E-Cigarette Toxicology.

Since the spread of tobacco from the Americas hundreds of years ago, tobacco cigarettes and, more recently, alternative tobacco products have become global products of nicotine addiction. Within the evolving alternative tobacco product space, electronic cigarette (e-cigarette) vaping has surpassed conventional cigarette smoking among adolescents and young adults in the United States and beyond. This review describes the experimental and clinical evidence of e-cigarette toxicity and deleterious health effects. Adverse health effects related to e-cigarette aerosols are influenced by several factors, including e-liquid components, physical device factors, chemical changes related to heating, and health of the e-cigarette user (e.g., asthmatic). Federal, state, and local regulations have attempted to govern e-cigarette flavors, manufacturing, distribution, and availability, particularly to underaged youths. However, the evolving e-cigarette landscape continues to impede timely toxicological studies and hinder progress made toward our understanding of the long-term health consequence of e-cigarettes.

Untargeted Metabolomics to Characterize the Urinary Chemical Landscape of E-Cigarette Users.

The health and safety of using e-cigarette products (vaping) have been challenging to assess and further regulate due to their complexity. Inhaled e-cigarette aerosols contain chemicals with under-recognized toxicological profiles, which could influence endogenous processes once inhaled. We urgently need more understanding on the metabolic effects of e-cigarette exposure and how they compare to combustible cigarettes. To date, the metabolic landscape of inhaled e-cigarette aerosols, including chemicals originated from vaping and perturbed endogenous metabolites in vapers, is poorly characterized. To better understand the metabolic landscape and potential health consequences of vaping, we applied liquid chromatography-mass spectrometry (LC-MS) based nontargeted metabolomics to analyze compounds in the urine of vapers, cigarette smokers, and nonusers. Urine from vapers (n = 34), smokers (n = 38), and nonusers (n = 45) was collected for verified LC-HRMS nontargeted chemical analysis. The altered features (839, 396, and 426 when compared smoker and control, vaper and control, and smoker and vaper, respectively) among exposure groups were deciphered for their structural identities, chemical similarities, and biochemical relationships. Chemicals originating from e-cigarettes and altered endogenous metabolites were characterized. There were similar levels of nicotine biomarkers of exposure among vapers and smokers. Vapers had higher urinary levels of diethyl phthalate and flavoring agents (e.g., delta-decalactone). The metabolic profiles featured clusters of acylcarnitines and fatty acid derivatives. More consistent trends of elevated acylcarnitines and acylglycines in vapers were observed, which may suggest higher lipid peroxidation. Our approach in monitoring shifts of the urinary chemical landscape captured distinctive alterations resulting from vaping. Our results suggest similar nicotine metabolites in vapers and cigarette smokers. Acylcarnitines are biomarkers of inflammatory status and fatty acid oxidation, which were dysregulated in vapers. With higher lipid peroxidation, radical-forming flavoring, and higher level of specific nitrosamine, we observed a trend of elevated cancer-related biomarkers in vapers as well. Together, these data present a comprehensive profiling of urinary biochemicals that were dysregulated due to vaping.

Characterisation of personalised air pollution exposure in pregnant women participating in a birth cohort study.

BACKGROUND: Air pollution is a health risk in pregnant women and children. Despite the importance of refined exposure assessment, the characterisation of personalised air pollution exposure remains a challenge in paediatric and perinatal epidemiology. OBJECTIVE: We used portable personal air monitors to characterise personalised exposure to air pollutants in pregnant women. METHODS: Between November 2019 and May 2022, we offered personal air monitors to pregnant women participating in a birth cohort in New York City. During pregnancy, women used air monitors, which measured particulate matter (PM), nitrogen dioxide (NO2 ), and volatile organic compounds (average use = 14 days). Data were stored in real-time on a secure database via synchronisation with a smartphone application. Of 497 women who agreed to use air monitors, 273 women (55%) were successful in using air monitors for longer than a day. For these participants, we identified daily patterns of exposure to air pollutants using functional principal component analysis (3827 days of air monitoring). RESULTS: Compared to women with no pollution data (n = 224), women who successfully used monitors were more likely to be non-Hispanic White and Asian (vs. Hispanic), nulliparous, unemployed, married/partnered, and received the device in-person (vs. mailed). We identified different daily patterns of exposure to air pollutants. The most dominant pattern for all pollutants was low exposure levels with little variations within 24 h, followed by a pattern that showed differences between day and night levels. NO2 had higher daily variations compared to PM. CONCLUSIONS: Small wearables are useful for the measurement of personalised air pollution exposure in birth cohorts and identify daily patterns that cannot be captured otherwise. Successful participation, however, depends on certain individual characteristics. Future studies should consider strategies in design and analysis to account for selective participation.

