Doctor of Philosophy, University of California Berkeley (2018)
Master of Health and Science, Johns Hopkins University (2015)
Bachelor of Science, Santa Clara University (2012)
Importance: Use of alternative tobacco products (ATPs) such as electronic cigarettes, chewing tobacco, pipes, cigars, cigarillos, little cigars, and hookah is rapidly increasing. Although marketing restrictions exist for cigarettes, marketing of ATPs is not yet fully regulated, and studies have not assessed the association between ownership of ATP promotional materials and subsequent ATP or cigarette initiation among adolescents and young adults.Objective: To estimate the association between marketing receptivity measured at baseline and ATP and any tobacco initiation 1 year later, including cigarettes, among adolescents and young adults.Design, Setting, and Participants: Longitudinal cohort study of adolescents and young adults aged 13 to 19 years recruited at high schools in California from July 2014 to October 2015, with follow-up 1 year later. Data were analyzed from January to March 2018.Exposures: Ownership of ATP-specific promotional material and ownership of any tobacco promotional materials (eg, samples, coupons, branded caps, t-shirts, or posters) assessed in wave 1.Main Outcomes and Measures: Outcomes were (1) ATP initiation and (2) either ATP or cigarette initiation in wave 2.Results: Of 757 participants (mean [SD] age at wave 1, 16.1 [1.1] years; 481 [63.5%] female; 166 [21.9%] Asian or Pacific Islander, 202 [26.7%] white, and 276 [36.4%] Latino), 129 (17.0%) initiated ATP use and 141 (18.6%) initiated ATP or cigarette use 1 year later. In unadjusted models, wave 2 ATP initiation was found to be significantly associated with wave 1 ownership of ATP promotional materials (odds ratio, 2.23; 95% CI, 1.26-3.97). After adjustment for wave 1 demographic covariates, the association between ownership of ATP promotional material and ATP initiation 1 year later yielded similar results (odds ratio, 2.13; 95% CI, 1.16-3.91). Results of models assessing a combined outcome variable of either ATP or cigarette ever use were not statistically significant.Conclusions and Relevance: Ownership of ATP promotional materials was associated with subsequent initiation of ATPs. The results of this study are consistent with the suggestion that current marketing restrictions for cigarettes, including restrictions of the distribution of samples, coupons, and other promotional material, should extend to ATPs.
View details for DOI 10.1001/jamanetworkopen.2019.4006
View details for PubMedID 31099874
The rise of noncigarette, alternative tobacco product (ATP) use among adolescents may be due in part to an increase in retail availability of ATPs. We examined whether proximity and density of tobacco retailers near students' homes are associated with a higher likelihood of initiating ATP use over time.Using data from 728 adolescents (aged 13-19 years at baseline) residing in 191 different neighborhoods and attending 10 different California high schools, longitudinal multilevel and cross-classified random effect models evaluated individual-level, neighborhood-level, and school-level risk factors for ATP initiation after 1 year. Covariates were obtained from the American Community Survey and the California Department of Education.The sample was predominantly female (63.5%) and was racially and ethnically diverse. Approximately one third of participants (32.5%) reported ever ATP use at baseline, with 106 (14.5%) initiating ATP use within 1 year. The mean number of tobacco retailers per square mile within a tract was 5.66 (standard deviation = 6.3), and the average distance from each participant's residence to the nearest tobacco retailer was .61 miles (standard deviation = .4). Living in neighborhoods with greater tobacco retailer density at baseline was associated with higher odds of ATP initiation (odds ratio = 1.22, 95% confidence interval = 1.07-2.12), controlling for individual and school factors.Tobacco retailers clustered in students' home neighborhood may be an environmental influence on adolescents' ATP use. Policy efforts to reduce adolescent ATP use should aim to reduce the density of tobacco retailers and limit the proximity of tobacco retailers near adolescents' homes and schools.
View details for DOI 10.1016/j.jadohealth.2019.09.004
View details for PubMedID 31784411
The rapid increase in e-cigarette use among adolescents and young adults has led to drastic changes in patterns of nicotine consumption worldwide. The use of e-cigarettes, many of which contain high levels of nicotine, is especially harmful in this age group and is associated with increased use of cigarettes and other substances among youth. While the risks of short- and long-term e-cigarette use and secondhand aerosol exposure remain only partially understood, e-cigarettes should not be recommended for smoking cessation for youth in any circumstances given the lack of evidence for effectiveness and potential harmful physical and mental health effects. The perceptions of low e-cigarette risk of adolescents and young adults combined with few market regulations and the appeal of youth-friendly flavors, have created ideal conditions for the e-cigarette industry to thrive and place millions of youth at risk of developing an addiction to nicotine. Policies and regulations aiming to prevent youth-directed marketing and sales of e-cigarette and all nicotine delivery products are needed to protect young people. Public health-led education campaigns and educational curricula are also needed to help inform youth and families about the risks of e-cigarette use. While more research is required to determine the best ways to help youth quit e-cigarette use, adolescent health providers can play a key role in screening and counseling youth about e-cigarette use and should be adequately trained and supported to care for youth with e-cigarette addiction.
