Barriers to implementation of pediatric emergency department interventions for parental tobacco use and dependence: a qualitative study using the theoretical domains framework

Background Pediatric emergency department (PED) and urgent care (UC) professionals can play a key role in delivering evidence-based guidelines to address parental tobacco use and child tobacco smoke exposure (TSE). Understanding PED/UC professionals’ perceptions regarding these guidelines is the first step in developing and implementing a TSE screening and counseling intervention in these settings. This study aimed to use the theoretical domains framework (TDF) to identify current screening and counseling behaviors of PED/UC professionals related to parental tobacco use and child TSE, and determine barriers and enablers that influence these behaviors. Methods Semi-structured, focused interviews were conducted with 29 actively practicing PED/UC clinical staff who worked at one large, Midwestern children’s hospital. The interview guide was informed by the TDF and included open-ended questions. Content analysis of interview transcripts was guided by the TDF. Nurses, physicians, and healthcare administrators were assessed overall and by group membership to ensure each group was represented based on their varying PED/UC roles. Results Fifty-one percent were nurses, 38% were physicians, and 11% were healthcare administrators. Most PED/UC professionals did not currently follow the guidelines, but perceived addressing parental tobacco use as part of their role. All 14 TDF domains were identified by nurses, physicians, and administrators in relation to counseling for parental tobacco use and child TSE. Domains with the most sub-themes were (1) knowledge: lack of knowledge about tobacco counseling, including implementing counseling, cessation resources/referrals, and thirdhand smoke; (2) beliefs about capabilities: not comfortable counseling parents, easier to discuss with parents who are receptive and to ask and advise when patients have a TSE-related complaint, and more likely to discuss if there were resources/referrals; and (3) environmental context and resources: barriers include lack of time, training, and resources and referral information to give to parents, and an enabler is using TSE-related complaints as a context to offer counseling. Conclusions Study findings provide a strong foundation for developing and implementing clinical practice guidelines regarding parental tobacco use and child TSE in the PED/UC setting. Future intervention development will address all TDF domains and test the implementation of the intervention in the PED/UC setting.

A Novel Model of Tobacco Smoke–Mediated Aortic Injury

Objective Tobacco smoke exposure is a major risk factor for aortic aneurysm development. However, the initial aortic response to tobacco smoke, preceding aneurysm formation, is not well understood. We sought to create a model to determine the effect of solubilized tobacco smoke (STS) on the thoracic and abdominal aorta of mice as well as on cultured human aortic smooth muscle cells (HASMCs). Methods Tobacco smoke was solubilized and delivered to mice via implanted osmotic minipumps. Twenty male C57BL/6 mice received STS or vehicle infusion. The descending thoracic, suprarenal abdominal, and infrarenal abdominal segments of the aorta were assessed for elastic lamellar damage, smooth muscle cell phenotype, and infiltration of inflammatory cells. Cultured HASMCs grown in media containing STS were compared to cells grown in standard media in order to verify our in vivo findings. Results Tobacco smoke solution caused significantly more breaks in the elastic lamellae of the thoracic and abdominal aorta compared to control solution ( P< .0001) without inciting an inflammatory infiltrate. Elastin breaks occurred more frequently in the abdominal aorta than the thoracic aorta ( P < .01). Exposure to STS-induced aortic microdissections and downregulation of α-smooth muscle actin (α-SMA) by vascular smooth muscle cells (VSMCs). Treatment of cultured HASMCs with STS confirmed the decrease in α-SMA expression. Conclusion Delivery of STS via osmotic minipumps appears to be a promising model for investigating the early aortic response to tobacco smoke exposure. The initial effect of tobacco smoke exposure on the aorta is elastic lamellar damage and downregulation of (α-SMA) expression by VSMCs. Elastic lamellar damage occurs more frequently in the abdominal aorta than the thoracic aorta and does not seem to be mediated by the presence of macrophages or other inflammatory cells.

Association Between Time Spent Outdoors and Risk of Multiple Sclerosis

Objective:This study aims to determine the contributions of sun exposure and ultraviolet radiation (UVR) exposure to risk of paediatric-onset multiple sclerosis (MS).Methods:Children with MS and controls recruited from multiple centres in the USA were matched on sex and age. Multivariable conditional logistic regression was used to investigate the association of time spent outdoors daily in summer, use of sun protection, and ambient summer UVR dose in the year prior to birth and the year prior to diagnosis, with MS risk, adjusting for sex, age, race, birth season, child’s skin colour, mother’s education, tobacco smoke exposure, being overweight, and Epstein-Barr virus infection.Results:332 children with MS (median disease duration: 7.3 months) and 534 controls were included after matching on sex and age. In a fully adjusted model, compared to spending <30 minutes outdoors daily during the most recent summer, greater time spent outdoors was associated with a marked reduction in the odds of developing MS, with evidence of dose-response (30 minutes to 1 hour: adjusted odds ratio (AOR)=0.48, 95% confidence interval [95%CI] 0.23-0.99, p=0.05; 1-2 hours: AOR=0.19, 95%CI 0.09-0.40, p<0.001). Higher summer ambient UVR dose was also protective for MS (AOR=0.76 per kJ/m2, 95%CI 0.62-0.94, p=0.01).Conclusions:If this is a causal association, spending more time in the sun during summer may be strongly protective against developing paediatric MS, as well as residing in a sunnier location.

