The difference of smoker’s topography has been found to be a function of sex, personality, nicotine yield, cigarette type (i.e., flavored versus non-flavored) ethnicity and etc. We evaluated the puffing behaviors of Korean smokers and its association with smoking-related biomarker levels. A sample of 300 participants was randomly recruited from metropolitan areas, South Korea. Topography measures during a 24-hour period were obtained using a CReSS pocket device. Korean male smokers smoked two puffs less per cigarette, compared to female smokers [15.0 (13.0–19.0) vs. 17.5 (15.0–21.0) as median (Interquartile range)], but had a significantly larger puff volume [62.7 (52.7–75.5) mL vs. 53.5 (42.0–64.2) mL); p = 0.012]. The interpuff interval was similar between men and women [8.9 (6.5–11.2) s vs. 8.3 (6.2–11.0) s; p = 0.122] but much shorter than other study results. A dose-response association (p = 0.0011) was observed between daily total puff volumes and urinary cotinine concentrations, after controlling for sex, age, household income level, nicotine addiction level. Understanding of the difference of topography measures, especially, larger puff volume and shorter interpuff interval of Korean smokers may help to overcome potential underestimation of internal dose of hazardous substitutes of smoking or corresponding its health effect.

Most studies on the association of in utero exposure to cigarette smoking and childhood overweight or obesity (OWO) were based on maternal self-reported smoking data and few were based on objective biomarkers. In this study, we evaluated the associations between self-reported and biomarkers of in utero exposure to cigarette smoking with risk of childhood OWO. We analyzed data from 2351 mother-child pairs in the Boston Birth Cohort, a US low-income minority cohort that enrolled children at birth and followed prospectively up to age 18 years. In utero smoking exposure was measured by maternal self-report and by maternal and cord plasma cotinine and hydroxycotinine metabolites. We assessed the individual and joint associations of each smoking exposure measure and maternal OWO with childhood OWO using multinomial logistic regressions. We used nested logistic regressions to investigate the childhood OWO prediction performance when adding maternal and cord plasma biomarkers as input covariates on top of self-reported data. Our results demonstrated that in utero cigarette smoking exposure defined by self-report and by maternal or cord metabolites were consistently associated with increased risk of long-term child OWO. Adding maternal and cord plasma biomarker information to self-reported data improved the prediction accuracy of long-term child OWO risk.

Abstract: Background: Exposure to ETS (Environmental Tobacco Smoke) is one of the most toxic environmental exposures. Objective: To investigate the impact of ETS on physiological, biochemical, psychological indicators, on the urine antioxidant capacity (AC) and oxidative damage to lipids in a pilot sample of healthy pregnant women. Methods: The exposure to ETS was investigated by a validated questionnaire, urine cotinine and the marker of oxidative damage to lipids - 8-isoprostane concentrations using an ELISA kit. Urine AC was determined by the spectrophotometric TEAC method. From the sample of pregnant women (n=319, average age 30.84 ± 5.09 years) in 80 the levels of cotinine and oxidative stress markers were analyzed. Results: From our sample, 5 % individuals (7.4 % objectified by cotinine) were current smokers and 25 % reported passive smoking in the household (18.8 % objectified by cotinine). The Kappa was 0.78 for smokers and 0.22 for ETS exposed non-smokers. Smokers as well as non-smokers had significantly higher (p<0.05) urine AC than ETS exposed non-smokers. Non-smokers had significantly lower levels of 8-isoprostane than smokers (p<0.01) and ETS-exposed non-smokers (p<0.05). Correlations between urine levels of cotinine and AC were positive in ETS exposed non-smokers. Conclusion: The harmful effect of active and passive smoking on oxidative stress parameters has been indicated.

We assessed if there were any sex-related differences in the ability of nicotine to increase plasma corticosterone secretion after single or repeated nicotine administration. For single-dose studies, male and female mice were habituated to the test room for 1 h and injected with saline or nicotine (0.25 or 1 mg/kg, s.c.). In repeated-dosing studies, mice were injected with saline or nicotine (1 mg/kg, s.c.) once daily for six days, and, on day 7, received nicotine (1 mg/kg, s.c.). The mice were euthanized 15 min later, and trunk blood was collected for the measurement of corticosterone, nicotine, and cotinine. Our results showed that saline or nicotine each significantly increased plasma corticosterone levels in both male and female mice, with a greater response in female mice. Plasma corticosterone levels were increased in male but not female mice after repeated compared to single nicotine administration. The level of cotinine, a biomarker of nicotine use, was significantly higher in female than in male mice. Taken together, these novel findings suggest that female mice responded to nicotine and stress of handling more than male mice and provide for the first-time quantitative data on the male-female differences in nicotine-induced elevations of corticosterone and of cotinine.