Faculty Bibliography

BACKGROUND:E-cigarette use (vaping) is an emerging public health problem. Depression has been found to be associated with e-cigarette use, and vaping and depression are each associated with elevated systemic inflammation. To date, the role of inflammation in the relationship between vaping and depression has not been explored. OBJECTIVE:To assess the independent associations between e-cigarette use, depression, and inflammation, and to investigate whether the likelihood of depression among current e-cigarette users is associated with systemic inflammation. METHODS:= 4961). Systemic inflammation was defined as serum C-reactive protein (CRP) ≥ 8.0 mg/L. Depressed individuals were characterized by a score ≥ 10 on the Patient Health Questionnaire-9 (PHQ-9). Current e-cigarette users were defined as individuals who vaped at least once in the past 30 days and these individuals were stratified by use: exclusive users (reported smoking less than 100 combustible cigarettes in their lifetime), dual users (reported current use of electronic and combustible cigarettes), and e-cigarette users who were previous smokers. Bivariate analyses were used to assess independent associations between vaping, depression, and inflammation; and weighted logistic regression analyses adjusting for BMI, sex, and economic status were used to determine the odds ratios (ORs) for depression by e-cigarette category stratified by differential CRP levels. RESULTS:-values > 0.05). CONCLUSION:While a pattern of greater ORs for depression among e-cigarette users with elevated CRP provides provocative findings that might suggest a potential role of inflammation in the association between vaping and depression, we failed to find evidence that inflammation clearly moderates this association. While it is possible that depression among e-cigarette users may be influenced by systemic inflammation, a reproduction of the current study is necessary among a larger cohort to elucidate the effect of inflammation on depression among e-cigarette users.

CONTEXT/BACKGROUND:Use of electronic cigarettes (e-cigarettes) has rapidly increased despite unclear longitudinal health effects. Once thought to be a safer alternative to tobacco smoke, it is possible that e-cigarettes expose the user to similar carcinogenic byproducts during the vaping process. These toxicants are metabolized and excreted in the urine, and may have oncogenic implications for bladder urothelium. OBJECTIVE:To characterize and summarize known urinary carcinogenic biomarkers in e-cigarette users as they relate to the risk of developing bladder cancer. EVIDENCE ACQUISITION/METHODS:A systematic literature search was performed using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, and included PubMed, Embase, Web of Science, and Cochrane Central Register of Controlled Trials (CENTRAL). Relevant articles published in peer-reviewed journals, through January 2019, that reported on urinary biomarkers in e-cigarettes users were included. Parent compounds and urinary biomarkers were classified according to the International Agency for Research on Cancer Monographs on the Evaluation of Carcinogenic Risks to Humans and cross referenced using the Collaborative on Health and the Environment, Toxicant and Disease Database to determine a link to bladder cancer, grouped by strength of evidence. EVIDENCE SYNTHESIS/RESULTS:Our initial search identified 1385 articles, 22 of which met final inclusion criteria and were included for analysis. In summation, these studies described 40 different parent compounds and four metals found in the urine of e-cigarette users. Since each parent compound can be metabolized several different ways, 63 unique toxicant or carcinogenic metabolite biomarkers were identified. Compared with nonuser controls, e-cigarette users had higher concentrations of urinary biomarkers of several carcinogenic compounds linked to bladder cancer. The majority of studies were limited by heterogeneous reporting and a dearth of control individuals who had never smoked. CONCLUSIONS:Biomarkers of carcinogens, several with a strong link to bladder cancer, are present in the urine of e-cigarette users. Long-term implications of urothelial exposure to these toxicants are unknown but concerning, given the similarities to tobacco smoke and its established relationship with bladder cancer. Further study on the urological safety of e-cigarettes is necessary. PATIENT SUMMARY/UNASSIGNED:Our review shows that several carcinogens that have a known link to bladder cancer are present in the urine of electronic cigarette (e-cigarette) users. Further study on the urological safety of e-cigarettes is necessary.

