Changes in oxidative stress levels during two weeks of smoking cessation treatment and their association with nutritional characteristics in Japanese smokers.

Although several experimental studies have reported that oxidative stress levels decrease during smoking cessation, how they change among general smokers has yet to be completely elucidated. In the present study, a total of 23 smokers who underwent smoking cessation treatment were observed for two-week changes in their levels of 8-OHdG and 8-isoprostane. Physical and nutritional characteristics were measured at the initial patient visit, and casual urine samples were collected at the initial visit and at a follow-up visit two weeks later. Oxidative stress was measured by a high performance liquid chromatography electrochemical detector, and the two-week difference in the levels of oxidative stress was assessed according to demographic and nutrient factors. Neither the urinary level of 8-OHdG nor that of 8-isoprostane decreased, although the cotinine level was decreased at two weeks. A Two-way repeated ANOVA revealed a significant interaction for fat intake by time for the change in the 8-OHdG level (P=0.03) and significant interactions for α-tocopherol intake (P=0.03), iron intake, and carbohydrate intake (P=0.03), all of which were time-dependent for the change in the 8-isoprostane level. The 8-OHdG level decreased among smokers with a high fat intake and was increased with a low fat intake. The 8-isoprostane levels were decreased among smokers with a high carbohydrate intake and increased with a low carbohydrate intake, decreased with a low iron intake and increased with a high iron intake and decreased with a low α-tocopherol intake and increased with a high α-tocopherol intake. Although the present study failed to observe a decrease in oxidative stress levels during the two-week smoking cessation period, we hypothesize that the intake levels of specific nutrients when initiating smoking cessation treatment may predict any subsequent changes in the oxidative stress levels.

Screening for secondhand smoke in schoolchildren in Japan.

BACKGROUND: There is no systematic screening for secondhand smoke exposure in children. METHODS: In 2002, we began a secondhand smoke screening (SSS) program for grade 4 elementary schoolchildren with the cooperation of public administration. The SSS program consisted of urinary cotinine measurement in children and a questionnaire survey of their parents. RESULTS: More than 1200 schoolchildren were enrolled in this program annually. The level of urinary cotinine in 30% of the children was >5 ng/mL, whereas in half of them it was undetectable. The major risk factor affecting cotinine level was mother's smoking. Average cotinine was significantly high in children who had a history of "short stature", "decayed tooth and/or periodontal disease," and "frequent stridor". In addition, the highest level of cotinine was detected in children whose father and/or mother smoked in the living room and the lowest level of cotinine was detected in children whose father and/or mother smoked on the veranda or outside the door. These levels, however, were two-fivefold higher than in children whose parents did not smoke. On follow-up questionnaire survey 4 years after initial SSS, significant elevated motivation for smoking cessation was noted. CONCLUSIONS: The SSS program is a very simple mass screen that can be done using only a urine test and is very effective for motivating parents to stop smoking with regard to cost benefit.

Urinary biomarkers for secondhand smoke.

The use of a biomarker is mandatory for quantitative analysis of exposure to secondhand smoke (SHS). This article summarizes urinary biomarkers of smoke exposure which can be now quantified. The most reliable urinary biomarkers to assess the exposure to SHS are NNAL 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol and NNAL-Glucuronides, which is metabolites of tobacco-specific nitrosamine. These substances were detected even in 50% of children who had undetectable level of cotinine (<0.5 ng/ml). Urinary cotinine, which is determined by a highly sensitive competing enzyme immunoassay, is also a useful biomarker. However, individual variability of CYP2A6 allele,in which nicotine is catalyzed to cotinine, affects the level of urinary cotinine. Approximately 20% of Japanese subjects have homozygotes or heterozygotes of the CYP2A6*4 allele, which has impaired nicotine metabolism and subsequently may underestimate the actual exposure to SHS. In assessing the exposure to SHS, therefore, individual variability of CYP2A6 gene polymorphism should be taken into consideration. The combination of urinary cotinine measurement and self-report of parents' smoking seems to be accurate to assess the exposure to SHS in mass screening.

Effects of maternal smoking during pregnancy on body composition in offspring.

