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Cigarette smoking is associated with increased risk of acute respiratory distress syndrome (ARDS) in patients after severe trauma; however, the mechanisms underlying this association are unknown. To determine whether cigarette smoking contributes to ARDS development after trauma by altering community composition of the lung microbiota. We studied the lung microbiota of mechanically ventilated patients admitted to the ICU after severe blunt trauma. To do so, we used 16S ribosomal RNA gene amplicon sequencing of endotracheal aspirate samples obtained on ICU admission (n = 74) and at 48 hours after admission (n = 30). Cigarette smoke exposure (quantified using plasma cotinine), ARDS development, and other clinical parameters were correlated with lung microbiota composition. Smoking status was significantly associated with lung bacterial community composition at ICU admission (P = 0.007 by permutational multivariate ANOVA [PERMANOVA]) and at 48 hours (P = 0.03 by PERMANOVA), as well as with significant enrichment of potential pathogens, including Streptococcus, Fusobacterium, Prevotella, Haemophilus, and Treponema. ARDS development was associated with lung community composition at 48 hours (P = 0.04 by PERMANOVA) and was characterized by relative enrichment of Enterobacteriaceae and of specific taxa enriched at baseline in smokers, including Prevotella and Fusobacterium. After severe blunt trauma, a history of smoking is related to lung microbiota composition, both at the time of ICU admission and at 48 hours. ARDS development is also correlated with respiratory microbial community structure at 48 hours and with taxa that are relatively enriched in smokers at ICU admission. The data derived from this pilot study suggest that smoking-related changes in the lung microbiota could be related to ARDS development after severe trauma.

To investigate how the two main electronic (e-) cigarette solvents-propylene glycol (PG) and glycerol (GL)-modulate the formation of toxic volatile carbonyl compounds under precisely controlled temperatures in the absence of nicotine and flavor additives. PG, GL, PG:GL = 1:1 (wt/wt) mixture, and two commercial e-cigarette liquids were vaporized in a stainless steel, tubular reactor in flowing air ranging up to 318°C to simulate e-cigarette vaping. Aerosols were collected and analyzed to quantify the amount of volatile carbonyls produced with each of the five e-liquids. Significant amounts of formaldehyde and acetaldehyde were detected at reactor temperatures ≥215°C for both PG and GL. Acrolein was observed only in e-liquids containing GL when reactor temperatures exceeded 270°C. At 318°C, 2.03±0.80 μg of formaldehyde, 2.35±0.87 μg of acetaldehyde, and a trace amount of acetone were generated per milligram of PG; at the same temperature, 21.1±3.80 μg of formaldehyde, 2.40±0.99 μg of acetaldehyde, and 0.80±0.50 μg of acrolein were detected per milligram of GL. We developed a device-independent test method to investigate carbonyl emissions from different e-cigarette liquids under precisely controlled temperatures. PG and GL were identified to be the main sources of toxic carbonyl compounds from e-cigarette use. GL produced much more formaldehyde than PG. Besides formaldehyde and acetaldehyde, measurable amounts of acrolein were also detected at ≥270°C but only when GL was present in the e-liquid. At 215°C, the estimated daily exposure to formaldehyde from e-cigarettes, exceeded United States Environmental Protection Agency (USEPA) and California Office of Environmental Health Hazard Assessment (OEHHA) acceptable limits, which emphasized the need to further examine the potential cancer and non-cancer health risks associated with e-cigarette use.