Risk Assessment of Passive Smoking Based on Analysis of Hair Nicotine and Cotinine as Exposure Biomarkers by In-Tube Solid-Phase Microextraction Coupled On-Line to LC-MS/MS

Passive smoking due to environmental tobacco smoke is a serious public health concern because it increases the risk of lung cancer and cardiovascular disease. However, the current status and effect of passive smoking in various lifestyles are not fully understood. In this study, we measured hair nicotine and cotinine levels as exposure biomarkers in non-smokers and assessed the risk from the actual situation of passive smoking in different lifestyle environments. Nicotine and cotinine contents in hair samples of 110 non-smoker subjects were measured by in-tube solid-phase microextraction with on-line coupling to liquid chromatography-tandem mass spectrometry, and self-reported lifestyle questionnaires were completed by the subjects. Nicotine and cotinine were detected at concentrations of 1.38 ng mg−1 and 12.8 pg mg−1 respectively in the hair of non-smokers, with levels significantly higher in subjects who reported being sensitive to tobacco smoke exposure. These levels were also affected by type of food intake and cooking method. Nicotine and cotinine in hair are useful biomarkers for assessing the effects of passive smoking on long-term exposure to environmental tobacco smoke, and our analytical methods can measure these exposure levels in people who are unaware of passive smoking. The results of this study suggest that the environment and places of tobacco smoke exposure and the lifestyle behaviors therein are important for the health effects of passive smoking.

Tobacco Smoke Exposure and Urinary Cadmium in Women from Northern Mexico

Cadmium (Cd), a carcinogenic metal also related to reproductive and cardiovascular diseases, is contained in tobacco and elevated concentrations of it in humans have been consistently associated with first-hand tobacco smoke; however, there is scarce and inconclusive evidence of the relationship between Cd and secondhand smoke (SHS) exposure. Our aim was to evaluate the association between exposure to tobacco, both active and SHS, with urinary Cd concentrations in Mexican women. In a cross-sectional analysis that included 998 women living in northern Mexico, we measured the concentration of creatinine-adjusted urinary Cd (µg-cadmium/g-creatinine) using inductively coupled plasma triple quadrupole (ICP-QQQ) in tandem mass spectrometry mode (MS/MS). We gathered tobacco smoking information through an in-person interview and formed seven groups: non-smokers without SHS exposure; non-smokers with SHS exposure; ex-smokers without SHS exposure <1 year of quitting; ex-smokers without SHS exposure ≥1 year of quitting, ex-smokers with SHS exposure <1 year of quitting; ex-smokers with SHS exposure ≥1 year of quitting and current smokers. The interview also yielded sociodemographic characteristics. We used linear multivariable regression models to estimate the association between Cd concentrations and tobacco smoke exposure. Compared to non-smokers without SHS exposure, we found higher Cd concentrations in ex-smokers with SHS exposure <1 year of quitting and current smokers (adjusted geometric means 0.51 vs. 1.01 and 0.69 µg-cadmium/g-creatinine, respectively). Our results do not support a conclusion that SHS exposure is a source of Cd body burden.

Parental Knowledge, Attitude, and Practice on Tobacco Use, Smoking Cessation, and Children's Environmental Tobacco Smoke Exposure

Background: Environmental tobacco smoke (ETS) exposure in children ranks one of the major public health problems in our time. Poor parental knowledge, attitude, and practice (KAP) on ETS often contribute to worse exposure of the kids. Thus, we aimed to document parental KAP regarding tobacco use, smoking cessation and children's ETS exposure, and to analyse how knowledge and attitude relate to practice.Methods: Self-administered KAP questionnaires were distributed to smoking parents recruited from the pediatric unit at the Prince of Wales Hospital, which provides pediatric service to a population of 1.2 million in Hong Kong. The 60-item questionnaire had a range of 0–38 for knowledge, 0–44 for attitude, and 0–40 for practice. Descriptive analyses were performed for KAP response, regression analyses were performed for the exploration of associations and identification of predictive indicators.Results: 145 smoking parents (mean age: 38.0 ± 6.7 yrs.; male: 85.5%) were included. Less than half (39.3%) of them reported a smoke-free policy at home. Among those parents who had private cars, less than half (45.2%) of them had smoke-free policy in their car that they never smoked in the car. Only 25.5% of the participants correctly answered ≥70% of the knowledge questions, and 11.8 % of the participants gave favorable responses to ≥70% of the attitude questions. The total knowledge and the total attitudes score were positively associated (r = 0.49, 95% CI: 0.35–0.79, p &lt; 0.001), yet they were only modestly correlated with parental practice on children's ETS exposure. By multivariate regressions, potential predictive factors for more favorable parental KAP included higher household income, lower parental nicotine dependence level and breastfeeding practice.Conclusions: Parental KAP related to tobacco use and children's ETS exposure needs improvement to address the significant gap between recommended and actual practice. The weak association between knowledge and practice suggested that parental education alone is not adequate to combat ETS exposure in children.

