk. Likewise, smoking “light” cigarettes does not reduce the risks.
Tobacco use most commonly leads to diseases affecting the heart and lungs, with smoking being a major risk factor for heart attacks, Chronic Obstructive Pulmonary Disease (COPD), emphysema, and cancer, particularly lung cancer, cancers of the larynx and mouth, and pancreatic cancer. Overall life expectancy is also reduced in regular smokers, with estimates ranging from 10 to 17.9  years fewer than nonsmokers. About two thirds of male smokers will die of illness due to smoking. The association of smoking with lung cancer is strongest, both in the public perception and etiologically. People who have smoked tobacco at some point have about a one in ten chance of developing lung cancer during their lifetime. If one looks at men who continue to smoke tobacco, the risk increases to one in six. Historically, lung cancer was considered to be a rare disease prior to World War I and was perceived as something most physicians would never see during their career. With the postwar rise in popularity of cigarette smoking came a virtual epidemic of lung cancer.
Male and female smokers lose an average of 13.2 and 14.5 years of life, respectively.
According to the results of a 50 year study of 34,439 male British doctors, at least half of all lifelong smokers die earlier as a result of smoking.
Smokers are three times as likely to die before the age of 60 or 70 as nonsmokers.[
In the United States alone, cigarette smoking and exposure to tobacco smoke results in at least 443,000 premature deaths annually.
In the United States alone, tobacco kills the equivalent of three jumbo jets full of people crashing every day, with no survivors, 365 days of the year. -ABC’s Peter Jennings On a worldwide basis, it’s 1 jumbo jet per hour, 24 hours a day, 365 days of the year. -WHO
The primary risks of tobacco usage include many forms of cancer, particularly lung cancer, cancer of the kidney, cancer of the larynx and head and neck, breast cancer, bladder, esophagus, pancreas, and stomach. There is some evidence suggesting an increased risk of myeloid leukemia, squamous cell sinonasal cancer, liver cancer, cervical cancer, colorectal cancer after an extended latency, childhood cancers and cancers of the gall bladder, adrenal gland and small intestine.
The risk of dying from lung cancer before age 85 is 22.1% for a male smoker and 11.9% for a female current smoker, in the absence of competing causes of death. The corresponding estimates for lifelong nonsmokers are a 1.1% probability of dying from lung cancer before age 85 for a man of European descent, and a 0.8% probability for a woman.
In smoking, long term exposure to compounds found in the smoke such as carbon monoxide, cyanide, and so forth—, are believed to be responsible for pulmonary damage and for loss of elasticity in the alveoli, leading to emphysema and COPD. The carcinogen acrolein and its derivatives also contribute to the chronic inflammation present in COPD.
Secondhand smoke is a mixture of smoke from the burning end of a cigarette, pipe or cigar and the smoke exhaled from the lungs of smokers. It is involuntarily inhaled, lingers in the air hours after cigarettes have been extinguished, and can cause a wide range of adverse health effects, including cancer, respiratory infections, and asthma. Nonsmokers who are exposed to secondhand smoke at home or work increase their heart disease risk by 25–30% and their lung cancer risk by 20–30%. Secondhand smoke has been estimated to cause 38,000 deaths per year, of which 3,400 are deaths from lung cancer in non-smokers.
Chronic obstructive pulmonary disease (COPD) caused by smoking, known as tobacco disease, is a permanent, incurable reduction of pulmonary capacity characterized by shortness of breath, wheezing, persistent cough with sputum, and damage to the lungs, including emphysema and chronic bronchitis.
A study of an outbreak of A(H1N1) influenza in an Israeli military unit of 336 healthy young men to determine the relation of cigarette smoking to the incidence of clinically apparent influenza, revealed that, of 168 smokers, 68.5 percent had influenza, as compared with 47.2 percent of nonsmokers. Influenza was also more severe in the smokers; 50.6 percent of the smokers lost work days or required bed rest, or both, as compared with 30.1 percent of the nonsmokers.