To provide insights into the cause of e-cigarette (e-cig) associated lung injury, we examined the effects of propylene glycol (PG) and glycerol (G), two common solvent carriers used to deliver nicotine/flavor, on markers of oxidative stress and inflammation in female B6C3F1 mice which had been used successfully in tobacco smoke (TS)-induced lung carcinogenesis. Mice exposed to air and TS were used as negative and positive controls, respectively. Using LC-MS/MS, we showed that PG/G alone, in the absence of nicotine, significantly increased the levels of 8-hydroxy-2'-deoxyguanosine (8-OHdG or its tautomer 8-oxodG), a biomarker of DNA oxidative damage, in lung and plasma of mice; moreover, addition of nicotine (12 and 24 mg/mL) in e-cig liquid appears to suppress the levels of 8-oxodG. Exposure to e-cig aerosols or TS induced nonsignificant increases of plasma C-reactive protein (CRP), a biomarker of inflammation; nonetheless, the levels of fibronectin (FN), a biomarker of tissue injury, were significantly increased by e-cig aerosols or TS. Although preliminary, our data showed that exposure to e-cig aerosols induced a higher score of lung injury than did control air or TS exposure. Our results indicate that the B6C3F1 mouse model may be suitable for an in-depth examination of the impact of e-cig on lung injury associated with oxidative stress and inflammation and this study adds to the growing evidence that the use of e-cig can lead to lung damage.

OBJECTIVES/OBJECTIVE:The goals of this study were to assess the air quality in subway systems in the northeastern United States and estimate the health risks for transit workers and commuters. METHODS: RESULTS: DISCUSSION/CONCLUSIONS:

Introduction/UNASSIGNED:Alternative tobacco products, including electronic cigarettes (e-cigarettes) and non-combustible tobacco products or heat-not-burn (HNB) products, are substitutes to conventional combustible cigarettes with the potential to impact urologic health, similar to traditional smoking. Most urologists, however, have limited knowledge of these products and are unfamiliar with their potential health implications. We conducted a review to assess the impact of e-cigarettes and HNB products on urologic health. Material and methods/UNASSIGNED:and Google Scholar. Articles were reviewed and categorized based on the potential impact on erectile dysfunction, semen quality, lower urinary tract symptoms, genitourinary malignancies, and smoking cessation. Data were extracted, analyzed and summarized. Results/UNASSIGNED:Mature data on the long-term impact of e-cigarette and HNB product use on urologic health are lacking. E-cigarette and HNB vapors appear to contain decreased concentrations of chemicals responsible for erectile dysfunction compared to tobacco smoke but may play a role through endothelial damage. Use of e-cigarettes is associated with lower sperm counts. No definitive data has shown a link between e-cigarette or HNB product use and lower urinary tract symptoms. Multiple carcinogens including those specifically linked to bladder cancer have been identified in the urine of e-cigarette and HNB product users. Limited data suggest e-cigarettes may aid in smoking cessation. Conclusions/UNASSIGNED:Urologists may benefit from understanding the urologic health concerns surrounding e-cigarettes and HNB product use and patients may benefit from being properly educated.

Food carts are common along streets in cities throughout the world. In North America, food cart vendors generally use propane, charcoal, or both propane and charcoal (P and C) for food preparation. Although cooking emissions are known to be a major source of indoor air pollution, there is limited knowledge on outdoor cooking's impact on the ambient environment and, in particular, the relative contribution of the different cooking fuels. This field study investigated the air pollution the public is exposed to in the micro-environment around 19 food carts classified into 3 groups: propane, charcoal, and P and C carts. Concentrations near the food carts were measured using both real-time and filter-based methods. Mean real-time concentrations of PM_2.5, BC_2.5, and particle counts were highest near the charcoal food carts: 196 μg/m³, 5.49 μg/m³, and 69,000 particles/cm³, respectively, with peak exposures of 1520 μg/m³, 67.9 μg/m³, and 235,000 particles/cm³, respectively. In order of pollution emission impacts: charcoal > P and C > propane carts. Thus, significant differences in air pollution emissions occurred in the vicinity of mobile food carts, depending on the fuel used in food preparation. Local air pollution polices should consider these emission factors in regulating food cart vendor operations.

