Perceptions, intentions, and actual use of a consumer nicotine gum

Abstract Background Little is known about perceptions, use intentions, and behaviors of adults regarding nicotine gum that is marketed and regulated as a consumer product rather than as a medicinal nicotine replacement therapy (NRT). Methods Survey data were collected from a Qualtrics online panel (N = 1000) of adults who had never used a consumer nicotine gum, recruited based on smoking behavior, and from current and former purchasers of one commercially available nicotine gum product (LUCY Chew and Park), recruited via emails to a customer database (N = 500). In addition to descriptive cross-sectional analyses, logistic regression was used to estimate the probability of intent to try and of product appeal among these different groups. Results Among online panel respondents, individuals who smoked with and without plans to quit showed high intention to try the product (odds ratios 15.6 [95% CI 9.3, 27.6] and 9.8 [95% CI 5.8, 17.3] respectively, compared to people who formerly smoked) and persons who had never smoked showed low intentions to try. These results stood regardless of flavor. Among current and former purchasers of the study product, 43.4% of persons who had smoked cigarettes regularly indicated they were motivated to try the product “to help me quit smoking.” Only 0.6% of young adult consumers of the nicotine gum (aged 21–30) had not tried tobacco products previously. Conclusions Consumer nicotine gum does not appear to attract those who have never used a tobacco product and the results for young adults suggest minimal appeal to youth. The study product was used primarily by individuals who currently smoke and/or use e-cigarettes but who wished to quit or reduce consumption. These results suggest that a consumer nicotine gum may reduce harm by substituting for higher-risk products such as combustible cigarettes

Inhaled particulate matter causes expression of nuclear factor (NF)-kappa B-related genes and oxidant-dependent NF-kappa B activation in vitro

High levels of ambient air pollution are associated with exacerbation of asthma and respiratory morbidity, yet little is known concerning the mechanisms of inflammation and toxicity by components of inhaled particulate matter (PM). Brief inhalation of PM2.5 (particles of an aerodynamic diameter of < 2.5 microns) (300 μ g/m3 air for 6 h followed by a period of 24 h in clean air) by either C3H/HeJ or C57/BL6 mice caused significant (P ⩽ 0.05) increases in steady-state messenger RNA (mRNA) levels of a number of nuclear factor (NF)- κ B–associated and/ or –regulated genes, including tumor necrosis factor- α and - β , interleukin-6, interferon- γ , and transforming growth factor- β . Lung mRNA levels of lymphotoxin- β and macrophage migration inhibitory factor were unchanged. In murine C10 alveolar cells and an NF- κ B–luciferase reporter cell line, exposure to PM2.5 at noncytotoxic concentrations resulted in increases in transcriptional activation of NF- κ B–dependent gene expression which were inhibited in the presence of catalase. Early and persistent increases in intracellular oxidants, as measured by flow cytometry and cell imaging using the oxidant probe 2 ′ -7 ′ -dichlorofluoroscin diacetate, were observed in epithelial cells exposed to PM2.5 and ultrafine carbon black particles. Studies here are the first to show NF- κ B–related inflammatory and cytokine gene expression after inhalation of PM2.5 and oxidant-dependent induction of NF- κ B activity by PM2.5 in pulmonary epithelial cells

Characterization of potential impurities and degradation products in electronic cigarette formulations and aerosols

AbstractE-cigarettes are gaining popularity in the U.S. as well as in other global markets. Currently, limited published analytical data characterizing e-cigarette formulations (e-liquids) and aerosols exist. While FDA has not published a harmful and potentially harmful constituent (HPHC) list for e-cigarettes, the HPHC list for currently regulated tobacco products may be useful to analytically characterize e-cigarette aerosols. For example, most e-cigarette formulations contain propylene glycol and glycerin, which may produce aldehydes when heated. In addition, nicotine-related chemicals have been previously reported as potential e-cigarette formulation impurities. This study determined e-liquid formulation impurities and potentially harmful chemicals in aerosols of select commercial MarkTen® e-cigarettes manufactured by NuMark LLC. The potential hazard of the identified formulation impurities and aerosol chemicals was also estimated. E-cigarettes were machine puffed (4-s duration, 55-mL volume, 30-s intervals) to battery exhaustion to maximize aerosol collection. Aerosols analyzed for carbonyls were collected in 20-puff increments to account for analyte instability. Tobacco specific nitrosamines were measured at levels observed in pharmaceutical grade nicotine. Nicotine-related impurities in the e-cigarette formulations were below the identification and qualification thresholds proposed in ICH Guideline Q3B(R2). Levels of potentially harmful chemicals detected in the aerosols were determined to be below published occupational exposure limits

Toxicological assessment of a prototype e-cigaret device and three flavor formulations: a 90-day inhalation study in rats

<p>A prototype electronic cigaret device and three formulations were evaluated in a 90-day rat inhalation study followed by a 42-day recovery period. Animals were randomly assigned to groups for exposure to low-, mid- and high-dose levels of aerosols composed of vehicle (glycerin and propylene glycol mixture); vehicle and 2.0% nicotine; or vehicle, 2.0% nicotine and flavor mixture. Daily targeted aerosol total particulate matter (TPM) doses of 3.2, 9.6 and 32.0 mg/kg/day were achieved by exposure to 1 mg/L aerosol for 16, 48 and 160 min, respectively. Pre-study evaluations included indirect ophthalmoscopy, virology and bacteriological screening. Body weights, clinical observations and food consumption were monitored weekly. Plasma nicotine and cotinine and carboxyhemoglobin levels were measured at days 28 and 90. After days 28, 56 and 90, lung function measurements were obtained. Biological endpoints after 90-day exposure and 42-day recovery period included clinical pathology, urinalysis, bronchoalveolar fluid (BALF) analysis, necropsy and histopathology. Treatment-related effects following 90 days of exposure included changes in body weight, food consumption and respiratory rate. Dose-related decreases in thymus and spleen weights, and increased BALF lactate dehydrogenase, total protein, alveolar macrophages, neutrophils and lung weights were observed. Histopathology evaluations revealed sporadic increases in nasal section 1–4 epithelial hyperplasia and vacuolization. Following the recovery period, effects in the nose and BALF were persistent while other effects were resolved. The no observed effect level based upon body weight decreases is considered to be the mid-dose level for each formulation, equivalent to a daily TPM exposure dose of approximately 9.6 mg/kg/day.</p