A review of the literature on the mechanisms of periodontal disease under the influence of smoking. The data on the spread of the harmful habit of mankind — smoking both traditional cigarettes and alternative types of smoking — are analyzed. Smoking is the most common epidemic in the world. Today, cigarettes are considered drugs because with each cigarette burned, a person receives a certain dose of nicotine, which over time causes addiction and the development of addiction, the most common type of domestic addiction, which is a serious social and medical problem. In addition, back in 2002, tobacco smoke was officially declared a carcinogen that does not have a safe level of exposure to it. Active and passive smoking are equally harmful to the body, undermining a person's health and threatening his life. The oral cavity (RP) is the first barrier to tobacco smoke in the human body. The effect of smoking on the organs and tissues of the RP, as well as on the whole body, is primarily determined by the intensity and duration of chemical, physical and thermal action, as well as individual morphofunctional features oral mucosa (SORP). Smoking adversely affects the organs of RP, causing smoker+specific diseases such as cancer, Tappeiner's leukoplakia, smoker's melanosis, and deepens and promotes the progression of pre+existing dental diseases, such as periodontal tissue. It is established that there is a correlation between the intensity and experience of smoking and the occurrence

Cigarette smoke is a complex mixture of chemicals, including several tobacco-specific nitrosamines (TSNA). Most TSNA are formed in tobacco during the post-harvest period, while a number are produced when a cigarette is burned. Considerable evidence supports the role of TSNA important causative factors for cancers of the lung, pancreas, esophagus, and oral cavity in people who use tobacco products. Of the known TSNA, nicotine-derived nitrosamine ketone (NNK) and N-nitrosonornicotine (NNN) are the most carcinogenic. Other TSNA include N'-nitrosoanatabine (NAT) and N-nitrosoanabasine (NAB). New tobacco products (e.g., e-cigarettes) designed to attract consumers who are concerned about the health effects of tobacco have been appearing on the market. Several studies have reported that certain TSNA have been detected in the replacement liquids and vapour of e-cigarettes, but the levels are generally considerably lower than in tobacco cigarettes. Additionally, the FDA recently announced its intention to regulate TSNA in e-cigarettes, cigar tobacco and pipe tobacco. With the rise of new technologies for reducing the use of tobacco products-such as e-cigarettes- to evaluate exposure levels to these harmful chemicals over time, researchers will be monitoring levels of TSNA in the body as a result of the use of these devices.

A general mathematical model is presented for predicting the concentration and fate of particulate matter in indoor air. Using a multicomponent sectional representation, the model accounts for the effects of ventilation, filtration, deposition onto surfaces, direct emission, and coagulation. Model predictions are compared with the evolution over time of the measured aerosol size distribution following combustion of a cigarette in a single room with a low air-exchange rate. Reasonable agreement is obtained; however, further experiments are required for full validation of additional capabilities