Slide2: Early information on smoking originates from artifacts of the Maya of the Yucatan reion of Mexico.

Smoking of tobacco was part of the religious rituls and political gatherings of the natives of the yutacan peninsula as shown in the artwork on a pottery vessel from the 10th century. Columbus and his crew were thus the first Europeans who became acquainted with tobacco smoking. Jean Nicot was the first person known to have grown tobacco in Europe. He introduced tobacco and tobacco smoke at the royal court of Paris, and used it to treat migraine headaches of King Charles IX . Nowadays, tobacco are used for the manufacture ofchewing tobacco, oral and nasal snuff, cigarettes, cigars, and pipe tobacco. Cigarette is the most popular one, which is use by 1.3 billion peole all over the world. Slide3: We notice and discuss about those chemicals because they have significant impact on human health. Slide4: Nicotine C10H14N2 is an alkoloid, contained in the leaves of several species of plants. Nicotine in cigarettes comes from dried tobacco leaf. Pharmacologic effects - it increases their heart rate, heart muscle oxygen consumption rate, and heart stroke volume Psychodynamic effects - the consumption of nicotine is also linked to raised alertness, euphoria, and a sensation of being relaxed. Addictive properties - nicotine is highly addictive. The American Heart Association says that nicotine (from smoking tobacco) is one of the hardest substances to quit - at least as hard as heroin. It is still in debate whether nicotine is a carcinogenic agents. Newest research proposed that nicotine increases the risk of breast cancer and promote cell instability and tumor growth.

Alkaloid is organic nitro base substances. when humans, mammals and most other types of animals are exposed to nicotine, it increases their heart rate, heart muscle oxygen consumption rate, and heart stroke volume People who regularly consume nicotine and then suddenly stop experience withdrawal symptoms, which may include cravings, a sense of emptiness, anxiety, depression, moodiness, irritability, and inattentiveness

Slide5: Nitrite is a strong N-nitrosating agent of secondary and tertiary amines. Most of the metals and metalloids are essential elements for the tobacco plant. In inhalation studies, nickel carbonyl (Ni[CO]4) induced a few pulmonary tumors in rats; upon intravenous injection of this compound, 19 out of 20 rats developed lung tumors Nitrosamine _Nitrite is a strong N-nitrosating agent of secondary and tertiary amines. _During curing and fermentation of tobacco, nitrate is partially reduced to nitrite. This lead to the forming of N-nitrosamine. _N-nitrosamines are strong carcinogens agents in mice,rats, hamsters and mink. Slide6: Phosphate fertilizers are the major source of these radioelements. minor contributions come from airborne particles carrying lead-210 and polonium-210. These particles are trapped by the trichomes on the undersides of the tobacco leaves. DDT concentration was significantly higher in cigar tobacco (10.0 - 53.0 g/g) than in cigarette tobacco (2.0 - 6.0 g/g), whereas DDD and endrin concentrations in cigar tobaccos (10 - 15 g/g and 0.0 - 0.5 ppm) and cigarette tobaccos (12 - 23 g/g and < 0.5 - 2 ppm) were comparable. _Contains at least 28 metals and more tham 10 metaloids. Ex: lead, arsenic, nickel, and mercury, are trace contaminants _Their concentrations range from 5,300 to 97,000 mg calcium/g tobacco to trace amounts, as in the case of mercury (0.05 mg/g tobacco) -> a part of these metals and metaloids will transfer into smoke and are inhaled. In additional, _ Tobacco cigarette contains or may contain radioactive elements such as Lead2010,Ra226 and Polonium210. _Cigarette tobaccos also have insect control agents- pesticides , that are applied to tobacco during cultivation of the tobacco. Ex: DDT, DDD Slide7: "Tar" is a black substance primarily derived from coal. They use it in the surface when making a road. Tar is used in the yellow part of the cigarette, the place you hold a cigartte when smoking.

Tar In solid form, tar is the brown, tacky substance that is left behind on the end of the cigarette filter. It stains a smoker's teeth and fingers brown and coats everything it touches with a brownishyellow film. Tar in cigarette smoke paralyzes the cilia in the lungs and contributes to lung diseases such as: +Emphysema +Bronchitis +Lung Cancer

Slide8: Carbon monoxide is one of the major contributors to the acute toxicity of cigar smoke. Latter you will be told about how carbon monoxide has significant effect on secondary smokers than primary smokers. Carboxylhemoglobin _Human hemoglobin has 210 times greater affinity for carbon monoxide than for oxygen. _ Inhaling tobacco smoke with up to 6 volume percent of CO diminishes the oxygen carrying capacity of the blood. _The concentration of CO intoxication (COHb) in the blood of nonsmokers amounts to about 0.5 percent, whereas in smokers it may reach 8 - 9 percent. _ In 1969, Hamill and ONeill reported two first cases of CO intoxication of cigar smokers. They are both secondary smokers. _In primary cigar smokers, COHb amounts to about 2 %; in secondary cigar smokers, the values are usually higher, up to 11%.