According to a study of 1,900 male cadets after the 1968 Hong Kong A2 influenza epidemic at a South Carolina military academy, compared with nonsmokers heavy smokers (more than 20 cigarettes per day), had 21% more illnesses and 20% more bed rest, light smokers (less than 20 cigarettes per day) had 10% more illnesses and 7% more bed rest.
The effect of cigarette smoking upon epidemic influenza was studied prospectively among 1,811 male college students. Clinical influenza incidence among those who daily smoked 21 or more cigarettes was 21% higher than that of non-smokers. Influenza incidence among smokers of 1 to 20 cigarettes daily was intermediate between non-smokers and heavy cigarette smokers.
Surveillance of a 1979 influenza out-break at a military base for women in Israel revealed that, Influenza symptoms developed in 60.0% of the current smokers vs. 41.6% of the nonsmokers.
Smoking seems to cause a higher relative influenza-risk in older populations than in younger populations. In a prospective study of community-dwelling people 60–90 years of age, during 1993, of unimmunized people 23% of smokers had clinical influenza as compared with 6% of non-smokers.
Smoking may substantially contribute to the growth of influenza epidemics affecting the entire population. However the proportion of influenza cases in the general non-smoking population attributable to smokers has not yet been calculated.
Inhalation of tobacco smoke causes several immediate responses within the heart and blood vessels. Within one minute the heart rate begins to rise, increasing by as much as 30 percent during the first 10 minutes of smoking. Carbon monoxide in tobacco smoke exerts its negative effects by reducing the blood’s ability to carry oxygen.
Smoking also increases the chance of heart disease, stroke, atherosclerosis, and peripheral vascular disease. Several ingredients of tobacco lead to the narrowing of blood vessels, increasing the likelihood of a blockage, and thus a heart attack or stroke. According to a study by an international team of researchers, people under 40 are five times more likely to have a heart attack if they smoke.
Latest research of the American biologists have determined that cigarette smoke also influences the process of cell division in the cardiac muscle and changes heart’s shape.
The usage of tobacco has also been linked to Buerger’s disease (thromboangiitis obliterans) the acute inflammation and thrombosis (clotting) of arteries and veins of the hands and feet.
The current Surgeon General’s Report concluded that there is no risk-free level of exposure to secondhand smoke. Even short exposures to secondhand smoke can cause blood platelets to become stickier, damage the lining of blood vessels, decrease coronary flow velocity reserves, and reduce heart rate variability, potentially increasing the risk of heart attack. New research indicates that private research conducted by cigarette company Philip Morris in the 1980s showed that secondhand smoke was toxic, yet the company suppressed the finding during the next two decades.
Although cigarette smoking causes a greater increase of the risk of cancer than cigar smoking, cigar smokers still have an increased risk for many health problems, including cancer, when compared to non-smokers. As for Environmental Tobacco Smoke (ETS, or “Second-hand Smoking”), the NIH study points to the large amount of smoke generated by one cigar, saying “cigars can contribute substantial amounts of tobacco smoke to the indoor environment; and, when large numbers of cigar smokers congregate together in a cigar smoking event, the amount of ETS produced is sufficient to be a health concern for those regularly required to work in those environments.”
Smoking tends to increase blood cholesterol levels. Furthermore, the ratio of high-density lipoprotein (the “good” cholesterol) to low-density lipoprotein (the “bad” cholesterol) tends to be lower in smokers compared to non-smokers. Smoking also raises the levels of fibrinogen and increases platelet production (both involved in blood clotting) which makes the blood viscous. Carbon monoxide binds to haemoglobin (the oxygen-carrying component in red blood cells), resulting in a much stabler complex than haemoglobin bound with oxygen or carbon dioxide—the result is permanent loss of blood cell functionality. Blood cells are naturally recycled after a certain period of time, allowing for the creation of new, functional erythrocytes. However, if carbon monoxide exposure reaches a certain point before they can be recycled, hypoxia (and later death) occurs. All these factors make smokers more at risk of developing various forms of arteriosclerosis. As the arteriosclerosis progresses, blood flows less easily through rigid and narrowed blood vessels, making the blood more likely to form a thrombosis (clot). Sudden blockage of a blood vessel may lead to an infarction (stroke). However, it is also worth noting that the effects of smoking on the heart may be more subtle. These conditions may develop gradually given the smoking-healing cycle (the human body heals itself between periods of smoking), and therefore a smoker may develop less significant disorders such as worsening or maintenance of unpleasant dermatological conditions, e.g. eczema, due to reduced blood supply. Smoking also increases blood pressure and weakens blood vessels.