Long-Term Trends in Secondhand Smoke Exposure in High-Rise Housing Serving Low-Income Residents in New York City: Three-Year Evaluation of a Federal Smoking Ban in Public Housing, 2018-2021.

INTRODUCTION: In July 2018, the U.S. Department of Housing and Urban Development passed a rule requiring public housing authorities to implement smoke-free housing (SFH) policies. We measured secondhand smoke (SHS) exposure immediately before, and repeatedly up to 36 months post-SFH policy implementation in a purposeful sample of 21 New York City (NYC) high-rise buildings (>15 floors): 10 NYC Housing Authority (NYCHA) buildings subject to the policy and 11 privately managed buildings in which most residents received housing vouchers (herein "Section 8"). AIMS AND METHODS: We invited participants from nonsmoking households (NYCHA n = 157, Section-8 n = 118) to enroll in a longitudinal air monitoring study, measuring (1) nicotine concentration with passive, bisulfate-coated filters, and (2) particulate matter (PM2.5) with low-cost particle sensors. We also measured nicotine concentrations and counted cigarette butts in common areas (n = 91 stairwells and hallways). We repeated air monitoring sessions in households and common areas every 6 months, totaling six post-policy sessions. RESULTS: After 3 years, we observed larger declines in nicotine concentration in NYCHA hallways than in Section-8, [difference-in-difference (DID) = -1.92 µg/m3 (95% CI -2.98, -0.87), p = .001]. In stairwells, nicotine concentration declines were larger in NYCHA buildings, but the differences were not statistically significant [DID= -1.10 µg/m3 (95% CI -2.40, 0.18), p = .089]. In households, there was no differential change in nicotine concentration (p = .093) or in PM2.5 levels (p = .385). CONCLUSIONS: Nicotine concentration reductions in NYCHA common areas over 3 years may be attributable to the SFH policy, reflecting its gradual implementation over this time. IMPLICATIONS: Continued air monitoring over multiple years has demonstrated that SHS exposure may be declining more rapidly in NYCHA common areas as a result of SFH policy adherence. This may have positive implications for improved health outcomes among those living in public housing, but additional tracking of air quality and studies of health outcomes are needed. Ongoing efforts by NYCHA to integrate the SFH policy into wider healthier-homes initiatives may increase policy compliance.

Effects of electronic cigarettes and hookah (waterpipe) use on home air quality.

INTRODUCTION: A major site of secondhand smoke exposure for children and adults is the home. Few studies have evaluated the impact of e-cigarette or hookah use on home air quality, despite evidence finding toxic chemicals in secondhand e-cigarette aerosols and hookah smoke. We assessed the effect of e-cigarette and hookah use on home air quality and compared it with air quality in homes where cigarettes were smoked and where no smoking or e-cigarette use occurred. METHODS: Non-smoking homes and homes where e-cigarettes, hookah or cigarettes were used were recruited in the New York City area (n=57) from 2015 to 2019. Particulate matter with diameter less than 2.5 µm (PM2.5), black carbon and carbon monoxide (CO) were measured during a smoking or vaping session, both in a 'primary' smoking room and in an adjacent 'secondary' room where no smoking or vaping occurred. Log transformed data were compared with postanalysis of variance Tukey simultaneous tests. RESULTS: Use of hookah significantly increased PM2.5 levels compared with non-smoking homes, in both the primary and secondary rooms, while use of e-cigarettes increased PM2.5 levels only in primary rooms. Additionally, in-home use of hookah resulted in greater CO concentrations than the use of cigarettes in primary rooms. CONCLUSIONS: Use of e-cigarettes or hookah increases air pollution in homes. For hookah, increases in PM2.5 penetrated even into rooms adjacent to where smoking occurs. Extending smoke-free rules inside homes to include e-cigarette and hookah products is needed to protect household members and visitors from passive exposure to harmful aerosols and gases.

