Multicomponent Behavioural Intervention during Pregnancy to Reduce Home Exposure to Second-Hand Smoke: A Pilot Randomised Controlled Trial in Bangladesh and India.

BACKGROUND: Pregnant women exposed to second-hand smoke (SHS) are at increased risk of poor birth outcomes. We piloted multicomponent behavioural intervention and trial methods in Bangalore, India, and Comilla, Bangladesh. METHODS: A pilot individual randomised controlled trial with economic and process evaluation components was conducted. Non-tobacco-using pregnant women exposed to SHS were recruited from clinics and randomly allocated to intervention or control (educational leaflet) arms. The process evaluation captured feedback on the trial methods and intervention components. The economic component piloted a service use questionnaire. The primary outcome was saliva cotinine 3 months post-intervention. RESULTS: Most pregnant women and many husbands engaged with the intervention and rated the components highly, although the cotinine report elicited some anxiety. Forty-eight (Comilla) and fifty-four (Bangalore) women were recruited. The retention at 3 months was 100% (Comilla) and 78% (Bangalore). Primary outcome data were available for 98% (Comilla) and 77% (Bangalore). CONCLUSIONS: The multicomponent behavioural intervention was feasible to deliver and was acceptable to the interventionists, pregnant women, and husbands. With the intervention, it was possible to recruit, randomise, and retain pregnant women in Bangladesh and India. The cotinine data will inform sample size calculations for a future definitive trial.

NHANES-based analysis of the correlation between leisure-time physical activity, serum cotinine levels and periodontitis risk.

OBJECTIVE: To investigate the association of leisure-time physical activity and serum cotinine levels with the risk of periodontitis in the general population and to further analyze the interaction between leisure-time physical activity and serum cotinine levels on the risk of periodontitis. METHODS: This was a cross-sectional study, extracting data from 9605 (56.19%) participants in the National Health and Nutrition Examination Survey (NHANES) database from 2009 to 2014, and analyzing the relationship and interaction effects of serum cotinine level, leisure time physical activity, and risk of periodontitis by weighted univariate logistic modeling; Effect sizes were determined using ratio of ratios (OR), 95% confidence intervals (95% CI). RESULTS: 5,397 (56.19%) of 9,605 participants had periodontitis; an increased risk of periodontitis was found in those in the leisure time physical activity intensity < 750 MET × min/week group (OR = 1.44, 95% CI: 1.17-1.78). Serum cotinine levels ≥ 0.05 ng/ml were associated with an increased risk of periodontitis (OR = 1.99, 95% CI: 1.69-2.33). The group with low leisure physical activity and serum cotinine levels ≥ 0.05 ng/ml had an increased risk of periodontitis compared to the group with high leisure physical activity and serum cotinine levels < 0.05 ng/ml (OR = 2.48, 95% CI: 1.88-3.27). Interaction metrics RERI = 0.90 (95% CI: 0.44-1.36) and API = 0.36 (95% CI: 0.18-0.55); CI for SI = 2.55 (95% CI: 1.03-6.28). for API 0.36. CONCLUSION: Leisure time physical activity intensity interacted with smoking exposure on periodontitis risk and may provide the general population with the opportunity to Increasing leisure-time physical activity and smoking cessation may provide recommendations for the general population.

Consumption of hookahs, e-cigarettes, and classic cigarettes and the impact on medically assisted reproduction treatment.

Smoking of classic cigarettes has been well-established as a health risk factor, including cardiovascular, neurological, and pulmonary diseases. Adverse effects on human reproduction have also been shown. Smokers are assumed to have a significantly lower chance of pregnancy, however, the impact of smoking on medically assisted reproduction (MAR) treatment outcomes is controversial. Moreover, smoking habits have changed during the last decades since e-cigarettes and hookahs, or water pipes, have become very popular, yet little is known regarding vaping or hookah-smoking patients undergoing MAR treatments. This prospective study aimed to examine the presence of benzo[a]pyrene, nicotine, and its main metabolite, cotinine, in human follicular fluid (FF) in non-smoking, smoking, and vaping/hookah-smoking patients and to evaluate the impact on female fertility. Human FF samples were collected from 320 women subjected to intracytoplasmic sperm injection (ICSI) cycles due to male subfertility. Gas chromatography combined with mass spectrometry was used to analyse the presence of benzo[a]pyrene, nicotine, and cotinine. A questionnaire was provided to assess patient consumption behaviour and to identify (1) non-smoking patients, (2) patients who consumed cigarettes, and (3) patients with exclusive consumption of e-cigarettes or hookahs. Data were analysed using linear and logistic regression, Fisher's exact test, and the Mann-Whitney U Test. Nicotine was present in 22 (6.8%) and cotinine in 65 (20.3%) of the 320 samples. The nicotine and cotinine concentrations per sample ranged from 0 to 26.3 ng/ml and 0-363.0 ng/ml, respectively. Benzo[a]pyrene was not detectable in any of the samples analysed. Nicotine and cotinine were also present in the FF of patients with exclusive consumption of e-cigarettes or hookahs. The clinical pregnancy rate, fertilization and maturation rates, and number of oocytes per oocyte pick-up were not statistically significantly different between non-smoking, smoking, or vaping/hookah-smoking patients. Smoking and the accumulation of smoking toxins in the FF have no impact on the outcome of MAR treatments-neither the clinical pregnancy rate, maturation and fertilization rates, nor the number of retrieved oocytes were affected. For the first time, nicotine and cotinine were quantified in the FF of patients exclusively vaping e-cigarettes or smoking hookahs. Since vaping liquids and hookah tobaccos contain potentially harmful substances, other adverse effects cannot be excluded.Trial registration ClinicalTrials.gov Identifier: NCT03414567.