Perhaps the most serious oral condition that can arise is that of oral cancer. However, smoking also increases the risk for various other oral diseases, some almost completely exclusive to tobacco users. The National Institutes of Health, through the National Cancer Institute, determined in 1998 that “cigar smoking causes a variety of cancers including cancers of the oral cavity (lip, tongue, mouth, throat), esophagus, larynx, and lung.” Pipe smoking involves significant health risks, particularly oral cancer. Roughly half of periodontitis or inflammation around the teeth cases attributed to current or former smoking. Smokeless tobacco causes gingival recession and white mucosal lesions. Up to 90% of periodontitis patients who are not helped by common modes of treatment are smokers. Smokers have significantly greater loss of bone height than nonsmokers, and the trend can be extended to pipe smokers to have more bone loss than nonsmokers. Smoking has been proven to be an important factor in the staining of teeth. Halitosis or bad breath is common among tobacco smokers. Tooth loss has been shown to be 2 to 3 times higher in smokers than in non-smokers. In addition, complications may further include leukoplakia, the adherent white plaques or patches on the mucous membranes of the oral cavity, including the tongue, and a loss of taste sensation or salivary changes.
Tobacco is also linked to susceptibility to infectious diseases, particularly in the lungs. Smoking more than 20 cigarettes a day increases the risk of tuberculosis by two to four times, and being a current smoker has been linked to a fourfold increase in the risk of invasive pneumococcal disease. It is believed that smoking increases the risk of these and other pulmonary and respiratory tract infections both through structural damage and through effects on the immune system. The effects on the immune system include an increase in CD4+ cell production attributable to nicotine, which has tentatively been linked to increased HIV susceptibility. The usage of tobacco also increases rates of infection: common cold and bronchitis, chronic obstructive pulmonary disease, emphysema and chronic bronchitis in particular.
Smoking reduces the risk of Kaposi’s sarcoma in people without HIV infection. One study found this only with the male population and could not draw any conclusions for the female participants in the study.
In a study of men ages 24 to 36 seeking treatment for infertility, Panayiotis Zavos, Ph.D., confirmed the results of earlier studies demonstrating that smoking harms sperm quality in every way, from longevity to motility. But Zavos also found that smoking affected sexual behavior. The smokers had sex an average of 5.7 times per month, while the nonsmokers reported an average of 11.6 encounters. And on a scale of 1 to 10, the smokers rated the quality of sex at a lackluster 5.2, compared to 8.7 for nonsmokers.”
Smokers report a variety of physical and psychological effects from smoking tobacco. Those new to smoking may experience nausea, dizziness, and rapid heart beat. The unpleasant symptoms will eventually vanish over time, with repeated use, as the body builds a tolerance to the chemicals in the cigarettes, such as nicotine.
Smokers report high levels of everyday stress. Several studies have monitored feelings of stress over time, and they find reduced stress after quitting.
The deleterious mood effects of abstinence explain why smokers suffer more daily stress than non-smokers, and become less stressed when they quit smoking. Deprivation reversal also explains much of the arousal data, with deprived smokers being less vigilant and less alert than non-deprived smokers or non-smokers.
Social and Behavioral
Medical researchers have found that smoking is a predictor of divorce. Smokers have 53% more divorce than nonsmokers.