Investigation of a river-tunnel effect on PM2.5 concentrations in New York City subway stations.

It is well-documented that subway stations exhibit high fine particulate matter (PM2.5) concentrations. Little is known about the potential of river-tunnels to increase PM2.5 concentrations in subways. We hypothesized a "river-tunnel" effect exists: Stations adjacent to poorly ventilated tunnels that travel beneath rivers exhibit higher PM2.5 concentrations than more distant stations. Accordingly, the PM2.5 concentrations were monitored at stations adjacent to and two- and three-stations distant from the river-tunnel. Multivariate linear regression analysis was conducted to disentangle how proximity to a river-tunnel and other factors (e.g., depth) influence concentrations. Stations adjacent to a river-tunnel had 80-130% higher PM2.5 concentrations than more distant stations. Moreover, distance from a river-tunnel was the strongest PM2.5-influencing factor This distance effect was not observed at underground stations adjacent to a river-bridge. The "river-tunnel" effect explains some of the inter-station variability in subway PM2.5 concentrations. These results support the need for improving ventilation systems in subways.

A combination of three antioxidants decreases the impact of rural particulate pollution in Normal human keratinocytes.

OBJECTIVE: It is well established that exposure of human skin to airborne pollution, particularly in the form of particulate matter sized 2.5 µm (PM2.5 ), is associated with oxidative stress, DNA damage and inflammation, leading to premature signs of skin aging. Because much of the damage results from oxidative stress, we examined the effects of a topical composition containing three antioxidants in an in vitro model system to assess the potential for amelioration of premature aging. The use of multiple antioxidants was of interest based on the typical composition of therapeutic skincare products. It is important to determine the efficacy of multiple antioxidants together and develop a short-term assay for larger scale efficacy testing. METHODS: Normal human epidermal keratinocytes were exposed to a rural-derived source of PM2.5 in the presence and absence of an antioxidant mixture of resveratrol, niacinamide and GHK peptide. Endpoints related to inflammation, premature aging and carcinogenicity were monitored after 5 h of exposure and included IL-6, CXCL10, MMP-1 and NRF2. Differentially expressed genes were monitored by RNA-seq. RESULTS: Pre-treatment of keratinocytes with the antioxidant preparation in the absence of PM2.5 reduced baseline levels of MMP-1, IL-6 and CYP1A1 and reduced PM2.5 -induced increases in all four endpoints, MMP-1, IL-6, CXCL10 and CYP1A1. Antioxidants significantly increased NRF2 protein in the presence of PM2.5 , indicating a protective response. RNA-seq interrogation of antioxidant-treated cells further showed increased expression of NRF2 inducible genes. The expression of CYP1A1 and genes related to aryl hydrocarbon activation were induced by PM2.5 and suppressed by antioxidants. CONCLUSIONS: Specific signalling pathways known to be correlated with skin inflammation and aging were examined based on their suitability for use in efficacy testing for the prevention of skin damage due to ambient hydrocarbon pollution. Endpoints examined after only 5 h of exposure provide a useful method amenable to high through-put screening. The results obtained reinforce the concept that a multiple antioxidant preparation, topically applied, may reduce pro-inflammatory signalling and cellular damage and thereby reduce premature skin aging due to exposure to rural-derived airborne pollution.