Unraveling the link: environmental tobacco smoke exposure and its impact on infertility among American women (18-50 years).

Purpose: The detrimental effects of environmental tobacco smoke (ETS) on women's reproductive health have been widely recognized. However, the detailed association between exposure to environmental tobacco smoke and the incidence of infertility remains under-explored. This investigation focuses on exploring this potential connection. Methods: For this analysis, we extracted data from the US National Health and Nutrition Examination Survey (NHANES) database, covering the years 2013 to 2018, focusing on individuals with recorded serum cotinine levels and infertility information. ETS exposure and fertility status were analyzed as independent and dependent variables, respectively. We applied weighted multivariate logistic regression method to evaluate the impact of ETS on infertility, including subgroup analyses for more detailed insights. Results: The study encompassed 3,343 participants. Logistic regression analysis revealed a notable positive correlation between ETS exposure and infertility, with an odds ratio (OR) of 1.64 (95% Confidence Interval [CI]: 1.14-2.36). We observed a non-linear relationship between ETS exposure and infertility risk. Notably, infertility risk increased by 64% in serum cotinine levels above 0.136 compared to that in serum cotinine levels below 0.011. Further, subgroup analysis and interaction tests showed consistent results across different segments, underscoring the robustness of the ETS-infertility link. Conclusion: Our findings suggest that environmental tobacco smoke exposure may be a contributing factor to infertility. These results reinforce the recommendation for women in their reproductive years to avoid ETS exposure, especially when planning for pregnancy.

Associations of active and passive tobacco exposure with elevated blood pressure in Korean adolescents.

OBJECTIVES: To test the hypothesis that tobacco exposure is associated with elevated blood pressure (EBP) in Korean adolescents, and that the association is dose dependent. METHODS: This cross-sectional study used data from the 2011-2020 Korea National Health and Nutrition Survey (KNHANES). Subjects were eligible if they were 13-18 years at the time of participation in KNHANES. Tobacco exposure was defined by urine cotinine level. The main outcomes were EBP and hypertension. Statistical analyses were conducted using SAS version 9.4 with appropriate sampling weights to account for the complex survey design, stratification, and cluster variable. RESULTS: A total of 2,518 adolescents was included in the analysis, representing 2.5 million Korean adolescents. The mean± standard deviation participant age was 15.3±1.7 years, and 55.3% were male. The number of participants with active tobacco smoke exposure was 283 (11.2%), passive tobacco smoke exposure was 145 (5.8%), and no smoke exposure was 2,090 (83.0%). Analysis of the 2,518 urine-cotinine-verified participants showed that tobacco smoke exposure had a significant effect on EBP: with an odds of elevated blood pressure of 3.00 (95% confidence interval [CI], 1.14 to 7.89). The odds of hypertension were 3.61 (95% CI, 1.13 to 11.49) in the active smoking group compared with the no tobacco exposure group after adjustment for potential confounders. CONCLUSIONS: It is necessary to present a range of public health plans to reduce tobacco exposure that affects adolescents' blood pressure, and further research with a larger number of participants using urine cotinine as a biomarker is needed.

Changes in biomarkers of exposure and withdrawal symptom among Chinese adult smokers after completely or partially switching from combustible cigarettes to an electronic nicotine delivery system.

This study assessed changes in biomarkers of exposure (BoE) after 5 days of completely or partially switching to an electronic nicotine delivery system (ENDS) use, compared with continued use of combustible cigarettes and smoking abstinence among Chinese adult smokers. A randomized, open-label, parallel-arm study was conducted among Chinese adult smokers who were naive ENDS users. Forty-six subjects were randomized to 4 study groups (n = 11-12 per group): exclusive ENDS use, dual use of ENDS and cigarettes, exclusive cigarettes use, and smoking abstinence. Subjects were confined in clinic for 5 consecutive days and product use was ad libitum. Nicotine and its metabolites (cotinine and 3-hydroxycotinine), and BoEs (AAMA, CEMA, HEMA, HMPMA, 3-HPMA, SPMA, exhaled CO, and exhaled NO) were measured. Withdrawal symptom was measured using MNWS throughout the 5-day period. Six urine BoEs of volatile organic compounds decreased by 55.1-84.1% in the exclusive ENDS use group, which is similar to the smoking abstinence group (67.2-87.4%). The level of decrease was 56.8-70.4% in the dual use group and 10.7-39.0% in the cigarettes group. Urine total nicotine exposure had a non-significant increase in the exclusive ENDS use group, and plasma nicotine and cotinine showed a trend of increasing day by day. After completely or partially switching to ENDS use among Chinese smokers, exposure to selected toxicants were significantly decreased. The results of this study add to the body of evidence that exposure to toxic substance decreased among smokers after complete or partial switch from combustible cigarettes to ENDS use. As part of transition to experienced ENDS use, this study found that smokers of the initial stage who have no prior ENDS experience may increase nicotine intake after switching to ENDS use.

