Passive smoking causes damage to human health due to pathologies largely similar to those caused by active smoking (smoking and the effects of smoking on health). It is causing more and more damage in industrialized and non-industrialized countries (Indonesia, for example, is one of the world's largest per capita consumers of tobacco).
In the USA this phenomenon brings up to 60,000 deaths every year in the 2000s, previously, in the 1980s, mortality had been reported from 35,000 to 40,000 deaths per year. The level of toxicity of passive smoking is much lower than that of active smoking, but in any case they involve substantial damage to the organism, constituting a risk factor for various heart diseases, the same WHO, the world health organization, has expressed highlighting its dangerousness, in front of 192 countries that have adopted the measures expressed there.
The study: Passive smoking induces nasal biofilms in children, published on the International journal of pediatric otorhinolaryngology, said how passive exposure of children to cigarette smoke has been implicated in several recalcitrant respiratory childhood disorders.
However, to our knowledge, no information is available regarding the connection between passive exposure to tobacco smoke and the formation of nasal biofilms in children. The present study was therefore geared at investigating the hypothesis that exposure of children to household passive smoking may induce the formation of nasal biofilms.
The study included 20 children between the ages of 6 and 12 years with a positive history of prolonged exposure to household passive smoke, and who required inferior turbinate reduction together with other procedures. Another 20 children who required similar surgeries but with negative history of exposure to household smoking formed the control group.
None of children, in the study and control groups, had evidence of adenoids or infective rhinosinusitis. At the time of surgery, a tiny biopsy was taken from the lower border of the inferior turbinate. The specimens were processed for scanning and transmission electron microscopy.
The nasal mucosa of 11 out of 20 children with positive history of exposure to passive smoking showed biofilm formation. Ten of these biofilms grew S. aureus. On the other hand, only one child in the control group showed nasal biofilm.
Longer exposure to tobacco smoke and higher urinary cotinine levels were associated with more frequent biofilm formation. Likewise, children of heavy smokers developed biofilms more frequently than other children. On the other hand, the age of the children and nasal allergy had no effect on the chances of biofilm formation.
This is a preliminary report showing that children exposed to household passive cigarette smoking may develop nasal biofilms. Development of these biofilms may increase susceptibility of affected children to persistent sinonasal and possibly other respiratory infections.