OBJECTIF: Il est bien établi que l'exposition de la peau humaine à la pollution atmosphérique, en particulier sous forme de particules d'une taille de 2,5 µm (PM2,5 ), est associée à un stress oxydatif, à des dommages à l'ADN et à une inflammation entraînant des signes prématurés de vieillissement cutané. Étant donné que la plupart des dommages résultent du stress oxydatif, nous avons examiné les effets d'une composition topique contenant trois antioxydants dans un système de modèle in vitro afin d'évaluer le potentiel d'amélioration du vieillissement prématuré. L'utilisation de plusieurs antioxydants a été intéressante en raison de la composition typique des produits thérapeutiques de soin de la peau. Il est important de déterminer l'efficacité de plusieurs antioxydants combinés et de développer un test à court terme pour des tests d'efficacité à plus grande échelle. MÉTHODES: Des kératinocytes épidermiques humains normaux ont été exposés à une source de PM2,5 rurale en présence et en l'absence d'un mélange antioxydant de resvératrol, de niacinamide et de peptide GHK. Les critères d'évaluation liés à l'inflammation, au vieillissement prématuré et à la carcinogénicité ont été surveillés après 5 heures d'exposition et comprenaient l'IL-6, CXCL10, MMP-1 et le NRF2. Les gènes exprimés de manière différentielle ont été surveillés par séquençage de l'ARN. RÉSULTATS: Le prétraitement des kératinocytes par la préparation antioxydante en l'absence de PM2,5 a réduit les taux initiaux de MMP-1, IL-6 et de CYP1A1 et a réduit les augmentations induites par les PM2,5 dans les quatre critères d'évaluation, MMP-1, IL-6, CXCL10 et CYP1A1. Les antioxydants ont significativement augmenté la protéine NRF2 en présence de PM2,5 , ce qui indique une réponse protectrice. L'interrogation des séquences d'ARN des cellules traitées par antioxydants a également montré une expression accrue des gènes inductibles par NRF2. L'expression du CYP1A1 et des gènes liés à l'activation des hydrocarbures aryles a été induite par les PM2,5 et supprimée par les antioxydants. CONCLUSIONS: Les voies de signalisation spécifiques connues pour être corrélées à l'inflammation cutanée et au vieillissement ont été examinées en fonction de leur adéquation à l'utilisation dans les tests d'efficacité pour la prévention des lésions cutanées dues à la pollution des hydrocarbures ambiants. Les critères d'évaluation examinés après seulement 5 heures d'exposition fournissent une méthode utile pouvant être utilisée pour un dépistage à haut débit. Les résultats obtenus renforcent le principe selon lequel une préparation antioxydante multiple, appliquée par voie topique, peut réduire la signalisation pro-inflammatoire et les dommages cellulaires et ainsi réduire le vieillissement prématuré de la peau résultant de l'exposition à la pollution atmosphérique d'origine rurale.

From Augmented to Virtual Reality in Plastic Surgery: Blazing the Trail to a New Frontier.

BACKGROUND: Augmented reality (AR) and virtual reality (VR)-termed mixed reality-have shown promise in the care of operative patients. Currently, AR and VR have well-known applications for craniofacial surgery, specifically in preoperative planning. However, the application of AR/VR technology to other reconstructive challenges has not been widely adopted. Thus, the purpose of this investigation is to outline the current applications of AR and VR in the operative setting. METHODS: The literature pertaining to the use of AR/VR technology in the operative setting was examined. Emphasis was placed on the use of mixed reality technology in surgical subspecialities, including plastic surgery, oral and maxillofacial surgery, colorectal surgery, neurosurgery, otolaryngology, neurosurgery, and orthopaedic surgery. RESULTS: Presently, mixed reality is widely used in the care of patients requiring complex reconstruction of the craniomaxillofacial skeleton for pre- and intraoperative planning. For upper extremity amputees, there is evidence that VR may be efficacious in the treatment of phantom limb pain. Furthermore, VR has untapped potential as a cost-effective tool for microsurgical education and for training residents on techniques in surgical and nonsurgical aesthetic treatment. There is utility for mixed reality in breast reconstruction for preoperative planning, mapping perforators, and decreasing operative time. VR has well- documented applications in the planning of deep inferior epigastric perforator flaps by creating three-dimensional immersive simulations based on a patient's preoperative computed tomography angiogram. CONCLUSION: The benefits of AR and VR are numerous for both patients and surgeons. VR has been shown to increase surgical precision and decrease operative time. Furthermore, it is effective for patient-specific rehearsal which uses the patient's exact anatomical data to rehearse the procedure before performing it on the actual patient. Taken together, AR/VR technology can improve patient outcomes, decrease operative times, and lower the burden of care on both patients and health care institutions.