Effect of children secondhand smoke exposure associated with GABA concentration: Influence from parents who are extremely heavy smokers in urban households.

BACKGROUND: Secondhand smoke (SHS) poses the most considerable health risk to children in urban households. However, limited evidence exists regarding the impact of children exposure to SHS on gamma-aminobutyric acid (GABA) levels. This study aimed to investigate the level of cotinine and GABA and their association with variables related to children exposed to SHS. METHODS: A cross-sectional analysis was conducted to assess urinary cotinine and GABA levels in respondents. The study involved 85 participants aged 2-4 years who resided with parents exhibiting heavy smoking habits in urban households in Bangkok, Thailand. Urinary cotinine and GABA concentrations were utilized as biomarkers and measured using an enzyme-linked immunosorbent assay kit. An independent t-test was employed to compare contributing factors with urinary cotinine metabolites. Spearman's correlation test was utilized to assess the relationship between cotinine metabolites and GABA concentration. RESULTS: The study found a correlation between urinary cotinine metabolites and GABA concentration among children's (r = 0.260, p-value = 0.016), particularly influenced by parents exhibiting extreme heavy smoking in urban households. Male children exhibited significantly higher urinary cotinine metabolite concentrations than females (p-value = 0.040). Moreover, significantly elevated levels of cotinine metabolites (57.37 ± 10.27 ng/ml) were observed in households where parents engaged in extreme heavy smoking. CONCLUSIONS: This research establishes a link between urinary cotinine metabolite levels and GABA concentration among children exposed to extreme heavy smoking by their parents in urban households. Consequently, smoking might impact neurobehavioral effects, potentially leading to insomnia. The study emphasizes the importance of promoting and safeguarding non-smokers from exposure to SHS in indoor workplaces, public spaces, and households, advocating for the implementation of smoke-free public health regulations.

Correlation analysis between smoke exposure and serum neurofilament light chain in adults: a cross-sectional study.

BACKGROUND: Smoke exposure is a prevalent and well-documented risk factor for various diseases across different organ systems. Serum neurofilament light chain (sNfL) has emerged as a promising biomarker for a multitude of nervous system disorders. However, there is a notable paucity of research exploring the associations between smoke exposure and sNfL levels. METHODS: We conducted a comprehensive analysis of the National Health and Nutrition Examination Survey (NHANES) cross-sectional data spanning the years 2013 to 2014. Serum cotinine levels were classified into the following three groups: < 0.05, 0.05-2.99, and ≥ 3 ng/ml. Multiple linear regression models were employed to assess the relationships between serum cotinine levels and sNfL levels. Additionally, we utilized restricted cubic spline analyses to elucidate the potential nonlinear relationship between serum cotinine and sNfL levels. RESULTS: A total of 2053 participants were included in our present research. Among these individuals, the mean age was 47.04 ± 15.32 years, and males accounted for 48.2% of the total study population. After adjusting the full model, serum cotinine was positively correlated with sNfl in the second group (ß = 0.08, 95%CI 0.01-0.15) and in the highest concentration of serum cotinine (ß = 0.10, 95%CI 0.01-0.19) compared to the group with the lowest serum cotinine concentrations. Current smokers, in comparison to non-smokers, exhibited a trend toward elevated sNfL levels (ß = 0.07, 95%CI 0.01-0.13). Furthermore, subgroup analyses revealed interactions between serum cotinine levels and different age groups (P for interaction = 0.001) and gender stratification (P for interaction = 0.015) on sNfL levels. CONCLUSION: The study suggested that serum cotinine was significantly and positively associated with sNfl levels in adult participants. Furthermore, current smokers tend to exhibit elevated sNfL levels. This research sheds light on the potential implications of smoke exposure on neurological function impairment and underscores the importance of further exploration in this area.

Association between secondhand smoke exposure and incident heart failure: The Multi-Ethnic Study of Atherosclerosis (MESA).

