Passive Smoking: Oral and Dental Effects

Passive smoking, also known as involuntary smoking , second hand smoking or exposure to environmental tobacco smoke (ETS), is defined as inhalation of the cigarette smoke of another individual or the exhale of a smoker (1). Passive smoking can adversely affect the health of non-smokers of all age groups (1). The association of passive smoking with life threatening conditions such as lung cancer, cardiovascular diseases, and sudden infant death syndrome has been well confirmed. Besides, passive smoking is correlated with low birth weight, asthma, bronchitis, pneumonia, otitis media, increased incidence of tuberculosis, Crohn's disease, learning disorders, developmental retardation, high systolic and diastolic blood pressure, child behavior disorders and spontaneous abortion (2-4). ETS contains over 4000 chemical agents adversely affecting the oral health of passive smokers (5). Co-tinine is a nicotine biomarker with a half-life longer than that of nicotine. Measurement of cotinine level is a suitable and reliable objective and quantitative screening tool for determination of exposure to ETS as it is for active smoking (5, 6). A dose-dependent correlation exists between the number of cigarettes smoked by a smoker and the plasma and saliva cotinine levels of his/her non-smoker companion (5). Passive smoking changes the normal oral and nasopharyngeal flora and may cause upper airway infection (2). It may decrease alveolar bone density (1) or cause severe periodontitis (7), implant failure (8), gingival pigmentation in children and adults (2, 4), primary and permanent tooth decay (2, 5) and tooth loss (6). It may also delay tooth development (9). Passive smoking is a risk factor for occurrence of or facial clefts as well (10). The cigarette smoke products in active and passive smoking result in edema and inflammation via the activity of pro-inflammatory agents and local vaso-constriction. Systemically, these products decrease the level of saliva IgA and serum IgG and suppress the function of T helper cells in host immunity responses (6). It appears that passive smoking, via the above-mentioned mechanisms and oxidative stress, can cause periodontal disease like severe periodon-titis, decrease the alveolar bone density and lead to tooth loss. In active smokers, in comparison to passive smokers, plaque accumulation is among the main causes of periodontal disease (7). Moreover, cigarette smoke, via the generation of products such as carbon monoxide and cyanides, delays wound healing and its nicotine content inhibits cell proliferation and osteoblastic activity and stimulates alkaline phosphatase activity. It adversely affects fibroblast activity and decreases the …