Mechanism Health effects of tobacco

1 mechanism

1.1 chemical carcinogens
1.2 radioactive carcinogens
1.3 nicotine

mechanism

chemical carcinogens

smoke, or partially burnt organic matter, contains carcinogens (cancer-causing agents). potential effects of smoking, such lung cancer, can take 20 years manifest themselves. historically, women began smoking en masse later men, increased death rate caused smoking amongst women did not appear until later. male lung cancer death rate decreased in 1975 — 20 years after initial decline in cigarette consumption in men. fall in consumption in women began in 1975 1991 had not manifested in decrease in lung cancer-related mortalities amongst women.

smoke contains several carcinogenic pyrolytic products bind dna , cause genetic mutations. particularly potent carcinogens polycyclic aromatic hydrocarbons (pah), toxicated mutagenic epoxides. first pah identified carcinogen in tobacco smoke benzopyrene, has been shown toxicate epoxide irreversibly attaches cell s nuclear dna, may either kill cell or cause genetic mutation. if mutation inhibits programmed cell death, cell can survive become cancer cell. similarly, acrolein, abundant in tobacco smoke, irreversibly binds dna, causes mutations , cancer. however, needs no activation become carcinogenic.

there on 19 known carcinogens in cigarette smoke. following of potent carcinogens:

polycyclic aromatic hydrocarbons tar components produced pyrolysis in smoldering organic matter , emitted smoke. several of these pah s toxic in normal form, however, many of can become more toxic liver. due hydrophobic nature of pah s not dissolve in water , hard expel body. in order make pah more soluble in water, liver creates enzyme called cytochrome p450 adds additional oxygen pah, turning mutagenic epoxides, more soluble, more reactive. first pah identified carcinogen in tobacco smoke benzopyrene, been shown toxicate diol epoxide , permanently attach nuclear dna, may either kill cell or cause genetic mutation. dna contains information on how cell function; in practice, contains recipes protein synthesis. if mutation inhibits programmed cell death, cell can survive become cancer cell, cell not function normal cell. carcinogenicity radiomimetic, i.e. similar produced ionizing nuclear radiation. tobacco manufacturers have experimented combustion less vaporizer technology allow cigarettes consumed without formation of carcinogenic benzopyrenes. although such products have become increasingly popular, still represent small fraction of market, , no conclusive evidence has shown prove or disprove positive health claims.
acrolein pyrolysis product abundant in cigarette smoke. gives smoke acrid smell , irritating, tear causing effect , major contributor carcinogenicity. pah metabolites, acrolein electrophilic alkylating agent , permanently binds dna base guanine, conjugate addition followed cyclization hemiaminal. acrolein-guanine adduct induces mutations during dna copying , causes cancers in manner similar pahs. however, acrolein 1000 times more abundant pahs in cigarette smoke , able react is, without metabolic activation. acrolein has been shown mutagen , carcinogen in human cells. carcinogenicity of acrolein has been difficult study animal experimentation, because has such toxicity tends kill animals before develop cancer. generally, compounds able react conjugate addition electrophiles (so-called michael acceptors after michael reaction) toxic , carcinogenic, because can permanently alkylate dna, mustard gas or aflatoxin. acrolein 1 of them present in cigarette smoke; example, crotonaldehyde has been found in cigarette smoke. michael acceptors contribute chronic inflammation present in tobacco disease.
nitrosamines group of carcinogenic compounds found in cigarette smoke not in uncured tobacco leaves. nitrosamines form on flue-cured tobacco leaves during curing process through chemical reaction between nicotine , other compounds contained in uncured leaf , various oxides of nitrogen found in combustion gasses. switching indirect fire curing has been shown reduce nitrosamine levels less 0.1 parts per million.

sidestream tobacco smoke, or exhaled mainstream smoke, particularly harmful. because exhaled smoke exists @ lower temperatures inhaled smoke, chemical compounds undergo changes can cause them become more dangerous. well, smoke undergoes changes ages, causes transformation of compound no more toxic no2. further, volatilization causes smoke particles become smaller, , more embedded deep lung of later breathes air.

radioactive carcinogens

in addition chemical, nonradioactive carcinogens, tobacco , tobacco smoke contain small amounts of lead-210(pb) , polonium-210 (po) both of radioactive carcinogens. presence of polonium-210 in mainstream cigarette smoke has been experimentally measured @ levels of 0.0263–0.036 pci (0.97–1.33 mbq), equivalent 0.1 pci per milligram of smoke (4 mbq/mg); or 0.81 pci of lead-210 per gram of dry condensed smoke (30 bq/kg).