AIMS: There are no studies on the association between secondhand smoke (SHS) exposure and incident heart failure (HF). This cohort study aimed to examine the associations of self-reported and urinary cotinine-assessed SHS exposure with incident HF. METHODS AND RESULTS: This study included 5548 non-active smoking participants aged 45-84 years and free of known cardiovascular diseases and HF at baseline who self-reported SHS exposure time in the Multi-Ethnic Study of Atherosclerosis (MESA) at baseline (2000-2002). A cohort subset of 3376 non-active smoking participants underwent urinary cotinine measurements. HF events were verified by medical records or death certificates and ascertained from baseline through 2019. Multivariable Cox proportional hazards regression analysis was used with adjustment for demographic variables, traditional cardiovascular risk factors, physical activity, tobacco pack-years and medications. During a median follow-up of 17.7 years, 353 and 196 HF events were identified in the self-report cohort and cohort subset, respectively. In the self-report cohort, compared with the SHS unexposed group (0 h/week), the highest tertile of the SHS exposed group (7-168 h/week) was not associated with incident HF (hazard ratio [HR] 0.70, 95% confidence interval [CI] 0.49-1.00; p = 0.052). In contrast, in the cohort subset, participants with detectable urinary cotinine >7.07 ng/ml had a higher risk of incident HF than those with undetectable urinary cotinine ≤7.07 ng/ml (HR 1.45, 95% CI 1.03-2.06; p = 0.034). There were no significant heterogeneities in HF risk by age, sex, race/ethnicity, or past smoking status. CONCLUSION: Secondhand smoke exposure reflected by modestly increased urinary cotinine (>7.07 ng/ml) rather than self-report in non-active smokers was associated with a 40-50% higher risk of any HF event.

Evaluation on the Sex-Specific Association Between Cigarette Smoke Exposure and Inflammation Markers-C-Reactive Protein and White Blood Cell Count.

INTRODUCTION: Cigarette smoke increases peripheral white blood cell (WBC) count. However, the dose-dependent association between smoking and C-reactive protein (CRP), an important inflammatory marker, has been reported as inconsistent. AIMS AND METHODS: Here, we evaluated the associations between smoking and CRP using both smoking questionnaires and urine cotinine as exposure markers. The Korea National Health and Nutrition Examination Survey data were used for analyzing the associations. Multiple regression analyses were performed to examine the associations between cigarette smoke exposure, as assessed by questionnaires and urine cotinine, and health effects, as measured by CRP and WBC count, controlling for potential confounders. The confounders, including age, sex, body mass index, blood pressure, cholesterol, glucose, alanine aminotransferase, and uric acid, were selected a priori based on the literature. RESULTS: A total of 11 435 participants were included for analysis. For the exposure-response relationship, the results indicated a significant increase in CRP levels in male smokers compared to male nonsmokers (p = .002), whereas no significant increase was found in female smokers compared to female nonsmokers (p = .680). For the dose-response relationship, a significant positive association was observed between urine cotinine and CRP in male smokers (p = .018), whereas no significant association was found in female smokers (p = .508). WBC count consistently showed significant exposure-response and dose-response relationships in both sexes. CONCLUSIONS: WBC count was found to be a consistent effect marker of cigarette smoke exposure, while the association between CRP level and smoking was inconsistent and varied by sex. The sex-specific response to cigarette smoke exposure warrants further exploration in future studies. IMPLICATIONS: Cigarette smoke exposure is known to increase inflammation and has been thought to increase CRP, a significant inflammation marker. However, recent studies have reported conflicting results regarding the dose-dependent association between cigarette smoke exposure and CRP. This study found that the association between smoking and CRP is inconsistent and varies by sex, showing significant exposure response in men but not in women. Furthermore, the study suggests that WBC count is a more consistent marker for cigarette smoke exposure.

Tobacco Smoke Exposure and Sleep Duration among U.S. Adolescents.

OBJECTIVES: Tobacco smoke exposure (TSE) and poor sleep are public health problems with their own set of consequences. This study assessed whether TSE was associated with sleep duration among U.S. adolescents. METHOD: We conducted a secondary analysis of 2013-2018 National Health and Nutrition Examination Survey data including 914 nontobacco-using adolescents ages 16-19 years. TSE measures included cotinine and self-reported home TSE groups including no home TSE, thirdhand smoke (THS) exposure, and secondhand smoke (SHS)+THS exposure. Sleep duration was assessed in hours and categorically as insufficient sleep (recommended hours). Weighted multiple linear regression and multinomial regression models were conducted. RESULTS: Adolescents with higher log-cotinine levels had higher number of sleep hours (ß = 0.31, 95%CI = 0.02,0.60) and were at increased odds of reporting excess sleep (AOR = 1.41, 95%CI = 1.40,1.42), but were at reduced odds of reporting insufficient sleep (AOR = 0.88, 95%CI = 0.87,0.89). Compared to adolescents with no home TSE, adolescents with home THS exposure and home SHS+THS exposure were at increased odds of reporting insufficient sleep (AOR = 2.27, 95%CI = 2.26,2.29; AOR = 2.75, 95%CI = 2.72,2.77, respectively) and excess sleep (AOR = 1.89, 95%CI = 1.87,1.90; AOR = 5.29, 95%CI = 5.23,5.34, respectively). CONCLUSIONS: TSE may affect insufficient and excess sleep duration among adolescents. Eliminating TSE may promote adolescent respiratory and sleep health.