World Trade Center dust induces nasal and neurological tissue injury while propagating reduced olfaction capabilities and increased anxiety behaviors.

Objective: Previous in vitro and in vivo World Trade Center particulate matter (WTCPM) exposure studies have provided evidence of exposure-driven oxidative/nitrative stress and inflammation on respiratory tract and aortic tissues. What remains to be fully understood are secondary organ impacts due to WTCPM exposure. This study was designed to test if WTC particle-induced nasal and neurologic tissue injury may result in unforeseen functional and behavioral outcomes.Material and Methods: WTCPM was intranasally administered in mice, evaluating genotypic, histopathologic, and olfaction latency endpoints.Results: WTCPM exposure was found to incite neurologic injury and olfaction latency in intranasally (IN) exposed mice. Single high-dose and repeat low-dose nasal cavity insults from WTCPM dust resulted in significant olfaction delays and enduring olfaction deficits. Anxiety-dependent behaviors also occurred in mice experiencing olfaction loss including significant body weight loss, increased incidence and time spent in hind stretch postures, as well as increased stationary time and decreased exploratory time. Additionally, WTCPM exposure resulted in increased whole brain wet/dry ratios and wet whole brain to body mass ratios that were correlated with exposure and increased exposure dose (p<0.05).Discussion: The potential molecular drivers of WTCPM-driven tissue injury and olfaction latency may be linked to oxidative/nitrative stress and inflammatory cascades in both upper respiratory nasal and brain tissues.Conclusion: Cumulatively, these data provide evidence of WTCPM exposure in relation to tissue damage related to oxidative stress-driven inflammation identified in the nasal cavity, propagated to olfactory bulb tissues and, potentially, over extended periods, to other CNS tissues.

Passive exposure to e-cigarette emissions is associated with worsened mental health.

BACKGROUND: Cigarette smoking, secondhand cigarette smoke (SHS) exposure, and e-cigarette use ("vaping") are each associated with increased rates of depressive symptoms and other internalizing mental health disorders. The prevalence of vaping has increased greatly, yet the mental health correlates of secondhand exposure to e-cigarette emissions are as yet to be investigated. This study examined the potential adverse mental health outcomes associated with different tobacco exposures (direct and passive), with a particular focus on the mental health correlates of secondhand exposure to e-cigarette emissions. METHODS: The Population Assessment of Tobacco and Health Study data collected from a sample of 16,173 Wave 4 adults were used to test the hypothesis that secondhand e-cigarette emissions exposure is associated with increased odds of internalizing mental health disorders. Individuals were categorized as exclusive cigarette smokers, exclusive e-cigarette users, cigarette and e-cigarette dual users, exclusive noncombustible tobacco users, secondhand smoke exposed non-users, secondhand e-cigarette emissions exposed non-users, and non-users with no current SHS/secondhand e-cigarette aerosol exposure. Adjusted weighted logistic regression analysis was used to investigate the association between exposure type and internalizing problems as assessed by scores on the Global Appraisal of Individual Needs-Short Screener (GAIN-SS), a widely used instrument for assessing mental health problems. RESULTS: Cigarette smokers (AOR = 2.53, 95% CI: 2.19-2.92), e-cigarette users (AOR = 3.14, 2.41-4.09), dual users (AOR = 3.37, 2.85-4.00), noncombustible tobacco users (AOR = 1.48, 1.01-2.17), SHS exposed non-users (AOR = 1.63, 1.37-1.94), and secondhand e-cigarette emissions exposed non-users (AOR = 1.43, 1.03-1.99) were each associated with increased odds of moderate to severe internalizing mental health problems as compared to unexposed non-users. Odds of internalizing problems among SHS and secondhand e-cigarette emissions exposed non-users did not differ (p = 0.46). CONCLUSIONS: This is the first study, to our knowledge, to identify an association between recent secondhand exposure to e-cigarette emissions and mental health problems, and the risk is comparable to that of SHS. Corroboration of this relationship needs further research to explicate directionality and mechanisms underlying this association.