research ncar radiochemist ed martell suggested radioactive compounds in cigarette smoke deposited in hot spots bronchial tubes branch, tar cigarette smoke resistant dissolving in lung fluid , radioactive compounds have great deal of time undergo radioactive decay before being cleared natural processes. indoors, these radioactive compounds can linger in secondhand smoke, , greater exposure occur when these radioactive compounds inhaled during normal breathing, deeper , longer when inhaling cigarettes. damage protective epithelial tissue smoking increases prolonged retention of insoluble polonium-210 compounds produced burning tobacco. martell estimated carcinogenic radiation dose of 80–100 rads delivered lung tissue of smokers die of lung cancer.

smoking average of 1.5 packs per day gives radiation dose of 60-160 msv/year, compared living near nuclear power station (0.0001 msv/year) or 3.0 msv/year average dose americans. of mineral apatite in florida used produce phosphate u.s.a. tobacco crops contains uranium, radium, lead-210 , polonium-210 , radon. radioactive smoke tobacco fertilized way deposited in lungs , releases radiation if smoker quits habit. combination of carcinogenic tar , radiation in sensitive organ such lungs increases risk of cancer.

in contrast, 1999 review of tobacco smoke carcinogens published in journal of national cancer institute states levels of polonium-210 in tobacco smoke not believed great enough impact lung cancer in smokers. in 2011 hecht has stated levels of po in cigarette smoke low involved in lung cancer induction ...

nicotine


nicotine molecule

nicotine, contained in cigarettes , other smoked tobacco products, stimulant , 1 of main factors leading continued tobacco smoking. nicotine highly addictive psychoactive chemical. when tobacco smoked, of nicotine pyrolyzed; dose sufficient cause mild somatic dependency , mild strong psychological dependency remains. amount of nicotine absorbed body smoking depends on many factors, including type of tobacco, whether smoke inhaled, , whether filter used. there formation of harmane (a mao inhibitor) acetaldehyde in cigarette smoke, seems play important role in nicotine addiction facilitating dopamine release in nucleus accumbens in response nicotine stimuli. according studies henningfield , benowitz, nicotine more addictive cannabis, caffeine, ethanol, cocaine, , heroin when considering both somatic , psychological dependence. however, due stronger withdrawal effects of ethanol, cocaine , heroin, nicotine may have lower potential somatic dependence these substances. half of canadians smoke have tried quit. mcgill university health professor jennifer o loughlin stated nicotine addiction can occur 5 months after start of smoking.

ingesting compound smoking 1 of rapid , efficient methods of introducing bloodstream, second injection, allows rapid feedback supports smokers ability titrate dosage. on average takes ten seconds substance reach brain. result of efficiency of delivery system, many smokers feel though unable cease. of attempt cessation , last 3 months without succumbing nicotine, able remain smoke-free rest of lives. there exists possibility of depression in attempt cessation, other psychoactive substances. depression common in teenage smokers; teens smoke 4 times develop depressive symptoms nonsmoking peers.

although nicotine play role in acute episodes of diseases (including stroke, impotence, , heart disease) stimulation of adrenaline release, raises blood pressure, heart , respiration rate, , free fatty acids, serious longer term effects more result of products of smouldering combustion process. has led development of various nicotine delivery systems, such nicotine patch or nicotine gum, can satisfy addictive craving delivering nicotine without harmful combustion by-products. can heavily dependent smoker quit gradually, while discontinuing further damage health.

recent evidence has shown smoking tobacco increases release of dopamine in brain, in mesolimbic pathway, same neuro-reward circuit activated drugs of abuse such heroin , cocaine. suggests nicotine use has pleasurable effect triggers positive reinforcement. 1 study found smokers exhibit better reaction-time , memory performance compared non-smokers, consistent increased activation of dopamine receptors. neurologically, rodent studies have found nicotine self-administration causes lowering of reward thresholds—a finding opposite of other drugs of abuse (e.g. cocaine , heroin). increase in reward circuit sensitivity persisted months after self-administration ended, suggesting nicotine s alteration of brain reward function either long lasting or permanent. furthermore, has been found nicotine can activate long-term potentiation in vivo , in vitro. these studies suggest nicotine’s trace memory may contribute difficulties in nicotine abstinence.

the carcinogenity of tobacco smoke not explained nicotine per se, not carcinogenic or mutagenic, although metabolic precursor several compounds are. in addition, inhibits apoptosis, therefore accelerating existing cancers. also, nnk, nicotine derivative converted nicotine, can carcinogenic.

it worth noting nicotine, although implicated in producing tobacco addiction, not addictive when administered alone. addictive potential manifests after co-administration of maoi, causes sensitization of locomotor response in rats, measure of addictive potential.