BACKGROUND: The aim of the present cross-sectional study was to use objective methods to assess the association between maternal smoking and body composition in offspring. METHODS: A total of 2508 grade 4 school children were enrolled; all underwent lifestyle disease and passive smoking screening. Children were classified into four groups according to their urinary cotinine level and maternal smoking status during or before pregnancy. Items measured on lifestyle disease screening were compared among the four groups. RESULTS: Only degree of obesity (DO) and body mass index (BMI) were significantly associated with maternal smoking during pregnancy. The prevalence of both DO >20% and DO >30%, and BMI >22% and BMI >25% was highest in children of mothers who smoked during pregnancy. These children had a tendency toward shorter height and increased weight although it was not statistically significant. There were no significant differences between maternal smoking status and lipid profile among groups. Confounders such as food, exercise and sleep were able to be eliminated. CONCLUSION: Maternal smoking during pregnancy may be an independent risk factor of changing body composition in offspring, that is, shorter height and increased weight.

Maternal smoking during pregnancy and offspring obesity: meta-analysis.

BACKGROUND: Recent reports have suggested that maternal smoking may increase the risk of development of obesity in the unborn child in later life, but relatively few cohort studies have been done on the relationship between maternal smoking during pregnancy and future development of metabolic syndrome. METHODS: A systematic review and meta-analysis of observational studies reporting effect estimates and 95% confidence intervals (95%CI) was conducted on the association between maternal smoking during pregnancy and obesity of future offspring. RESULTS: Seventeen papers were identified from 444 English-language papers (key word search: maternal smoking and obesity) in PubMed. All papers showed a positive association between maternal smoking during pregnancy and childhood obesity. The meta-analysis, using the DerSimonian-Laird method, found the association to be statistically significant. In association with maternal smoking during pregnancy and body mass index with more than 95%CI in the offspring aged 3-33 years, the pooled odds ratio calculated from 16 of these 17 studies was 1.64 (95%CI: 1.42-1.90). After adjustment for publication bias, the pooled adjusted odds ratio was 1.52 (95%CI: 1.36-1.70). In addition, confounders of maternal obesity, low social status, low birthweight and not being breast-fed seemed to be risk factors for offspring obesity. CONCLUSION: Maternal smoking during pregnancy may cause future obesity and metabolic syndrome.

Enzyme-linked immunosorbent assay of nicotine metabolites.

INTRODUCTION: The level of cotinine in biological specimens, such as serum, urine, and saliva, measured by gas or liquid chromatography is the most validated and reliable indicator of exposure to tobacco smoke. However, chromatographic methods are not always suitable for all types of situations. METHODS: We validated a commercially available enzyme-linked immunosorbent assay (ELISA) that uses a polyclonal antibody to cotinine as a practical alternative to chromatographic methods. RESULTS: The cotinine antibody cross-reacts to 3-hydroxycotinine (3HC) and its glucuronide, thus generating a value for immunoreactive (IR) cotinine, which is a complex comprising cotinine, 3HC, and 3HC-glucuronide. The levels of IR cotinine in the urine of kindergarten children closely correlated with those of cotinine measured by gas chromatography-mass spectrometry (GC-MS) and reflected the smoking behavior of their parents more precisely than cotinine levels determined by GC-MS. DISCUSSION: Our findings showed that the cotinine-based ELISA can be a practical biomarker of exposure to tobacco smoke.

A passive smoking screening program for children.

BACKGROUND: There has been no report to date on mass screening of passive smoking in children using biomarkers. METHOD: To identify children exposed to actual environmental tobacco smoke (ETS), 261 children were divided into the following 3 groups: (A) both parents smoke; (B) one parent smokes; and (C) no parent smokes. Child urinary cotinine measurement and a parent questionnaire were obtained. RESULTS: Urinary cotinine was positive (>10 ng/ml) in 92 (35.2%) of the 261 children. Of the 92 children, 29 were classified into group A, 47 into group B, and 16 into group C. The percentages of children who tested positive for urinary cotinine in groups A, B, and C were 56.9%, 31.1%, and 27.1%, respectively. However, in group B, the percentage of children who tested positive for urinary cotinine was significantly higher if only the mother smoked (47.1%) than if only the father smoked (29.1%) (P<0.05). The mean+SD urinary cotinine level in group A was 12.9+/-6.5 ng/ml, and that in group B was 10.4+/-3.8 ng/ml if the mother smoked and 5.4+/-2.6 ng/ml if the father smoked. CONCLUSIONS: This smoking screening program may be useful in identifying children with actual ETS exposure and motivating their parents to either quit smoking or modify their smoking behavior around children.