Prevalence of Underreported Nicotine Exposure Among US Nonsmoking Adults: A Comparison of Self-Reported Exposure and Serum Cotinine Levels From NHANES 2013-2020.

INTRODUCTION: Secondhand smoke (SHS) poses a significant health risk. However, individuals who do not smoke may be unaware of their exposure, thereby failing to take protective actions promptly. AIMS AND METHODS: We assessed the prevalence of underreported nicotine exposure in a nationally representative sample of US nonsmoking adults using data from the US National Health and Examination Survey. Individuals with underreported nicotine exposure were defined as those who reported no exposure to all tobacco products (traditional tobacco, nicotine replacements, and e-cigarettes) or SHS, yet had detectable levels of serum cotinine (>0.015 ng/mL). We fitted logistic regression models to determine sociodemographic and chronic condition factors associated with underreported nicotine exposure. RESULTS: Our analysis included 13 503 adults aged 18 years and older. Between 2013 and 2020, the prevalence of self-reported SHS exposure, serum cotinine-assessed nicotine exposure, and underreported nicotine exposure among US nonsmokers were 22.0%, 51.2%, and 34.6%, respectively. Remarkably, 67.6% with detectable serum cotinine reported no SHS exposure. Males, non-Hispanic blacks, individuals of other races (including Asian Americans, Native Americans, and Pacific Islanders), and those without cardiovascular diseases were more likely to underreport nicotine exposure than their counterparts. The median serum cotinine value was higher in respondents who reported SHS exposure (0.107 ng/mL) than in those who reported no exposure (0.035 ng/mL). We estimate that approximately 56 million US residents had underreported nicotine exposure. CONCLUSIONS: Over a third of US nonsmokers underreport their nicotine exposure, underlining the urgent need for comprehensive public awareness campaigns and interventions. Further research into sociodemographic determinants influencing this underreporting is needed. IMPLICATIONS: Understanding the extent of underreported nicotine exposure is crucial for developing effective public health strategies and interventions. It is imperative to bolster public consciousness about the risks associated with SHS. Additionally, surveillance tools should also incorporate measures of exposure to outdoor SHS and e-cigarette vapor to enhance the quality of data monitoring. Findings from this study can guide tobacco control initiatives and inform smoke-free air legislation.

Inflammatory marker levels in children with tobacco smoke exposure.

BACKGROUND: Tobacco smoke exposure (TSE) has inflammatory and immunosuppressive effects which may be associated with altered levels of inflammatory markers and pediatric illnesses. OBJECTIVE: The primary objective was to examine the associations of cotinine-confirmed and parent-reported child TSE patterns and discharge diagnoses with C-reactive protein (CRP), IL-8, and IL-10 in 0-11-year-old pediatric emergency department (PED) patients who lived with ≥ 1 smoker. METHODS: Saliva samples were obtained from 115 children with a mean (SD) age of 3.5 (3.1) years during the PED visit (T0). Saliva was analyzed for cotinine, CRP, IL-8, and IL-10. Parents self-reported their children's TSE patterns; children's medical records were reviewed to identify and categorize discharge diagnoses. Linear regression models were utilized to find T0 associations of cotinine-confirmed and parent-reported child TSE patterns, and PED diagnoses with each inflammatory marker. All models were adjusted for child race/ethnicity, child sex, annual household income, and housing type. The TSE models also adjusted for child discharge diagnosis. RESULTS: At T0, the geometric mean (GeoM) of cotinine was 4.1 ng/ml [95 %CI = 3.2-5.2]; the GeoMs of CRP, IL-8, and IL-10 were 3,326 pg/ml [95 %CI = 2,696-4,105], 474 pg/ml [95 %CI = 386-583], and 1.1 pg/ml [95 %CI = 0.9-1.3], respectively. Parent-reported child TSE patterns were positively associated with ln-transformed CRP levels, while adjusting for the covariates (ß^ = 0.012 [95 %CI:0.004-0.020], p = 0.037). In the parent-reported child TSE pattern model, there were significant positive associations between the covariate of child age with CRP and IL-8 levels (p = 0.028 and p < 0.001, respectively). Children with a bacterial diagnosis had higher IL-8 levels (p = 0.002) compared to the other diagnosis groups. CONCLUSIONS: Results indicate that parent-reported child TSE increases the expression of CRP in ill children and supports prior work demonstrating that IL-8 is higher in children with TSE who have bacterial infections. These findings should be examined in future research with ill children with and without TSE.

Analysis of wastewater from 2013 to 2021 detected a recent increase in nicotine use in Queensland, Australia.