View details for DOI 10.1016/j.jadohealth.2019.10.007
View details for PubMedID 31780385
Most smoke-free legislation to reduce secondhand smoke (SHS) exposure exempts waterpipe (hookah) smoking venues. Few studies have examined SHS exposure in waterpipe venues and their employees.We surveyed 276 employees of 46 waterpipe tobacco venues in Istanbul, Moscow, and Cairo. We interviewed venue managers and employees and collected biological samples from employees to measure exhaled carbon monoxide (CO), hair nicotine, saliva cotinine, urine cotinine, urine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), and urine 1-hydroxypyrene glucuronide (1-OHPG). We estimated adjusted geometric mean ratios (GMR) of each SHS biomarker by employee characteristics and indoor air SHS measures.There were 73 nonsmoking employees and 203 current smokers of cigarettes or waterpipe. In nonsmokers, the median (interquartile) range concentrations of SHS biomarkers were 1.1 (0.2, 40.9) µg/g creatinine urine cotinine, 5.5 (2, 15) ng/mL saliva cotinine, 0.95 (0.36, 5.02) ng/mg hair nicotine, 1.48 (0.98, 3.97) pg/mg creatinine urine NNAL, 0.54 (0.25, 0.97) pmol/mg creatinine urine 1-OHPG, and 1.67 (1.33, 2.33) ppm exhaled CO. An 8-hour increase in work hours was associated with higher urine cotinine (GMR: 1.68, 95% CI: 1.20, 2.37) and hair nicotine (GMR: 1.22, 95% CI: 1.05, 1.43). Lighting waterpipes was associated with higher saliva cotinine (GMR: 2.83, 95% CI: 1.05, 7.62).Nonsmoking employees of waterpipe tobacco venues were exposed to high levels of SHS, including measurable levels of carcinogenic biomarkers (tobacco-specific nitrosamines and PAHs).Smoke-free regulation should be extended to waterpipe venues to protect nonsmoking employees and patrons from the adverse health effects of SHS.
View details for DOI 10.1093/ntr/ntx125
View details for PubMedID 28582531
View details for PubMedCentralID PMC6350617
Cigarette smoking is inversely associated with DNA methylation of the aryl hydrocarbon receptor repressor (AHRR; cg05575921). However, the association between secondhand tobacco smoke (SHS) exposure and AHRR methylation is unknown.DNA methylation of AHRR cg05575921 in CD14+ monocyte samples, from 495 never-smokers and 411 former smokers (having quit smoking ≥15 years) from the Multi-Ethnic Study of Atherosclerosis (MESA), was cross-sectionally compared with concomitantly ascertained self-reported SHS exposure, urine cotinine concentrations, and estimates of air pollutants at participants' homes. Linear regression was used to test for associations, and covariates included age, sex, race, education, study site, and previous smoking exposure (smoking status, time since quitting, and pack-years).Recent indoor SHS exposure (hours per week) was inversely associated with cg05575921 methylation (β ± SE = -0.009 ± 0.003, p = .007). The inverse effect direction was consistent (but did not reach significance) in the majority of stratified analyses (by smoking status, sex, and race). Categorical analysis revealed high levels of recent SHS exposure (≥10 hours per week) inversely associated with cg05575921 methylation (β ± SE = -0.28 ± 0.09, p = .003), which remained significant (p < .05) in the majority of stratified analyses. cg05575921 methylation did not significantly (p < .05) associate with low to moderate levels of recent SHS exposure (1-9 hours per week), urine cotinine concentrations, years spent living with people smoking, years spent indoors (not at home) with people smoking, or estimated levels of air pollutants.High levels of recent indoor SHS exposure may be inversely associated with DNA methylation of AHRR in human monocytes.DNA methylation is a biochemical alteration that can occur in response to cigarette smoking; however, little is known about the effect of SHS on human DNA methylation. In the present study, we evaluated the association between SHS exposure and DNA methylation in human monocytes, at a site (AHRR cg05575921) known to have methylation inversely associated with current and former cigarette smoking compared to never smoking. Results from this study suggest high levels of recent SHS exposure inversely associate with DNA methylation of AHRR cg05575921 in monocytes from nonsmokers, albeit with weaker effects than active cigarette smoking.
