Several investigations have been conducted regarding adverse effects of ETS exposure in adults, while in pediatrics most studies have focused on correlation between ETS exposure and respiratory diseases[11, 12]
. In this case-control study we intended to investigate the relationship between esophagitis and UCL in children. Our results revealed that the mean UCL was higher in patients group than in the control group. Moreover, the odds ratio indicated that exposure to ETS increases the risk of developing esophagitis. The higher median UCL in esophagitis group also confirmed the same results. Our results are in line with the study of Wielkoszynski et al that proposed nicotine metabolites are higher in esophagitis patients than healthy children
. Shabib et al has also found that passive smoking is a risk factor for esophagitis in children
In our study, we measured UCL instead of using questionnaires, this makes our study more reliable than studies that are only based on history of self-administered questionnaires. Self-reported history of ETS exposure has a low validity and reliability, it may mainly result from reluctance of parents on providing data on their smoking habits
Additionally, air ventilation, smoking patterns, nicotine yield in different cigarette brands, and the time of exposure to ETS varies widely that can affect validity of questionnaires. However, by measuring biomarkers for recent ETS exposure the bias created by above-mentioned factors may be reduced.
According to our findings, the mean UCL in children whose parents were cigarette smokers was higher than in children with non-smoker parents, this suggests correlation between passive smoking and UCL. The odds ratio also confirmed this issue as well. On the other hand, UCL was found to be higher in younger children that can be caused by the longer time younger children spend in close proximity to their parents.
Crowding index did not differ in the two groups which may be due to unequal air conditioning, number of windows and smoking pattern in each condition. However, it is expected that the adverse effects of ETS be raised in high-density populations exposed to tobacco smoke.
Our study had its own limitations. The major limitation of our study was lack of a specific cutoff point for urinary cotinine in pediatrics. There are several studies in adults regarding urinary cotinine cutoffs for passive smokers, non-smokers and active smokers, while in children few studies have investigated the cotinine levels and more research is needed to assess the values
. On the other hand, uptake, distribution, metabolism, and excretion of nicotine vary widely in each individual that can affect the results accordingly. Another limitation of our study was due to the short half-life of cotinine that cannot determine the time, frequency and pattern of tobacco exposure. Therefore, long-term cotinine levels must be measured to evaluate the exact ETS exposure in children because the pattern of smoking may be different shortly before sampling. Other issue to be in mind is that although we tried to homogenize our cases and also controls, socioeconomic status and living areas may differ and it was unenvitable.
We chose controls from outpatient healthy consecutive cases who visited the hospital for general health care or vaccination. We could not perform endoscopy or biopsy and the possibility exists that controls had esophagitis but the physicians examined children and found clinically no signs and symptoms of gastrointestinal disease.