Previous wastewater-based epidemiology (WBE) studies have reported decreasing trends of nicotine and tobacco use in Australia before 2017, but there is concern that increasing illicit use of nicotine in vaping products and illicit tobacco could reverse this progress. This study aimed to assess temporal trends of nicotine consumption and specifically tobacco consumption via wastewater analysis in a population in Australia between 2013 and 2021. One week of daily wastewater samples were analyzed every two months from February 2013 to December 2021 in a regional city serving ∼100,000 people. A total of 340 daily samples were analyzed for anabasine (tobacco specific biomarker) and nicotine metabolites, cotinine and hydroxycotinine, using direct injection method by liquid chromatography with tandem mass spectrometry. Daily consumption estimates were calculated from daily flow data, population estimates and previously reported excretion factors. Linear spline regression was performed to identify periods when significant change of slopes occurred and to evaluate the temporal trends. Tobacco use monitored using anabasine as a biomarker, showed a decreasing trend over the whole period with a higher rate of decrease during the first two years (2013-2014, 21 % decrease) compared to the later 7 years (2015-2021, 10 % decrease). Nicotine use, monitored using cotinine and hydroxycotinine, showed a downward trend between 2013 and 2018 (2013-2014: 18 % decrease, p < 0.05; 2015-2016: 6 % increase, p = 0.48; Feb-Dec 2017: 15 % decrease, p = 0.39) followed by a significant increase from 2018 to 2021 (40 % increase, p < 0.001). This finding suggests the increasing use of non-tobacco nicotine-based products. Additionally, the tobacco use estimate by wastewater analysis was higher than the tobacco sales data, which suggests the use of illicit tobacco in the catchment.

Systemic inflammation mediates the association between environmental tobacco smoke and depressive symptoms: A cross-sectional study of NHANES 2009-2018.

BACKGROUND: Depression is associated with both environmental tobacco smoke (ETS) and inflammation. However, whether systemic inflammation mediates the ETS-depression relationship is unclear. METHODS: We analyzed 19,612 participants from the 2009-2018 National Health and Nutrition Examination Survey (representing approximately 206,284,711 USA individuals), utilizing data of depressive symptoms (assessed by Patient Health Questionnaire-9), blood cotinine level (an ETS biomarker), dietary inflammatory index (DII, assessed by 24-h dietary recall) and inflammation, represented by immune-inflammation index (SII) and systemic inflammation response index (SIRI). RESULTS: Weighted multivariable logistic regression showed that a higher blood cotinine level is significantly associated with a higher depressive symptoms risk (OR = 1.79, 1.35-2.38). After adjusting for covariates, the effect in smokers (OR = 1.220, 95 % CI: 1.140-1.309) is larger than that in non-smokers (OR = 1.150, 95 % CI: 1.009-1.318). Compared to the lowest level, depressive symptoms risks in participants with the highest level of SII, SIRI and DII are 19 % (OR = 1.19, 1.05-1.35), 15 % (OR = 1.15, 1.01-1.31) and 88 % (OR = 1.88, 1.48-2.39) higher, respectively. Weighted linear regression demonstrated positive correlations of SII (ß = 0.004, 0.001-0.006), SIRI (ß = 0.009, 0.005-0.012) and DII (ß = 0.213, 0.187-0.240) with blood cotinine level. Restricted cubic splines model showed a linear dose-response relationship between blood cotinine and depressive symptoms (Pnon-linear = 0.410), with decreasing risk for lower DII. And SII and SIRI respectively mediate 0.21 % and 0.1 % of the association between blood cotinine and depressive symptoms. LIMITATION: Cross-sectional design, and lack of medication data for depression. CONCLUSIONS: Positive association of ETS (blood cotinine) with depressive symptoms risk is partly mediated by systemic inflammation, and anti-inflammatory diet could be beneficial.

Influence of tobacco product wastes in a protected coastal reserve adjacent to urbanization.

The present study, conducted at the Kendall-Frost Mission Bay Marsh Reserve in San Diego, California, aimed to assess tobacco-related pollutants in urban waters, a topic with limited prior research. Across 26 events occurring between November 2019 and February 2022, encompassing both wet and dry seasons at two outfall sites (Noyes St. and Olney St.), water and sediment samples were subjected to analysis for nicotine and cotinine levels, with Noyes St. displaying wide variation in nicotine concentrations, reaching a peak of 50.75 ng/L in water samples, whereas Olney St. recorded a peak of 1.46 ng/L. Wet seasons consistently had higher nicotine levels in water, suggesting the possibility of tobacco litter entering the reserve through stormwater runoff. Cotinine was detected in both sites in both water and sediment samples; however, these levels were considerably lower in comparison to nicotine concentrations. Limited research assesses aquatic environmental pollution from tobacco use and disposal, especially in protected areas like urban natural reserves. This study was conducted at the Kendall-Frost Mission Bay Marsh Reserve in San Diego, California, to evaluate tobacco-related pollutants in San Diego's urban waters. Twenty-six sampling events between November 2019 and February 2022, spanning wet and dry seasons at two outfall sites, were conducted. Nicotine and cotinine, a major ingredient of tobacco and its metabolite, were analyzed in the collected water and sediment samples. Nicotine concentrations differed substantially between the outfall locations (Noyes St. and Olney St.), with Noyes St. displaying wide variations, averaging at 9.31 (±13.24) ng/L with a maximum concentration of 50.75 ng/L, and Olney St. at 0.53 (±0.41) ng/L with a maximum concentration of 1.46 ng/L in water samples. In both locations, the nicotine concentrations in water samples were higher during wet seasons than dry seasons, and this pattern was more significant at Noyes St. outfall than at Olney St. outfall, which received not only stormwater runoff but also was connected to Mission Bay. Although this pattern did not directly align with sediment nicotine levels at both sites, maximum nicotine concentration in Noyes St. sediments during wet seasons was approximately 120 times higher than in Olney St. sediments. Regarding cotinine, Noyes St. outfall water averaged 3.17 ng/L (±1.88), and Olney St. water averaged 1.09 ng/L (±1.06). Similar to nicotine, the cotinine concentrations were higher in Noyes St. water and sediment compared to Olney St., but overall, the cotinine concentrations in both water and sediment were much lower than the corresponding nicotine concentrations. The study identifies urban stormwater runoff as a potential source of nicotine and cotinine pollution in a protected reserve, implicating tobacco product litter and human tobacco use as contributing factors.