The usage of tobacco also creates cognitive dysfunction, which include: increased risk of Alzheimer’s disease and decline in cognitive abilities, reduced memory and cognitive abilities in adolescent smokers, brain shrinkage (cerebral atrophy).
In many respects, nicotine acts on the nervous system in a similar way to caffeine. Some writings have stated that smoking can also increase mental concentration; one study documents a significantly better performance on the normed Advanced Raven Progressive Matrices test after smoking.
Most smokers, when denied access to nicotine, exhibit symptoms such as irritability, jitteriness, dry mouth, and rapid heart beat. The onset of these symptoms is very fast, nicotine’s half-life being only 2 hours. Withdrawal symptoms can appear even if the smoker’s consumption is very limited or irregular, appearing after only 4–5 cigarettes in most adolescents. An ex-smoker’s chemical dependence to nicotine will cease after approximately ten to twenty days, although the brain’s number of nicotine receptors is permanently altered, and the psychological dependence may linger for months or even many years. Unlike some recreational drugs, nicotine does not measurably alter a smoker’s motor skills, judgement, or language abilities while under the influence of the drug. Tobacco withdrawal has been shown to cause clinically significant distress.
Most notably, some studies have found that patients with Alzheimer’s disease are more likely not to have smoked than the general population, which has been interpreted to suggest that smoking offers some protection against Alzheimer’s. However, the research in this area is limited and the results are conflicting; some studies show that smoking increases the risk of Alzheimer’s disease. A recent review of the available scientific literature concluded that the apparent decrease in Alzheimer risk may be simply due to the fact that smokers tend to die before reaching the age at which Alzheimer normally occurs. “Differential mortality is always likely to be a problem where there is a need to investigate the effects of smoking in a disorder with very low incidence rates before age 75 years, which is the case of Alzheimer’s disease,” it stated, noting that smokers are only half as likely as non-smokers to survive to the age of 80.
Former and current smokers have a lower incidence of Parkinson’s disease compared to people who have never smoked, although the authors stated that it was more likely that the movement disorders which are part of Parkinson’s disease prevented people from being able to smoke than that smoking itself was protective. Another study considered a possible role of nicotine in reducing Parkinson’s risk: nicotine stimulates the dopaminergic system of the brain, which is damaged in Parkinson’s disease, while other compounds in tobacco smoke inhibit MAO-B, an enzyme which produces oxidative radicals by breaking down dopamine.
A very large percentage of schizophrenics smoke tobacco as a form of self medication. The high rate of tobacco use by the mentally ill is a major factor in their decreased life expectancy, which is about 25 years shorter than the general population. Following the observation that smoking improves condition of people with schizophrenia, in particular working memory deficit, nicotine patches had been proposed as a way to treat schizophrenia. Some studies suggest that a link exists between smoking and mental illness, citing the high incidence of smoking amongst those suffering from schizophrenia and the possibility that smoking may alleviate some of the symptoms of mental illness, but these have not been conclusive.
Recent studies have linked smoking to anxiety disorders, suggesting the correlation (and possibly mechanism) may be related to the broad class of anxiety disorders, and not limited to just depression. Current and ongoing research attempt to explore the addiction-anxiety relationship.
Data from multiple studies suggest that anxiety disorders and depression play a role in cigarette smoking. A history of regular smoking was observed more frequently among individuals who had experienced a major depressive disorder at some time in their lives than among individuals who had never experienced major depression or among individuals with no psychiatric diagnosis. People with major depression are also much less likely to quit due to the increased risk of experiencing mild to severe states of depression, including a major depressive episode. Depressed smokers appear to experience more withdrawal symptoms on quitting, are less likely to be successful at quitting, and are more likely to relapse.
