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Introduction: Many electronic cigarette manufacturers have begun offering liquids containing "nicotine salts," which are formed when an acid is mixed in a solution with free-base nicotine. Type of salt could play a significant role in the abuse liability of electronic cigarette liquids. As a first step to understanding nicotine salts, this study sought to identify the types of acids present in 23 commercially available electronic cigarette liquids.Aims and methods: Twenty-three electronic cigarette liquids advertised as containing nicotine salts were purchased for analysis. These liquids were tested for the presence of 11 different organic acids that were deemed likely to be used in a nicotine salt formulation. Liquids were analyzed using a combination of liquid chromatography-mass spectrometry and gas chromatography-mass spectrometry methods, then compared to authentic acid standards for identification.Results: Six of the 11 possible acids were identified in the liquids, from most to least common: lactic, benzoic, levulinic, salicyclic, malic, and tartaric acid. Acid(s) could not be identified in one of the liquids. Though most liquids contained only one type, three of the liquids contained multiple acids.Conclusions: These data demonstrate that several types of salts/acids are currently being used in electronic cigarette liquids. The type and concentration of salt(s) used in these liquids may differentially alter sensations in the throat and upper airway, and overall pharmacology of the aerosols by altering liquid pH and from flavor and sensory characteristics of the acids themselves.Implications: This study demonstrates that at least six different types of acids are being used to create the nicotine salts in electronic cigarette liquids, with the acids lactic, benzoic, and levulinic being the most frequently identified. Identification of these acids can serve as the foundation for future research to determine if type of nicotine salt alters pharmacological and to

ObjectiveIn an urban adolescent population, we evaluated sources of exposure to secondhand smoke exposure (SHS), examined differences in exposure by race/ethnicity, age and sex, and determined the relationship between exposure source(s) and the biomarkers cotinine and NNAL.MethodsParticipants were recruited from a public hospital-based outpatient clinic in San Francisco, CA, USA.ResultsOf a sample of N = 298 adolescents screened, 235 were biologically confirmed to be exposed to tobacco smoke. Of those, N = 16 were active smokers and N = 219 were exposed to SHS; 91 (39%) were heavily SHS exposed (median cotinine = 0.76 ng/mL) and 128 (54%) had light SHS exposure (median cotinine = 0.11 ng/mL). Within those SHS exposed, the most common source of exposure was in a public area. No significant racial/ethnic differences were found, although African American adolescents were more likely to live in a home that allowed smoking. Older adolescents were more likely to be exposed across several difference sources, and females more likely to be exposed in a car and in public areas. Past 7-day exposure in the home, in a car, and current blunt use were significantly related to biomarkers of exposure.ConclusionsUrban adolescents are exposed to SHS across a variety of sources. Although exposure in a public area is most common, exposure in the home and in cars significantly influences tobacco biomarker levels. Interventions to reduce exposure would have the greatest impact in this population if they focused on reducing exposure in the home and in cars. History of blunt use is a strong determinant of tobacco exposure.

IntroductionApproximately the same percentage of male high school students in the United States currently uses conventional smokeless tobacco as smokes cigarettes, resulting in toxin exposure.MethodsThis study assessed tobacco product use (smokeless, combustible, and electronic cigarettes) and nicotine and carcinogen exposures in a sample of 594 male rural high school baseball players-a population traditionally at risk for smokeless tobacco use. Salivary specimens were assayed for cotinine (a biomarker of nicotine exposure) and urine specimens for 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL, a biomarker of the carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) using liquid chromatography-tandem mass spectrometry.ResultsThe prevalence of past 30-day use of any tobacco product was 29%. Past 7-day smokeless tobacco use (prevalence: 13%) was associated with the highest levels of cotinine and NNAL observed in the sample, whether smokeless tobacco was used exclusively (geometric means: cotinine 11.1 ng/mL; NNAL 31.9 pg/mg-creatinine) or in combination with combustible products (geometric means: cotinine 31.6 ng/mL; NNAL 50.0 pg/mg creatinine). Cotinine and NNAL levels were incrementally higher in each increasing category of smokeless tobacco use frequency. However, observed levels were lower than previously reported for adults, likely reflecting less smokeless use per day among adolescents.ConclusionsBased on these biomarker observations, adolescents who use conventional smokeless tobacco products are exposed to substantial levels of nicotine and NNK. Although exposed to lower levels than adult smokeless users, the findings are concerning given the young age of the sample and tendency for smokeless tobacco users to increase use intensity over time.ImplicationsThis study demonstrates that adolescents using smokeless tobacco are exposed to levels of nicotine and NNK that increase with use frequency and that exceed exposures among peers using o

