]]>Tooth decay]]> is the most common chronic childhood disease in the United States. The annual treatment cost for childhood tooth decay is estimated to be at least $4.5 billion. Left untreated, tooth decay in children may result in pain, dysfunction, poor appearance, and even difficulties with speech development. In addition, despite reductions in smoking in the overall population, the proportion of U. S. children exposed to environmental smoke is more than 50%.

The relationship between tooth decay and ETS is complicated. Common wisdom notwithstanding, sweets do not directly cause tooth decay. Instead, sugar enables a bacteria called the Streptococcus mutans to dissolve the tooth’s enamel through the build up of lactic acid. Researchers believe that parents who smoke may be more likely to transmit the S. mutans bacteria to their children when they kiss them. ETS may also encourage the activity of S. mutans in children’s mouths by interfering with the normal function of their immune system.

ETS also increases inflammation of the respiratory tract, causing children to breathe through their mouths, which in turn leads to reduced saliva production. Reduced saliva production means less saliva to wash away lactic acid on the teeth.

Keeping all this in mind, and controlling for a multitude of other variables which may affect a child’s dental health, a study published in the March 12, 2003 issue of the Journal of the American Medical Association found that there is indeed an association between ETS and the risk of tooth decay among children.

About the study

The researchers used data from the Third National Health and Nutrition Examination (NHANES III) Survey (1988-1994) for 3,531 children between the ages of four and eleven to determine the relationship between serum cotinine levels and the presence of tooth decay. (Cotinine is a byproduct of nicotine and is used to estimate the degree of exposure to ETS.) All of the children included in the study received both dental examinations and serum cotinine level measurements.

Exposure to ETS was defined as a cotinine level between 0.2 ng/mL and 10 ng/mL. Children age twelve and older were excluded from the study in order to reduce the possibility of confusion with early active smoking. Children younger than twelve with serum cotinine levels above 10 ng/mL were excluded for the same reason.

Tooth decay was defined as decayed (unfilled) or filled teeth.

The findings

Twenty-five percent of the children in the study had at least one unfilled decayed tooth and 33% had at least one filling. Fifty-three percent had cotinine levels consistent with exposure to ETS. Elevated cotinine levels (exposure to ETS) were significantly associated with decayed and filled baby teeth, but not in permanent teeth. This relationship persisted even after adjusting for age, sex, race, family income, geographic region, frequency of dental visits, sugar intake, and blood lead level. The researchers estimated the absolute risk of tooth decay from ETS was 27% for decayed teeth and 14% for filled teeth.

How does this affect you?

The study concluded that there is an association between environmental smoke and the risk for tooth decay among children.

Although the study could not demonstrate conclusively that ETS is the cause of tooth decay, the results are consistent with what is known regarding the biologic effects of ETS on dental health. The finding that ETS was associated with tooth decay in baby teeth but not in permanent teeth suggests that exposure early in life is key to this process.

The researchers concede there may be additional variables not controlled for in the study, which contribute to the incidence of tooth decay in children, and that the issue requires further investigation. However, if the link between ETS and tooth decay is substantiated, health interventions for tooth decay should take into account ETS exposure. The promotion of a child’s dental health is yet one more reason to ensure that children have the opportunity to grow up in a smoke-free environment.