Smokers Artistas brand<unk>  package of Mexico from the Museo del Objeto del Objeto collection The harm from smoking comes from the many toxic chemicals in the natural tobacco leaf and those formed in smoke from burning tobacco. People keep smoking because the nicotine, the primary psychoactive chemical in<unk> s, is highly addictive.<unk> s, like narcotics, have been described as "strategically addictive," with the addictive properties being a core component of the business strategy. About half of smokers die from a smoking-related cause. Smoking harms nearly every organ of the body. Smoking leads most commonly to diseases affecting the heart, liver, and lungs, being a major risk factor for heart attacks, strokes, chronic obstructive pulmonary disease (COPD) (including emphysema and chronic bronchitis), and cancer (particularly lung cancer, cancers of the larynx and mouth, and pancreatic cancer). It also causes peripheral vascular disease and hypertension. Children born to women who smoke during pregnancy are at higher risk of congenital disorders, cancer, respiratory disease, and sudden death. On average, each<unk>  smoked is estimated to shorten life by 11 minutes. Starting smoking earlier in life and smoking<unk> s higher in tar increases the risk of these diseases. The World Health Organization estimates that tobacco kills 8 million people each year as of 2019 and 100 million deaths over the course of the 20th century.<unk> s produce an aerosol containing over 4,000 chemical compounds, including nicotine, carbon monoxide, acrolein, and oxidant substances. Over 70 of these are carcinogens. The most important chemical compounds causing cancer are those that produce DNA damage since such damage appears to be the primary underlying cause of cancer. Cunningham et al. combined the microgram weight of the compound in the smoke of one<unk>  with the known genotoxic effect per microgram to identify the most carcinogenic compounds in<unk>  smoke. The seven most important carcinogens in tobacco smoke are shown in the table, along with DNA alterations they cause. +The most genotoxic cancer causing chemicals in<unk>  smoke Compound Micrograms per<unk>  Effect on DNA Ref. Acrolein 122.4 Reacts with deoxyguanine and forms DNA crosslinks, DNA-protein crosslinks and DNA adducts Formaldehyde 60.5 DNA-protein crosslinks causing chromosome deletions and re-arrangements Acrylonitrile 29.3 Oxidative stress causing increased 8-oxo-2'-deoxyguanosine 1,3-butadiene 105.0 Global loss of DNA methylation (an epigenetic effect) as well as DNA adducts Acetaldehyde 1448.0 Reacts with deoxyguanine to form DNA adducts Ethylene oxide 7.0 Hydroxyethyl DNA adducts with adenine and guanine Isoprene 952.0 Single and double strand breaks in DNA "Ulcerative colitis is a condition of nonsmokers in which nicotine is of therapeutic benefit." A recent review of the available scientific literature concluded that the apparent decrease in Alzheimer disease risk may be simply because smokers tend to die before reaching the age at which it 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 nonsmokers to survive to the age of 80. Gateway theory A very strong argument can be made about the association between adolescent exposure to nicotine by smoking conventional<unk> s and the subsequent onset of using other dependence-producing substances. Strong, temporal, and dose-dependent associations have been reported, and a plausible biological mechanism (via rodent and human modeling) suggests that long-term changes in the neural reward system take place as a result of adolescent smoking. Adolescent smokers of conventional<unk> s have disproportionately high rates of comorbid substance use, and longitudinal studies have suggested that early adolescent smoking may be a starting point or "gateway" for substance use later in life, with this effect more likely for persons with attention deficit hyperactivity disorder (ADHD). Although factors such as genetic comorbidity, innate propensity for risk-taking, and social influences may underlie these findings, both human neuroimaging and animal studies suggest a neurobiological mechanism also plays a role. In addition, behavioral studies in adolescent and young adult smokers have revealed an increased propensity for risk-taking, both generally and in the presence of peers, and neuroimaging studies have shown altered frontal neural activation during a risk-taking task as compared with nonsmokers. In 2011, Rubinstein and colleagues used neuroimaging to show decreased brain response to a natural reinforcer (pleasurable food cues) in adolescent light smokers (1–5<unk> s per day), with their results highlighting the possibility of neural alterations consistent with nicotine dependence and altered brain response to reward even in adolescent low-level smokers. Second-hand smoke Second-hand smoke is a mixture of smoke from the burning end of a<unk>  and the smoke exhaled from the lungs of smokers. It is involuntarily inhaled, lingers in the air for hours after<unk> s have been extinguished, and can cause a wide range of adverse health effects, including cancer, respiratory infections, and asthma. Nonsmokers who are exposed to second-hand smoke at home or work increase their heart disease risk by 25–30% and their lung cancer risk by 20–30%. Second-hand smoke has been estimated to cause 38,000 deaths per year, of which 3,400 are deaths from lung cancer in nonsmokers. Sudden infant death syndrome, ear infections, respiratory infections, and asthma attacks can occur in children who are exposed to second-hand smoke. Scientific evidence shows that no level of exposure to second-hand smoke is safe.
Cigarette
Tobacco smoke
Electronic cigarette
Ventilated cigarette
Smokeless tobacco
Dissolvable tobacco
Herbal cigarette
Allergen