View details for DOI 10.1093/ntr/ntw219
View details for Web of Science ID 000402066600008
View details for PubMedID 27613907
View details for PubMedCentralID PMC6075517
Modern tobacco regulatory science requires an understanding of which biomarkers of cardiovascular injury are most sensitive to cigarette smoking exposure.We studied self-reported current smokers from the Multi-Ethnic Study of Atherosclerosis. Smoking intensity was defined by number of cigarettes/day and urinary cotinine levels. Subclinical cardiovascular injury was assessed using markers of inflammation [high-sensitivity C-reactive protein (hsCRP), interleukin 6 & 2 (IL-2 & IL-6), tumor necrosis factor alpha (TNF-α)], thrombosis (fibrinogen, D-dimer, homocysteine), myocardial injury (troponin T; TnT), endothelial damage (albumin: creatinine ratio), and vascular function [aortic & carotid distensibility, flow-mediated dilation (FMD)]. Biomarkers were modeled as absolute and percent change using multivariable-adjusted linear regression models adjusted for cardiovascular risk factors and smoking duration.Among 843 current smokers, mean age was 58 (9) years, 53% were men, 39% were African American, mean number of cigarettes per day was 13 (10), and median smoking duration was 39 (15) years. Cigarette count was significantly associated with higher hsCRP, IL-6 and fibrinogen (β coefficients: 0.013, 0.011, 0.60 respectively), while ln-transformed cotinine was associated with the same biomarkers (β coefficients: 0.12, 0.04, 5.3 respectively) and inversely associated with aortic distensibility (β coefficient: -0.13). There was a limited association between smoking intensity and homocysteine, D-dimer, and albumin:creatinine ratio in partially adjusted models only, while there was no association with IL-2, TNF-α, carotid distensibility, FMD, or TnT in any model. In percent change analyses, relationships were strongest with hsCRP.Smoking intensity was associated with early biomarkers of CVD, particularly, markers of systemic inflammation. Of these, hsCRP may be the most sensitive.
View details for DOI 10.1016/j.atherosclerosis.2017.01.021
View details for Web of Science ID 000397406500016
View details for PubMedID 28237909
View details for PubMedCentralID PMC5404388
To investigate public compliance with legislation to prohibit smoking within public buildings and the extent of tobacco smoking in outdoor areas in Turkey.Using a standardized observation protocol, we determined whether smoking occurred and whether ashtrays, cigarette butts and/or no-smoking signs were present in a random selection of 884 public venues in 12 cities in Turkey. We visited indoor and outdoor locations in bars/nightclubs, cafes, government buildings, hospitals, restaurants, schools, shopping malls, traditional coffee houses and universities. We used logistic regression models to determine the association between the presence of ashtrays or the absence of no-smoking signs and the presence of individuals smoking or cigarette butts.Most venues had no-smoking signs (629/884). We observed at least one person smoking in 145 venues, most frequently observed in bars/nightclubs (63/79), hospital dining areas (18/79), traditional coffee houses (27/120) and government-building dining areas (5/23). For 538 venues, we observed outdoor smoking close to public buildings. The presence of ashtrays was positively associated with indoor smoking and cigarette butts, adjusted odds ratio, aOR: 315.9; 95% confidence interval, CI: 174.9-570.8 and aOR: 165.4; 95% CI: 98.0-279.1, respectively. No-smoking signs were negatively associated with the presence of cigarette butts, aOR: 0.5; 95% CI: 0.3-0.8.Additional efforts are needed to improve the implementation of legislation prohibiting smoking in indoor public areas in Turkey, especially in areas in which we frequently observed people smoking. Possible interventions include removing all ashtrays from public places and increasing the number of no-smoking signs.
View details for DOI 10.2471/BLT.15.158238
View details for Web of Science ID 000372674200006
View details for PubMedID 26908959
View details for PubMedCentralID PMC4750436
Few studies have evaluated the association between secondhand smoke (SHS) and subclinical cardiovascular disease among ethnically diverse populations. This study assesses the impact of SHS on inflammation and atherosclerosis (carotid intima-media thickness, coronary artery calcification, and peripheral arterial disease).We examined 5032 nonsmoking adults aged 45 to 84 years without prior cardiovascular disease participating in the Multi-Ethnic Study of Atherosclerosis (MESA) from 2000 to 2002. SHS exposure was determined by self-report, and urinary cotinine was measured in a representative subset (n=2893). The multi-adjusted geometric mean ratios (95% CIs) for high-sensitivity C-reactive protein and interleukin-6 comparing 407 participants with SHS ≥12 h/wk versus 3035 unexposed participants were 1.13 (1.02-1.26) and 1.04 (0.98-1.11), respectively. The multi-adjusted geometric mean ratio for carotid intima-media thickness was 1.02 (0.97-1.07). Fibrinogen and coronary artery calcification were not associated with SHS. The prevalence of peripheral arterial disease (ankle-brachial index ≤0.9 or ≥1.4) was associated with detectable urinary cotinine (odds ratio, 2.10; 95% CI, 1.09-4.04) but not with self-reported SHS. Urinary cotinine was not associated with inflammation or carotid intima-media thickness.Despite limited exposure assessment, this study supports the association of SHS exposure with inflammation and peripheral arterial disease.
View details for DOI 10.1161/JAHA.115.002965
View details for PubMedID 27993830
View details for PubMedCentralID PMC5210438
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