Effects of E-Cigarette Aerosols with Varying Levels of Nicotine on Biomarkers of Oxidative Stress and Inflammation in Mice.

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.

World Trade Center Dust induces airway inflammation while promoting aortic endothelial dysfunction.

Respiratory ailments have plagued occupational and public health communities exposed to World Trade Center (WTC) dust since the September 11, 2001 attack on the Twin Towers in Lower Manhattan. We proposed that these ailments were proposed to be induced by inhalation exposure to WTC particulate matter (WTCPM), that was released during the collapse of the buildings and its subsequent resuspension during cleanup. We investigated this hypothesis using both an in vitro and an in vivo mouse intranasal (IN) exposure models to identify the inflammatory potential of WTCPM with specific emphasis on respiratory and endothelial tissue responses. The in vitro exposure studies found WTCPM exposure to be positively correlated with cytotoxicity and increased NO2- production in both BEAS-2B pulmonary epithelial cells and THP-1 macrophage cells. The in vivo C57BL/6 mouse studies found significant increases in inflammatory markers including increases in polymorphonuclear neutrophil (PMN) influx into nasal and bronchoalveolar lavage fluids (NLF and BALF), as well as increased levels of total protein and cytokine/chemokines levels. Concurrently, NLF, BALF, and serum NO2- levels exhibited significant homeostatic temporal deviations as well as temporal myograohic aortic dysfunction in myography studies. Respiratory exposure to- and evidence -based retention of- WTCPM may have contributed to chronic systemic effects in exposed mice that r resembled to observed effects in WTCPM-exposed human populations. Collectively, these findings are reflective of WTCPM exposure and its effect(s) on respiratory and aortic tissues, highlighting potential dysfunctional pathways that may precipitate inflammatory events, while simultaneously altering homeostatic balances. The tight interplay between these balances, when chronically altered, may contribute to- or result in- chronically diseased pathological states.

Toxicity of particles emitted by fireworks.

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: Significant increases in ROS, in both cell types, were dependent upon the type of firework but not particle size. The in vitro ROS activity was correlated with lung inflammation produced in groups of mice treated by oropharyngeal aspiration with 0, 50, or 100 µg fireworks PM10/mouse. Trace metal analyses of the PM10 samples showed significant differences in metal content among fireworks type. Interestingly, the PM10 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.

A protocol for measuring the impact of a smoke-free housing policy on indoor tobacco smoke exposure.

BACKGROUND: Tobacco remains a leading cause of preventable death in the U.S., responsible for more than 440,000 deaths each year. Approximately 10% of these deaths are attributable to exposure of non-smokers to secondhand smoke (SHS). Residents living in public multi-unit housing (MUH) are at excess risk for SHS exposure compared to the general population. On November 30, 2016, the U.S. Department of Housing and Urban Development (HUD) passed a rule requiring all public housing agencies to implement smoke-free housing (SFH) policies in their housing developments by July 30, 2018. METHODS: As part of a larger natural experiment study, we designed a protocol to evaluate indoor SHS levels before and after policy implementation through collection of repeat indoor air samples in non-smoking apartments and common areas of select high-rise NYCHA buildings subject to the HUD SFH rule, and also from socio-demographically matched private-sector high-rise control buildings not subject to the rule. A baseline telephone survey was conducted in all selected buildings to facilitate rapid recruitment into the longitudinal study and assess smoking prevalence, behaviors, and attitudes regarding the SFH policy prior to implementation. Data collection began in early 2018 and will continue through 2021. DISCUSSION: The baseline survey was completed by 559 NYCHA residents and 471 comparison building residents (response rates, 35, and 32%, respectively). Smoking prevalence was comparable between study arms (15.7% among NYCHA residents and 15.2% among comparison residents). The majority of residents reported supporting a building-wide smoke-free policy (63.0 and 59.9%, respectively). We enrolled 157 NYCHA and 118 comparison non-smoking households into the longitudinal air monitoring study and performed air monitoring in common areas. Follow up surveys and air monitoring in participant households occur every 6 months for 2.5 years. Capitalizing on the opportunity of this federal policy rollout, the large and diverse public housing population in NYC, and robust municipal data sources, this study offers a unique opportunity to evaluate the policy's direct impacts on SHS exposure. Methods in this protocol can inform similar SFH policy evaluations elsewhere.