Evidence suggests that non-smokers are up to twice as likely as smokers to develop Parkinson’s disease or Alzheimer’s disease. A plausible explanation for these cases may be the effect of nicotine, a cholinergic stimulant, decreasing the levels of acetylcholine in the smoker’s brain; Parkinson’s disease occurs when the effect of dopamine is less than that of acetylcholine. In addition, nicotine stimulates the mesolimbic dopamine pathway (as do other drugs of abuse), causing an effective increase in dopamine levels. Opponents counter by noting that consumption of pure nicotine may be as beneficial as smoking without the risks associated with smoking, although this is unlikely due to the importance of the MAO-B inhibitor compounds of tobacco in preventing neurodegenerative diseases.
A number of studies have shown that tobacco use is a significant factor in miscarriages among pregnant smokers, and that it contributes to a number of other threats to the health of the fetus. Second-hand smoke appears to present an equal danger to the fetus, as one study noted that “heavy paternal smoking increased the risk of early pregnancy loss.”
Studies suggest that smoking decreases appetite, but did not conclude that overweight people should smoke or that their health would improve by smoking. This is also a cause of heart diseases.However due to some new processes of treating tobacco, especially in the case of cigarette, heavy smokers tend to become overweight as the processing involves large quantities of starch.This effect is not seen in occasional smokers. Smoking also decreases weight by overexpressing the gene AZGP1 which stimulates lipolysis.
Preliminary reports suggest that smoking can decrease the incidence of acne prophylactically. This was seen by a decreased percentage ratio of patients needing acne medication versus the percentage of entire population of smokers. (A smaller percentage of patients who smoked needed medication than found in the population as a whole).
A protective effect of current smoking against ulcerative colitis, although smoking increases the risk of Crohn’s disease, the other form of inflammatory bowel disease. There is some evidence for decreased rates of endometriosis in infertile smoking women, although other studies have found that smoking increases the risk in infertile women. There is little or no evidence of a protective effect in fertile women. Some preliminary data from 1996 suggested a reduced incidence of uterine fibroids, but overall the evidence is unconvincing.
A new research has found that women who smoke are at significantly increased risk of developing an abdominal aortic aneurysm, a condition in which a weak area of the abdominal aorta expands or bulges.
Several types of “Smoker’s Paradoxes”, (cases where smoking appears to have specific beneficial effects), have been observed; often the actual mechanism remains undetermined.
- Risk of ulcerative colitis has been frequently shown to be reduced by smokers on a dose-dependent basis; the effect is eliminated if the individual stops smoking.
- Smoking appears to interfere with development of:
- Kaposi’s sarcoma
- breast cancer among women carrying the very high risk BRCA gene
- atopic disorders such as allergic asthma
A plausible mechanism of action in these cases may be the nicotine in tobacco smoke acting as an anti-inflammatory agent and interfering with the disease process.
Smoking can also reduce rates of uterine fibroids. This may be due to estrogen inhibition, as opposed to general inhibition of inflammation.
Particular forms of tobacco use
Chewing tobacco has been known to cause cancer, particularly of the mouth and throat. According to the International Agency for Research on Cancer, “Some health scientists have suggested that smokeless tobacco should be used in smoking cessation programmes and have made implicit or explicit claims that its use would partly reduce the exposure of smokers to carcinogens and the risk for cancer. These claims, however, are not supported by the available evidence.” Oral and spit tobacco increase the risk for leukoplakia a precursor to oral cancer.
Like other forms of tobacco use, cigar smoking poses a significant health risk depending on dosage: risks are greater for those who inhale more when they smoke, smoke more cigars, or smoke them longer. The risk of dying from any cause is significantly greater for cigar smokers, with the risk particularly higher for smokers less than 65 years old, and with risk for moderate and deep inhalers reaching levels similar to cigarette smokers. Little cigars are commonly inhaled and likely pose the same health risks as cigarettes. The increased risk for those smoking 1–2 cigars per day is too small to be statistically significant, and the health risks of the 3/4 of cigar smokers who smoke less than daily are not known and are hard to measure; although it has been claimed that people who smoke few cigars have no increased risk, a more accurate statement is that their risks are proportionate to their exposure. Health risks are similar to cigarette smoking in nicotine addiction, periodontal health, tooth loss, and many types of cancer, including cancers of the mouth, throat, and esophagus. Cigar smoking also can cause cancers of the lung and larynx, where the increased risk is less than that of cigarettes. Many of these cancers have extremely low cure rates. Cigar smoking also increases the risk of lung and heart diseases such as chronic obstructive pulmonary disease.