Slide9: Hydrogen cyanide is proven to have a detrimental effect on the cilia. The cilia are a part of the lung clearance system in humans. When the lung clearance system is impaired and toxic agents build up, the likelihood of developing a disease increases.

Slide10: Benzene is used in the manufacturing of other chemicals, including:

nylon polystyrene pesticides gasoline

People that smoke three packs of cigarette per day increase their exposure by an estimated 6 to 15 micrograms per day. PAHs also considered as one of the most human carcinogens Benzen and Polynuclear aromatic hydrocarbon

Benzene is but one of the most poisonous and carcinogenic chemical compounds found in air tainted with cigarette smoke.

_In additon, smokers contact with benzen orally.

PAHs are a group of over 100 different chemicals consisting of carbon and hydrogen in fused-ring structures .

Safely exposure to PAHs via inhalation is estimated to range from 0.2 to 3 micrograms per day. Smoking one pack of unfiltered cigarette per day increases this estimate by an additional 2 to 5 micrograms per day.

Slide11, 12 Secondary smoke can be deadlier than the smoke the actual smoker breathes. This is because second hand smoke is made from a mixture of two forms of tobacco smoke. The sidestream smoke even has higher concentrations of cancer-causing agents (carcinogens) than the mainstream smoke. And, it contains smaller particles than mainstream smoke, which make their way into the bodys cells more easily. After all the research done about secondary smoke here are some conclusions experts have made out of it. It can definitely cause diseases, which includes lung cancer to non-smokers. Children whose parents smoke constantly develop more respiratory problems. When you separate the smokers from the non-smokers, but still are in the same place. It does not eliminate the threat or the exposure of the non-smokers. If you are a non-smoker, and is now worried to the point of panicking towards your house or a place that smells like an ashtray. Fear not, cigarette odor hasnt been known to cause any problems. The only problem it gives is that it will make you stink. If you are a smoker and really care about people around you; try to reduce smoking or smoke away from them as much as possible.

Smoking, it was now maintained affected the health of millions of non-smoking Americans, mostly women and children, by exposing them to the dangers of involuntary smoking.

Secondary smoke is cigarette smoke that non-smokers inhale from nearby smokers.

Sidestream smoke the smoke that comes from the end of a lighted cigarette, pipe, or cigar and Mainstream smoke the smoke that is exhaled by a smoker

There are 35,000 to 40,000 people who die each year from heart disease and 3,000 people die from lung cancer. These people are non-smokers , but they have the same symptoms as the smokers.

Second hand tobacco smoke contains 4,000 chemical compounds, 60 of which are known to cause cancer

Evidences: _ Again, the smoke of tobacco cigarette contain nicotine, metals and metaloids, benzen, aromatic hydrocarbon, hydro cyanide and carbon monoxide

In primary cigar smokers, COHb (formed by carbon monoxide) amounts to about 2 %; in secondary cigar smokers, the values are usually higher, up to 11%.

As a primary or secondary smokers, you may or will have to suffer these kinds of diseases: 1. Heart Diseases 2. Lung Diseases 3. Lung and other Cancers. 4. Diabetes. 5. Impotence. Body cant absorb gluten in ceareal