BackgroundThe changing prevalence and patterns of tobacco use, the advent of novel nicotine delivery devices, and the development of new biomarkers prompted an update of the 2002 Society for Research on Nicotine and Tobacco (SRNT) report on whether and how to apply biomarker verification for tobacco use and abstinence.MethodsThe SRNT Treatment Research Network convened a group of investigators with expertise in tobacco biomarkers to update the recommendations of the 2002 SNRT Biochemical Verification Report.ResultsBiochemical verification of tobacco use and abstinence increases scientific rigor and is recommended in clinical trials of smoking cessation, when feasible. Sources, appropriate biospecimens, cutpoints, time of detection windows and analytic methods for carbon monoxide, cotinine (including over the counter tests), total nicotine equivalents, minor tobacco alkaloids, and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol are reviewed, as well as biochemical approaches to distinguishing cigarette smoking from use of electronic nicotine delivery devices (ENDS).ConclusionsRecommendations are provided for whether and how to use biochemical verification of tobacco use and abstinence. Guidelines are provided on which biomarkers to use, which biospecimens to use, optimal cutpoints, time windows to detection, and methodology for biochemical verifications. Use of combinations of biomarkers is recommended for assessment of ENDS use.ImplicationsBiochemical verification increases scientific rigor, but there are drawbacks that need to be assessed to determine whether the benefits of biochemical verification outweigh the costs, including the cost of the assays, the feasibility of sample collection, the ability to draw clear conclusions based on the duration of abstinence, and the variability of the assay within the study population. This paper provides updated recommendations from the 2002 SRNT report on whether and how to use biochemical markers in determining tobacco use an

Comparisons of systemic exposure to toxicants during monitored cigarette smoking, electronic cigarette (e-cigarette) use, and abstention are needed to enhance our understanding of the risks of e-cigarette use (vaping). In a cross-over study, we measured 10 mercapturic acid metabolites of volatile organic compounds (VOCs) in 24-hour urine samples collected from 36 dual users (8 women) of e-cigarettes and cigarettes during 2 days of ad libitum vaping or cigarette-only use, and 2 days of enforced abstention. Concentrations of VOC metabolites were higher during smoking compared with vaping, except for the methylating agents metabolite. The fold-difference in concentrations when smoking relative to vaping ranged from 1.31 (1.06-1.61; geometric mean, 95% confidence interval; 1,3-butadiene) to 7.09 (5.88-8.54; acrylonitrile). Metabolites of acrylamide [fold difference of 1.21 (1.03-1.43)] and benzene [1.46 (1.13-1.90)] were higher during vaping compared with abstention. The 1,3-butadiene and propylene oxide metabolites were higher in variable-power tank users compared with users of cig-a-likes. E-cigarettes expose users to lower levels of toxic VOCs compared with cigarette smoking, supporting their harm reduction potential among smokers. However, some e-cigarettes expose users to VOCs such as acrylamide, benzene, and propylene oxide, and may pose health risks to nonsmoking users. The results of our study will inform regulators in assessing e-cigarettes with respect to the balance between its potential harm reduction for adult smokers and risk to nonsmoking users.

Thirdhand cigarette smoke (THS) is a newly described toxin that lingers in the indoor environment long after cigarettes have been extinguished. Emerging results from both cellular and animal model studies suggest that THS is a potential human health hazard. DNA damage derived from THS exposure could have genotoxic consequences that would lead to the development of diseases. However, THS exposure-induced interference with fundamental DNA transactions such as replication and transcription, and the role of DNA repair in ameliorating such effects, remain unexplored. Here, we found that THS exposure increased the percentage of cells in S-phase, suggesting impaired S-phase progression. Key DNA damage response proteins including RPA, ATR, ATM, CHK1, and BRCA1 were activated in lung cells exposed to THS, consistent with replication stress. In addition, THS exposure caused increased 53BP1 foci, indicating DNA double-strand break induction. Consistent with these results, we observed increased micronuclei formation, a marker of genomic instability, in THS-exposed cells. Exposure to THS also caused a significant increase in phosphorylated RNA Polymerase II engaged in transcription elongation, suggesting an increase in transcription-blocking lesions. In agreement with this conclusion, ongoing RNA synthesis was very significantly reduced by THS exposure. Loss of nucleotide excision repair exacerbated the reduction in RNA synthesis, suggesting that bulky DNA adducts formed by THS are blocks to transcription. The adverse impact on both replication and transcription supports genotoxic stress as a result of THS exposure, with important implications for both cancer and other diseases.