Black raspberry restores the expression of the tumor suppressor p120ctn in the oral cavity of mice treated with the carcinogen dibenzo[a,l]pyrene diol epoxide

One of the major risk factors for head and neck squamous cell carcinoma (HNSCC) is tobacco smoke exposure, but the mechanisms that can account for disease development remain to be fully defined. Utilizing our HNSCC mouse model, we analyzed oral squamous cell carcinomas (OSCC) induced by the active metabolite of a common smoke constituent, dibenzo[a,l]pyrene diol-epoxide (DBPDE). Analyzing protein expression by either immunofluorescence or immunohistochemistry, we identified biologic processes that are dysregulated in premalignant and invasive cancer lesions induced by DBPDE. Interestingly, p120ctn expression is downregulated in both stages of the disease. In addition to decreased p120ctn expression, there was also increased proliferation (as measured by Ki67), inflammation (as measured by NFkB (p65) expression), neovascularization (as measured by CD31) and recruitment of Ly6G-positive immune cells as well as strong EGFR expression. We also examined the effect of the chemopreventive agent black raspberry (BRB) on p120ctn and EGFR protein expression in DBPDE treated mice. p120ctn, but not EGFR, protein expression increased in mice treated with BRB. Our results suggest that modulation of p120ctn may, in part, account for the mechanism by which BRB inhibits DBPDE induced OSCC in mice.

Association Between Cigarette Smoking and Ovarian Reserve Among Women Seeking Fertility Care

Background This study examined the association of smoking with ovarian reserve in a cross-sectional study of 207 women enrolled in the Louisville Tobacco Smoke Exposure, Genetic Susceptibility, and Infertility (LOUSSI) Study and assessed effect modification by NAT2 acetylator phenotype. Methods Information on current smoking status was collected using a structured questionnaire and confirmed by cotinine assay. Serum anti-Müllerian hormone (AMH) levels were used to assess ovarian reserve. Diminished ovarian reserve (DOR) was defined as AMH < 1ng/mL. Single nucleotide polymorphisms in the NAT2 gene, which metabolizes toxins found in cigarette smoke, were analyzed to determine NAT2 acetylator status. Linear and logistic regression were used to determine the effects of smoking on ovarian reserve and evaluate effect modification by NAT2. Regression analyses were stratified by polycystic ovary syndrome (PCOS) status and adjusted for age. Results Current smoking status, either passive or active, was not significantly associated with DOR. For dose-response assessed using self-report, the odds of DOR increased significantly for every additional cigarette currently smoked (odds ratio, OR:1.08; 95% confidence interval, 95%CI:1.01–1.15); additionally, every 1 pack-year increase in lifetime exposure was associated with an increased odds of DOR among women without PCOS (OR: 1.08 95%CI: 0.99–1.18). These trends appear to be driven by the heavy or long-term smokers. Effect modification by NAT2 genotype was not established. Conclusion A history of heavy smoking, but not current smoking status, may indicate increased risk of diminished ovarian reserve.

Comparison of Levels of Three Tobacco Smoke Exposure Biomarkers in Children of Smokers

Objectives: Cotinine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), and N-oxides are biomarkers of tobacco smoke exposure (TSE) used to assess short- and longer-term TSE. The objective of this study was to assess the associations between these TSE biomarkers, sociodemographics, parental smoking, and child TSE patterns among 0–17-year-olds. Methods: A convenience sample of 179 pediatric patients (mean (SD) age = 7.9 (4.3) years) who lived with ≥1 smoker and who had parental assessments completed and urine samples analyzed for the three TSE biomarkers of interest were included. Biomarker levels were log-transformed, univariate regression models were built and Pearson correlations were assessed. Results: In total, 100% of children had detectable levels of cotinine and >96% had detectable NNAL and N-oxide levels. The geometric means of cotinine, NNAL, and N-oxide levels were 10.1 ng/mL, 25.3 pg/mL, and 22.9 pg/mL, respectively. The mean (SD) number of daily cigarettes smoked by parents was 10.6 (6.0) cigarettes. Child age negatively correlated with urinary cotinine (r = −0.202, p = 0.007) and log NNAL levels (r = −0.275, p < 0.001). The highest log-cotinine levels were in children who were younger, of African American race, and whose parents had a lower education, an annual income ≤USD15,000, and no smoking bans. The highest log-NNAL and N-oxide levels were in children whose parents had a lower education, had no smoking bans, and were around higher numbers of cigarettes. Conclusion: Children of smokers who were younger, African American, and had no smoking bans had the highest TSE biomarker levels. Targeted interventions are needed to reduce TSE levels among high-risk children.