Passive Smoking & Cancers Of Head & Neck

Tobacco smoke contains about 200 toxic substances, and 70 of these are identified as carcinogens. It is widely known that both active and passive cigarette smoking is toxic to the human body. Tobacco smoke includes many carcinogenic substances, but among them, benzopyrene and nitrosoamine are particularly strong carcinogens. While benzopyrene exists in particulate form, nitrosoamine which mainly exists in gaseous form can also be found in particulate form. The association between active and passive cigarette smoking and carcinogenesis has been clarified in cancers of the lung, oral cavity, pharynx, larynx, nasal cavity, paranasal sinuses, larynx, oesophagus, stomach, large intestine, liver, kidney, pancreas, urinary bladder, and uterine cervix. Since the risk of carcinogenesis is higher in the lung, oral cavity, pharynx, and larynx directly exposed to tobacco smoke than in other regions, it is assumed that direct stimulations, such as chemical and mechanical stimulations, on the nasal, paranasal sinus, pharyngeal, and laryngeal epithelium by tobacco smoke strongly influence carcinogenesis. On that basis, regarding the fluid dynamics of tobacco smoke, when smoke passes through regions with a large volume, such as the nasal cavity/paranasal sinuses and oral cavity, the unit smoke passage area is large, smoke flow rate is slow, and concentration is low, whereas the unit smoke passage area narrows, smoke flow rate increases, and concentration rises in regions with a small volume, such as the pharynx and larynx. The airway anatomy is complex, and the strength and resistance as a lumen vary among the regions.

Passive smoking (Involuntary smoking or second-hand smoke) entails exposure to human carcinogens, which are present in tobacco smoke. The composition of involuntary smoking includes both mainstream smoke and sidestream smoke. Mainstream smoke is inhaled and exhaled by smokers; sidestream smoke is released between puffs into the air from the burning cone. Metabolites of the tobacco-specific carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) were observed in the urine of non-smokers exposed to involuntary smoking. In animal experiments, this carcinogen is thought to induce adenocarcinomas rather than squamous cell carcinomas of lung cancer, and NNK and NNN, which is a metabolite of NNK, together induce oral cavity tumours. The evidence in tobacco smoke carcinogen biomarkers, such as urinary compounds, protein adducts and DNA adducts, supports that involuntary smoking carcinogens are metabolized by passive smokers and have the potential to increase cancer risk.

Studies have shown evidence for a carcinogenic effect of involuntary smoking on head and neck organs, particularly the pharynx and the larynx. There is evidence that people exposed to second-hand smoke (passive smoking) at home or in the workplace may have a small increase in their risk of mouth and oropharyngeal cancer. Since people spend most of their time at home and the workplace, these are more likely to be the places for involuntary smoking exposure. Even if the excess risk is small, its large prevalence makes it an important environmental carcinogen. Since smoking is a modifiable behaviour by public health intervention, it is of interest to investigate the association between involuntary smoking exposure and the risk of head and neck cancer, thereby bring out required behavioural changes.