Importance/UNASSIGNED:Secondhand smoke (SHS) exposure is associated with many health conditions in children and adults. Millions of individuals in the US are currently exposed to SHS in their homes. Objective/UNASSIGNED:To investigate whether a federal ban on smoking in public housing settings was associated with a decrease in indoor SHS levels in New York City public housing developments 12 months after the policy's implementation. Design, Setting, and Participants/UNASSIGNED:This cohort study tracked indoor air quality longitudinally from April 2018 to September 2019 and used difference-in-differences analysis to examine SHS exposure before vs after implementation of the 2018 federal smoke-free housing (SFH) policy in 10 New York City Housing Authority (NYCHA) buildings vs 11 matched low-income buildings not subject to the SFH policy (ie, Section 8 buildings). Exposures/UNASSIGNED:Federal SFH policy implementation, beginning July 30, 2018. Main Outcomes and Measures/UNASSIGNED:Comparison of nicotine concentration levels from passive, bisulfate-coated filters before vs 12 months after implementation of the federal SFH policy. Secondary outcomes included changes in particulate matter less than 2.5 μm in diameter, measured with low-cost particle monitors, and counts of cigarette butts in common areas. Results/UNASSIGNED:Air quality was measured repeatedly in a total of 153 NYCHA and 110 Section 8 nonsmoking households as well as in 91 stairwells and hallways. Before the SFH policy implementation, air nicotine was detectable in 19 of 20 stairwells (95.0%) in NYCHA buildings and 15 of 19 stairwells (78.9%) in Section 8 buildings (P = .19) and in 17 of 19 hallways (89.5%) in NYCHA buildings and 14 of 23 hallways (60.9%) in Section 8 buildings (P = .004). Nicotine was detected less frequently inside nonsmoking apartments overall (26 of 263 [9.9%]) but more frequently in NYCHA apartments (20 of 153 [13.1%]) than in Section 8 apartments (6 of 110 [5.5%]) (P = .04). One year after policy implementation, there was no differential change over time in nicotine concentrations measured in stairwells (DID, 0.03 μg/m3; 95% CI, -0.99 to 1.06 μg/m3) or inside nonsmoking households (DID, -0.04 μg/m3; 95% CI, -0.24 to 0.15 μg/m3). Larger decreases in nicotine concentration were found in NYCHA hallways than in Section 8 hallways (DID, -0.43 μg/m3; 95% CI, -1.26 to 0.40 μg/m3). Conclusions and Relevance/UNASSIGNED:The findings suggest that there was no differential change in SHS in NYCHA buildings 12 months after SFH policy implementation. Additional support may be needed to ensure adherence to SFH policies.

BACKGROUND:Particle matter (PM) has been associated with increased morbidity and mortality rates across the world. This study was designed to test the hypotheses that pyrotechnic firework displays introduce significant amounts of toxic metals into the atmosphere and are hazardous to human health. Size-selective emissions from 10 different fireworks displays were collected during particle generation in a dynamic, stainless steel chamber and tested for toxicity in cells. A subset of 2 particle types were tested in vivo in mice. At doses that did not produce cytotoxicity in an LDH assay, in vitro reactive oxygen species (ROS) formation was measured in bronchial epithelial airway (BEAS-2B) and human pulmonary microvascular endothelial (HPMEC-ST1.6R) cell lines treated with size-fractionated particles from the emissions of fireworks. RESULTS:sample for the fireworks type producing the greatest in vitro ROS response in BEAS-2B cells contained ~ 40,000 and ~ 12,000 ppm of lead and copper, respectively. This sample also produced the greatest inflammatory response (i.e., increased neutrophils in bronchoalveolar lavage fluid) in mice. CONCLUSIONS:These findings demonstrate that pyrotechnic display particles can produce adverse effects in mammalian cells and lungs, thus suggesting that further research is needed to expand our understanding of the contribution of metal content to the adverse health effects of fireworks particles. This information will lead to the manufacture of safer fireworks.