Genetic determinants of susceptibility to silver nanoparticle-induced acute lung inflammation in mice.

Silver nanoparticles (AgNPs) are employed in a variety of consumer products; however, in vivo rodent studies indicate that AgNPs can cause lung inflammation and toxicity in a strain- and particle type-dependent manner, but mechanisms of susceptibility remain unclear. The aim of this study was to assess the variation in AgNP-induced lung inflammation and toxicity across multiple inbred mouse strains and to use genome-wide association (GWA) mapping to identify potential candidate susceptibility genes. Mice received doses of 0.25 mg/kg of either 20-nm citrate-coated AgNPs or citrate buffer using oropharyngeal aspiration. Neutrophils in bronchoalveolar lavage fluid (BALF) served as markers of inflammation. We found significant strain- and treatment-dependent variation in neutrophils in BALF. GWA mapping identified 10 significant single-nucleotide polymorphisms (false discovery rate, 15%) in 4 quantitative trait loci on mouse chromosomes 1, 4, 15, and 18, and Nedd4l (neural precursor cell expressed developmentally downregulated gene 4-like; chromosome 18), Ano6 (anocatmin 6; chromosome 15), and Rnf220 (Ring finger protein 220; chromosome 4) were considered candidate genes. Quantitative RT-PCR revealed significant inverse associations between mRNA levels of these genes and neutrophil influx. Nedd4l, Ano6, and Rnf220 are candidate susceptibility genes for AgNP-induced lung inflammation that warrant additional exploration in future studies.-Scoville, D. K., Botta, D., Galdanes, K., Schmuck, S. C., White, C. C., Stapleton, P. L., Bammler, T. K., MacDonald, J. W., Altemeier, W. A., Hernandez, M., Kleeberger, S. R., Chen, L.-C., Gordon, T., Kavanagh, T. J. Genetic determinants of susceptibility to silver nanoparticle-induced acute lung inflammation in mice.

Secondhand hookah smoke: an occupational hazard for hookah bar employees.

BACKGROUND: Despite the increasing popularity of hookah bars, there is a lack of research assessing the health effects of hookah smoke among employees. This study investigated indoor air quality in hookah bars and the health effects of secondhand hookah smoke on hookah bar workers. METHODS: Air samples were collected during the work shift of 10 workers in hookah bars in New York City (NYC). Air measurements of fine particulate matter (PM2.5), fine black carbon (BC2.5), carbon monoxide (CO), and nicotine were collected during each work shift. Blood pressure and heart rate, markers of active smoking and secondhand smoke exposure (exhaled CO and saliva cotinine levels), and selected inflammatory cytokines in blood (ineterleukin (IL)-1b, IL-6, IL-8, interferon γ (IFN-γ), tumour necrosis factor (TNF-α)) were assessed in workers immediately prior to and immediately after their work shift. RESULTS: The PM2.5 (gravimetric) and BC2.5 concentrations in indoor air varied greatly among the work shifts with mean levels of 363.8 µg/m3 and 2.2 µg/m3, respectively. The mean CO level was 12.9 ppm with a peak value of 22.5 ppm CO observed in one hookah bar. While heart rate was elevated by 6 bpm after occupational exposure, this change was not statistically significant. Levels of inflammatory cytokines in blood were all increased at postshift compared to preshift testing with IFN-Υ increasing from 0.85 (0.13) to 1.6 (0.25) (mean (standard error of the mean; SEM)) pg/mL (p<0.01). Exhaled CO levels were significantly elevated after the work shift with 2 of 10 workers having values >90 ppm exhaled CO. CONCLUSIONS: These results demonstrate that hookah bars have elevated concentrations of indoor air pollutants that appear to cause adverse health effects in employees. These data indicate the need for further research and a marked need for better air quality monitoring and policies in such establishments to improve the indoor air quality for workers and patrons.