Association between parental smoking and child exposure to environmental tobacco smoke in Israel.

BACKGROUND: Environmental tobacco smoke (ETS) exposure in children can cause delayed lung development and lifelong cardiovascular damage. The aim of this study was to measure ETS exposure in children in Israel in 2020-2021 using urinary cotinine (UC) measurements and to assess correlates of ETS exposure, including parental smoking. METHODS: In the framework of the National Human Biomonitoring Program, spot urine samples and questionnaire data were collected from 166 children aged 4-12 years, during the years 2020-2021. We collected urine samples in 233 adults, 69 of whom were parents of children included in the study. Parents of participating children were asked about parental smoking, child's exposure to ETS and smoking policy at home. Cotinine and creatinine were measured in urine. Creatinine-adjusted and unadjusted urine cotinine (UC) geometric means were calculated. Associations between potential correlates and UC concentrations were analyzed in univariate and multivariate analyses. For 69 child-parent pairs, correlation between child and parental UC was analyzed. RESULTS: Based on urinary cotinine measurement, 65.2% of children of smokers are exposed to ETS, compared to 20.7% of children in non-smoking families. Greater numbers of smokers living in the home (beta = 1.27, p < 0.01), and low maternal education (beta = - 2.32, p < 0.01) were associated with higher levels of UC in a multivariate analysis. Spearman correlations showed a positive moderate correlation between UC in 69 child-parent pairs (r = 0.52, p < 0.01). CONCLUSIONS: In order to reduce child exposure to ETS, smoking parents should be urgently targeted for smoking cessation and smoke-free home interventions. Further interventions are needed to protect all children from ETS.

Household smoking impact on the oral health of 5- to 7-years-old children.

BACKGROUND: Children's exposure to secondhand smoke, particularly by their parents, could adversely affect their oral health. Thereby, this study aimed to assess the oral health status of children subjected to household smoking and the impact of smoking patterns on the severity of oral health deterioration. METHODS: A total of 210 healthy children were enrolled in this case-control study and allocated into children subjected to household smoking (HS) and control groups. Participants' guardians were asked to complete a questionnaire regarding sociodemographic characteristics and parental smoking habits. All participants were subjected to clinical dental examination to assess dental caries (ICDAS), hypomineralized primary molars (HSPM), and gingival status (GI). Stimulated saliva samples were collected to assess saliva composition and characteristics. Urine samples were collected and analyzed for cotinine concentration. Data were analyzed using SPSS (v.25) software at a test value of p ≤ 0.05. The t-student test was used to find significant differences between participants' age, gingival index score, saliva pH, flow rate, sIgA, and cotinine level. The Chi-square test was used to test for the significance of parental employment, number of rooms, gender, sweets consumption, brushing frequency, and HMPM. The correspondence analysis was used to test for significance of parents' levels of education, type of house ventilation, ICDAS score, smoking form, frequency, and smoking pattern. The correlation between cotinine level and sIgA was tested for association using Bivariate correlation test. RESULTS: The HS group showed a significantly increased risk for dental caries (p < 0.000), HSPM lesions (p = 0.007), and GI score (p < 0.000). A significant reduction in salivary flow rate, saliva pH, and sIgA were evident in HS group (p < 0.000). Parental consumption of more than 20 cigarettes/day was accompanied by increased dental caries activity (p < 0.000) and higher risk for increased severity of gingival inflammation (p < 0.000) of children in the HS group. Children of parents who smoke cigarettes and use the hubble/bubble anywhere in the house found to have greater distribution of HSPM (p < 0.000). Reduced sIgA values were found to be significantly associated with increased cotinine concentrations in HS children (p < 0.000). CONCLUSIONS: Frequent exposure to household smoking could be associated with an increased risk of dental caries progression, enamel hypomineralization, gingival inflammation, and saliva characteristics changes in children.