A common belief among users is that the smoke is significantly less dangerous than that from cigarettes. The water moisture induced by the hookah makes the smoke less irritating and may give a false sense of security and reduce concerns about true health effects. Doctors at institutions including the Mayo Clinic have stated that use of hookah can be as detrimental to a person’s health as smoking cigarettes, and a study by the World Health Organization also confirmed these findings.
Each hookah session typically lasts more than 40 minutes, and consists of 50 to 200 inhalations that each range from 0.15 to 0.50 liters of smoke. Reports by the World Health Organization and the American Cancer Society have shown that, in a one-hour hookah session, users consume about 100 to 200 times the smoke and about 70 times the nicotine as they do in one cigarette.
A study in the Journal of Periodontology found that water pipes smokers were five times more likely than non-smokers to show signs of gum disease. People who smoked water pipes had five times the risk of lung cancer as non-smokers.
The water used to filter the chemicals does not work efficiently to remove all the harmful chemicals.
A study on hookah smoking and cancer in Pakistan was published in 2008. Its objective was “to find serum CEA levels in ever/exclusive hookah smokers, i.e. those who smoked only hookah (no cigarettes, bidis, etc.), prepared between 1 and 4 times a day with a quantity of up to 120 g of a tobacco-molasses mixture each (i.e. the tobacco weight equivalent of up to 60 cigarettes of 1 g each) and consumed in 1 to 8 sessions”. Carcinoembryonic antigen (CEA) is a marker found in several forms of cancer. Levels in exclusive hookah smokers were lower compared to cigarette smokers although the difference was not statistically significant between a hookah smoker and a non-smoker. Also the study concluded that heavy hookah smoking (2–4 daily preparations; 3–8 sessions a day ; >2 hrs to ≤ 6 hours) substantially raises CEA levels.
Users of snuff are believed to face less cancer risk than smokers, but are still at greater risk than people who do not use any tobacco products. They also have an equal risk of other health problems directly linked to nicotine such as increased rate of atherosclerosis.
The late-19th century invention of automated cigarette-making machinery in the American South made possible mass production of cigarettes at low cost, and cigarettes became elegant and fashionable among society men as the Victorian era gave way to the Edwardian. In 1912, American Dr. Isaac Adler was the first to strongly suggest that lung cancer is related to smoking. In 1929, Fritz Lickint of Dresden, Germany, published a formal statistical evidence of a lung cancer–tobacco link, based on a study showing that lung cancer sufferers were likely to be smokers. Lickint also argued that tobacco use was the best way to explain the fact that lung cancer struck men four or five times more often than women (since women smoked much less).
Prior to World War I, lung cancer was considered to be a rare disease, which most physicians would never see during their career. With the postwar rise in popularity of cigarette smoking, however, came an epidemic of lung cancer.
In 1950, Richard Doll published research in the British Medical Journal showing a close link between smoking and lung cancer. Four years later, in 1954 the British Doctors Study, a study of some 40 thousand doctors over 20 years, confirmed the suggestion, based on which the government issued advice that smoking and lung cancer rates were related. The British Doctors Study lasted till 2001, with results published every ten years and final results published in 2004 by Doll and Richard Peto. Much early research was also done by Alton Ochsner. Reader’s Digest magazine for many years published frequent anti-smoking articles. In 1964 the United States Surgeon General’s Report on Smoking and Health, led millions of American smokers to quit, the banning of certain advertising, and the requirement of warning labels on tobacco products.
The Canadian province of British Columbia has the Tobacco Damages and Health Care Costs Recovery Act.