Maciej L. Goniewicz’s research while affiliated with Roswell Park Comprehensive Cancer Center and other places

Importance It remains unknown whether nicotine intake among youths who vape is lower, comparable, or higher than among youths who smoke. Objective To examine potential differences in biomarkers of exposure to nicotine (1) between adolescents who smoke tobacco, vape, both vape and smoke (dual use), or do not use; (2) between adolescents in 3 countries; and (3) by nicotine content and form in the vaping product last used among adolescents who exclusively vaped. Design, Setting, and Participants This population-based, observational cross-sectional study invited adolescents aged 16 to 19 years in Canada, England, and the US who had previously completed national surveys to participate in a biomarker study based on their vaping and smoking status. Participants completed questionnaires and self-collected urine samples between September 2019 and January 2022. Analyses were conducted in February 2023 and between January and June 2024. Exposures Vaping, tobacco smoking, dual use, or no use in the past 7 days. Main Outcomes and Measures Urine concentration of cotinine, trans-3′-hydroxycotinine (3OH-cotinine), and total nicotine equivalents (TNE-2; molar sum of cotinine and 3OH-cotinine), normalized for creatinine concentration. Results Among the 364 participants (mean [SD] age, 17.6 [1.1] years; 203 females [55.8%]) who provided usable urine samples and completed questionnaires, no differences in TNE-2 concentration were observed between adolescents who exclusively vaped (n = 73; geometric mean [SD], 3.10 [16.69] nmol/mg creatinine), exclusively smoked (n = 68; geometric mean [SD], 3.78 [18.00] nmol/mg creatinine), or both vaped and smoked (n = 77; geometric mean [SD], 6.07 [19.08] nmol/mg creatinine) in the past week, adjusting for creatinine concentration, age, sex, country, and cannabis use. All vaping and/or smoking groups had higher concentrations of TNE-2 than no use (n = 146; geometric mean [SD], 0.19 [1.14] nmol/mg creatinine; P < .001 for all contrasts). Among adolescents who exclusively vaped (n = 73), TNE-2 concentrations were not significantly different between those who reported using products containing more than 20 mg/mL nicotine (n = 33; geometric mean [SD], 4.35 [18.25] nmol/mg creatinine) and containing 20 mg/mL nicotine or less (n = 28; geometric mean [SD], 5.13 [15.64] nmol/mg creatinine). Reported use of vaping products containing nicotine salts (n = 23) was associated with higher concentration of TNE-2 (geometric mean [SD], 10.78 [18.03] nmol/mg creatinine) than reported use of products without nicotine salts (n = 29; geometric mean [SD], 2.72 [15.42] nmol/ng creatinine; P = .03) or reporting “don’t know” (n = 14; geometric mean [SD], 1.55 [15.01] nmol/ng creatinine; P = .009). Similar patterns of exposure were observed for cotinine and 3OH-cotinine. Conclusions and Relevance This cross-sectional study found that vaping was associated with similar nicotine exposure as smoking among adolescents. Reported use of a nicotine salt product was associated with higher nicotine exposure among those who exclusively vaped, consistent with findings from laboratory and population studies indicating greater dependence for nicotine salt e-cigarettes.

Background Few studies examine biomarkers of exposure to vaping and tobacco products among youth. We compared biomarkers for toxicants between youth who vape, smoke, “dual-use”, or neither. Methods Participants ages 16 to 19 years in Canada, England, and the United States completed surveys and self-collected urine samples between September 2019 and January 2022 (N = 364). Urine was tested for metabolites of tobacco-specific nitrosamine NNK (4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone) and six volatile organic compounds. Regression models examined differences in biomarker concentrations by past-week tobacco smoking and vaping, adjusting for creatinine, age, sex, country, and cannabis use. Results Compared with no vaping/smoking, exclusive vaping was associated with similar exposure to acrolein and acrylonitrile but higher exposure to toluene (P = 0.04) and acrylamide (P = 0.034, only in sensitivity analysis using past 24-hour measure). Compared with dual use or exclusive smoking, exclusive vaping was associated with lower exposure to NNK, acrolein, acrylamide, and acrylonitrile (P ≤ 0.01) but higher toluene exposure than dual use (P = 0.012). Exposure was similar for dual-use and exclusive smoking. Benzene and xylene biomarkers were detected in <5% and not compared. Among those smoking, NNK exposure was higher in the United States (geometric mean = 25.4 pg/mg creatinine) versus Canada (16.1 pg/mg; P = 0.006) and England (14.1 pg/mg; P = 0.018). Conclusions Youth exclusively vaping had similar exposure as no vaping/smoking except for two volatile organic compounds and lower exposure than smoking or dual use except toluene. Higher NNK levels among US youth who smoke likely reflect differences in tobacco blend. Impact Findings are generally consistent with literature indicating lower toxicant exposure from vaping versus smoking but elevated exposure versus no use for some.