Association between secondhand smoke exposure and severe headaches or migraine in never-smoking adults.

OBJECTIVE: The study aimed to examine the relationship between secondhand smoke (SHS) exposure and severe headaches or migraine in never-smoking adults verified by serum cotinine. BACKGROUND: Current evidence about the association between self-reported SHS exposure and headaches or migraine is limited and contradictory. An important issue lies in the lack of actual SHS exposure assessment through biomarkers. METHODS: We conducted a cross-sectional study on 4560 never-smoking adults from the National Health and Nutrition Examination Survey (NHANES), 1999-2004. The SHS exposure was evaluated by measuring serum cotinine concentrations. The information regarding severe headaches or migraine was based on self-reporting. RESULTS: The overall prevalence rate of severe headaches or migraine was 20% (919/4560). After adjusting for relevant covariates, we found that heavy SHS exposure (serum cotinine at 1 to 10 ng/mL) was positively associated with severe headaches or migraine (OR: 2.02, 95% CI [1.19, 3.43]); however, no significant association was found between low SHS exposure (serum cotinine at 0.05 to 0.99 ng/mL) and severe headaches or migraine (OR: 1.15, 95% CI [0.91, 1.47]). Restricted cubic spline analysis showed that the natural logarithm of serum cotinine had a linear relationship with severe headaches or migraine (p = 0.335 for nonlinearity). Stratified analysis indicated that individuals with a BMI of <25 (p < 0.001 for interaction) and sedentary activity (p = 0.016 for interaction) modified the relationship between SHS exposure and severe headaches and migraine. Even after altering the definition of SHS exposure, excluding drugs that might affect the metabolism of serum cotinine, and multiple imputation, our sensitivity analysis results remained stable. CONCLUSIONS: The study demonstrated that heavy SHS exposure (serum cotinine at 1 to 10 ng/mL) had a significant positive association with severe headaches or migraine in never-smoking adults. Prospective studies are necessary to verify this relationship in the future.

Does smoking exposure alter the effect of non-surgical periodontal therapy?

DESIGN: This prospective longitudinal observational study aimed to explore the impact of varying levels of smoking exposure on periodontal healing over a 12-month period following non-surgical periodontal therapy. COHORT SELECTION: The study included 80 individuals in the age range of 20-70 years, who were both, smokers at baseline, and also diagnosed with periodontitis. Initially, all participants were enrolled in a smoking cessation program and were provided with non-surgical periodontal therapy (NSPT). Subsequently, all patients were recalled after every 3 months for supportive periodontal care and data collection. Socio-demographic features and periodontal health parameters were recorded, which included clinical attachment level (CAL), periodontal pocket depth (PPD), bleeding on probing, etc. For smoking, data about frequency, duration and salivary carbon monoxide and cotinine levels were recorded. DATA ANALYSIS: Descriptive statistics was used to depict and compare periodontal health and smoking parameters at different time intervals. In addition, exploratory factor analysis method was employed to identify distinct patterns of smoking behavior over a 1-year study period. Accordingly, patients were classified into three categories. Lastly, in order to assess the impact of NSPT among patients in different smoking categories, mixed-effects regression modeling was used. RESULTS: The distribution of smokers was light smokers/quitters (46 individuals), moderate smokers (17 individuals) and heavy smokers (17 individuals). With NSPT an improvement in the mean CAL, PPD, and number of sites with PPD ≥4/5/6/7 mm was observed in all light, moderate and heavy smokers. Mean CAL (±SD) changed from 3.2 ± 1.5 to 2.5 ± 1.3, 3.5 ± 1.6 to 2.6 ± 1.3, and 4.2 ± 1.5 to 3.6 ± 1.3 and mean PPD changed from 2.5 ± 0.8 to 1.9 ± 0.4, 2.6 ± 1.0 to 2.0 ± 0.7, and 2.7 ± 0.8 to 2.1 ± 0.5 in light, moderate and heavy smokers respectively. Similar changes were observed in other periodontal and smoking parameters, e.g., salivary cotinine levels changed from baseline to 1 year, from 276.0 ± 155.7 to 213.8 ± 160.6, 564.8 ± 77.8 to 518.6 ± 197.6, and 764.0 ± 205.9 to 728.9 ± 116.7 in different smoking categories. Lastly, regression coefficients (RCs) were evaluated using regression modeling. RCs (and confidence intervals) for light and moderate smokers were CAL = -0.7 (-0.9 to -0.6), PPD -0.6 (-0.7 to -0.5) and CAL -0.4 (-0.1 to 0.3), PPD -0.4 (-0.8 to -0.1) respectively. In heavy smokers, a positive value of the regression coefficient for CAL was observed, indicating a trend of "increase in CAL value" (RC = 0.5, -0.1 to 1.2). CONCLUSIONS: The study concluded that in smokers, NSPT done along with SPC yielded positive results. However, these results were influenced by the level of smoking exposure in a dose-response manner.