Foodborne : ng c thc phm Colic: au bng Deterioration: gy hi

cramp: vp b

bloating: sng phng

pile up: tch t vomit: nn ma

suffer from inappetence:bing n

Paracetamol is metabolised primarily in the liver, into non-toxic products. Three metabolic pathways are notable: . Glucuronidation is believed to account for 40% to two-thirds of the metabolism of paracetamol.[73] . Sulfation (sulfate conjugation) may account for 2040%.[73] . N-hydroxylation and rearrangement, then GSH conjugation, accounts for less than 15%. The hepatic cytochrome P450 enzyme system metabolizes paracetamol, forming a minor yet significant alkylating metabolite known as NAPQI (N-acetyl-p-benzo-quinone imine).[74] NAPQI is then irreversibly conjugated with the sulfhydryl groups of glutathione. [74] All three pathways yield final products that are inactive, non-toxic, and eventually excreted by the kidneys. In the third pathway, however, the intermediate product NAPQI is toxic. NAPQI is primarily responsible for the toxic effects of paracetamol; this constitutes an example of toxication. Production of NAPQI is due primarily to two isoenzymes of cytochrome P450: CYP2E1 and CYP1A2. The P450 gene is highly polymorphic, however, and individual differences in paracetamol toxicity are believed due to a third isoenzyme, CYP2D6. Genetic polymorphisms in CYP2D6 may contribute to significantly different rates of production of NAPQI. Furthermore, individuals can be classified as "extensive", "ultrarapid", and "poor" metabolizers (producers of NAPQI), depending on their levels of CYP2D6 expression. Although CYP2D6 metabolises paracetamol into NAPQI to a lesser extent than other P450 enzymes, its activity may contribute to paracetamol toxicity in extensive and ultrarapid metabolisers, and when paracetamol is taken at very large doses.[75] At usual doses, NAPQI is quickly detoxified by conjugation.[74] Following overdose, and possibly also in extensive and ultrarapid metabolizers, this detoxification pathway becomes saturated, and, as a consequence, NAPQI accumulates. Paracetamol c chuyn ha ch yu gan thnh cc sn phm khng c hi. Ba con ng trao i cht ng ch : . Glucuronidation c cho l chim 40% n hai phn ba ca qu trnh trao i cht ca paracetamol [73]. . Sulfat (sulfate lin hp) c th chim 20-40%. [73] . N-hydroxyl ha v sp xp li, sau lin hp GSH, chim t hn 15%. h thng enzyme gan cytochrome P450 chuyn ha paracetamol, hnh thnh mt tr v thnh nin(t ngh l tin cht) cha ng k alkylating l NAPQI (Nacetyl-p-benzo-quinone imine) [74]. NAPQI sau l khng th o ngc kt hp vi cc nhm sulfhydryl ca glutathione [74]. Tt c ba con ng mang li sn phm cui cng khng c hot tnh, khng c hi, v c bi tit bi thn. Tuy nhin trong con ng th ba, sn phm trung gian NAPQI l c hi. NAPQI l tc nhn ch yu cho cc hiu ng c hi ca paracetamol, iu ny to thnh mt v d ca nhim c. Sn xut NAPQI ch yu do hai isoenzymes ca cytochrome P450 l: CYP2E1 v CYP1A2. Gen P450 rt a hnh, tuy nhin, v s khc bit c nhn trong c tnh ca paracetamol c cho l do isoenzyme 3: CYP2D6. a hnh di truyn trong CYP2D6 c th ng gp t l khc nhau ng k trong s sn xut NAPQI. Hn na, c nhn c th c phn loi l "rng ri", "cc nhanh", v "ngho" chuyn ha (nh sn xut ca NAPQI), ty thuc vo mc ca CYP2D6 biu hin. Mc d CYP2D6 chuyn ha paracetamol thnh NAPQI n mt mc t hn so vi cc enzym khc P450, hot ng ca n c th ng gp vo c tnh ca paracetamol trong metabolisers m rng v cc nhanh, khi paracetamol c ly liu rt ln [75] liu thng thng, NAPQI nhanh chng c kh bi lin hp [74] Sau khi qu liu, v c th cng trong s chuyn ha rng ri v cc nhanh, con ng gii c ny tr nn bo ha, v NAPQI c tch ly.

Recommended dose is of 1,000 mg per single dose and up to 3,000 mg per day for adults. The maximum daily dose of acetaminophen is 4,000 mg, and liver failure has been observed as low as 6,000 mg per day. The overdose threshold may be lowered in people taking other drugs, in chronic alcoholics and in serious undernourished; if the overdose is spread over a period of time the threshold may be higher, as the initial paracetamol dose is effectively metabolized. Often there are no symptoms in the first 24 hours following overdose, although there may be mild nausea and vomiting. Then loss of appetite, sweating, extreme tiredness, unusual bleeding and pain in the upper right part

of stomach may arise, followed by jaundice, confusion and loss of consciousness due to the deterioration of liver function . The treatment against paracetamol overdose is aimed at removing the drug from body and replacing the GSH. To reach this aim N-acetylcysteine is administered: it acts as a precursor of GSH and help the body in replacing it. In case of severe liver damage a transplant may be requested.