Objectives This is a protocol for a Cochrane Review (intervention). The objectives are as follows: Primary objectives To evaluate the benefits and harms of oral nicotine pouches when used to help people transition away from combustible tobacco use (smoking) To evaluate the impact of oral nicotine products on the prevalence of combustible tobacco use Secondary objectives To evaluate the benefits and harms of oral nicotine pouches when used to help people transition away from other non‐combustible tobacco/commercial nicotine product use To evaluate the impact of oral nicotine products on the prevalence of use of other non‐combustible tobacco/commercial nicotine products

The increasing shift from cannabis smoking to cannabis vaping is largely driven by the perception that vaping to form an aerosol represents a safer alternative to smoking and is a form of consumption appealing to youth. Herein, we compared the chemical composition and receptor-mediated activity of cannabis smoke extract (CaSE) to cannabis vaping extract (CaVE) along with the biological response in human bronchial epithelial cells. Chemical analysis using HPLC and GC/MS revealed that cannabis vaping aerosol contained fewer toxicants than smoke; CaSE and CaVE contained teratogens, carcinogens, and respiratory toxicants. A bioluminescence resonance energy transfer (BRET)-based biosensor detected the receptor-mediated activity of the extracts, primarily driven by Δ9-THC concentration. RNA- sequencing showed both CaSE and CaVE induced similar transcriptional responses, significantly upregulating genes within pathways related to inflammation, cancer, and cellular stress. This was paralleled by downregulation of pathways related to lipid synthesis and metabolism similarly from both CaSE and CaVE. Targeted metabolomics revealed significant changes in metabolites involved in lipid and membrane metabolism, energy production, nucleotide/DNA/RNA pathways, and oxidative stress response, suggesting potential impairment of lung epithelial cell repair and function. Additionally, the upregulation of 5-hydroxymethylcytosine (5hmC) indicates epigenetic changes potentially contributing to inflammation, oxidative stress, and an increased risk of cancer. These findings challenge the notion that cannabis vaping is risk-free, highlighting an urgent need for comprehensive research into its respiratory health effects. This comparison of cannabis consumption methods offers insights that could inform public health policies and raise consumer awareness regarding the potential risks of inhaling cannabis aerosol.

Background/Objectives: Electronic cigarettes (e-cigarettes) are commonly used by former smokers as an alternative product to conventional cigarettes and also by young adults and adolescents to deliver nicotine. E-cigarettes are thought to be a less harmful and more socially acceptable alternative to tobacco smoking; however, their long-term effects on health, including oral health, are currently unknown. Methods: A literature search for relevant papers indexed in the literature from 2016 to 2023 was conducted using the PubMed, Scopus, and Google Scholar databases. In our paper, we included clinical trials and both in vivo and in vitro research concerning the impact of e-cigarettes on oral health. Results: E-cigarettes impact the oral cavity, which is directly exposed to inhaled chemicals present in e-cigarette aerosols. The use of e-cigarettes has been linked to teeth discoloration and dental caries, promoting the development of periodontal diseases and causing oral mucosa lesions, including oral cancer. E-cigarette aerosols might also negatively affect the oral microbiome by suppressing the growth of commensal bacteria and increasing the population of bacteria responsible for developing numerous oral disorders. E-cigarettes also impact saliva composition and its properties, including reducing saliva’s antibacterial and antioxidant properties, which may subsequently lead to the promotion of oral diseases. Conclusions: The outcomes suggest that e-cigarette usage may cause the development of oral diseases, however further longitudinal studies of a larger and homogenous group of e-cigarette users are required.