Nigeria is a significant tobacco market and influential country in Africa. Nigeria ratified the WHO Framework Convention on Tobacco Control (FCTC) in 2005. We reviewed Nigeria's tobacco control legislation since 2000 and compliance of the National Tobacco Control Act (NTCA) 2015 with the FCTC. We reviewed the National Tobacco Control Bills 2011 (proposed by legislature) and 2014 (proposed by Executive), the NTCA 2015, and media stories on tobacco control from 2008 to 2017. The NTCA, despite being more comprehensive than Nigeria's first Tobacco Smoking (Control) law of 1990, maintained provisions promoted by the tobacco industry, for example: allowing designated smoking areas in hospitality venues, higher educational institutions, and transportation venues; a loophole in the advertising restrictions allowing communications with consenting adults; and having the Manufacturers Association of Nigeria (MAN) (which includes tobacco companies) on the National Tobacco Control Committee charged with working with the Ministry of Health to implement the law. The industry is also directly involved with the Standards Organisation of Nigeria (SON) in preparing regulations on cigarette constituents and emissions. In an unprecedented step globally, the law requires that implementing regulations be approved by the National Assembly, giving the industry another opportunity to weaken this law further by lobbying the legislators to favor the industry. As of January 2018, the law was still not being enforced. The NTCA can be strengthened through implementation guidelines still being developed. The industry should be prevented from interfering with through MAN and SON, as required by FCTC Article 5.3. The tobacco industry works to block Framework Convention on Tobacco Control implementation even after a country ratifies the treaty. The Nigerian case illustrates that it is essential for health authorities to remain vigilant and ensure that the tobacco industry does not play a decision-making role in the process of tobacco legislation and regulation either directly or indirectly. The unprecedented step of requiring approval of implementing regulations for the Nigerian law should not be allowed to become a precedent in other countries.

Kim H Nguyen and colleagues examine how tobacco companies applied their knowledge of flavours, colours, and child focused marketing to develop leading children’s sugar sweetened drink brands. These techniques continue to be used by drinks companies despite industry agreement not to promote unhealthy products in this way

Electronic-cigarette, or vaping, product use-associated lung injury (EVALI) is a syndrome of acute respiratory failure characterized by monocytic and neutrophilic alveolar inflammation. Epidemiological and clinical evidence suggests a role of vitamin E acetate (VEA) in the development of EVALI, yet it remains unclear whether VEA has direct pulmonary toxicity. To test the hypotheses that aerosolized VEA causes lung injury in mice and directly injures human alveolar epithelial cells, we exposed adult mice and primary human alveolar epithelial type II (AT II) cells to an aerosol of VEA generated by a device designed for vaping oils. Outcome measures in mice included lung edema, BAL analysis, histology, and inflammatory cytokines; outcomes included cell death, cytokine release, cellular uptake of VEA, and gene-expression analysis. Comparison exposures in both models included the popular nicotine-containing JUUL aerosol. We discovered that VEA caused dose-dependent increases in lung water and BAL protein compared with control and JUUL-exposed mice in association with increased BAL neutrophils, oil-laden macrophages, multinucleated giant cells, and inflammatory cytokines. VEA aerosol was also toxic to AT II cells, causing increased cell death and the release of monocyte and neutrophil chemokines. VEA was directly absorbed by AT II cells, resulting in the differential gene expression of several inflammatory biological pathways. Given the epidemiological and clinical characteristics of the EVALI outbreak, these results suggest that VEA plays an important causal role.

ObjectiveAnalyse the transnational tobacco companies’ (TTCs) memoranda of understanding (MoUs) on illicit trade and how they could undermine the WHO Framework Convention on Tobacco Control (FCTC) and the Protocol to Eliminate Illicit Trade in Tobacco Products (Protocol).MethodsReview of tobacco industry documents and websites, reports, news and media items using standard snowball search methods.ResultsFacing increasing pressure from governments and the FCTC to address illicit tobacco trade during the late 1990s, TTCs entered into voluntary partnerships embodied in MoUs with governments’ law enforcement and customs agencies. One of the earliest known MoUs was between Philip Morris International and Italy in 1999. TTCs agreed among themselves to establish MoUs individually but use the Italian MoU as a basis to establish similar connections with other governments to pre-empt more stringent regulation of illicit trade. TTCs report to have signed over 100 MoUs since 1999, and promote them on their websites, in Corporate Social Responsibility reports and in the media as important partnerships to combat illicit tobacco trade. There is no evidence to support TTCs’ claims that these MoUs reduce illicit trade. The terms of these MoUs are rarely made public. MoUs are non-transparent partnerships between government agencies and TTCs, violating FCTC Article 5.3 and the Protocol. MoUs are not legally binding so do not create an accountability system or penalties for non-compliance, rendering them ineffective at controlling illicit trade.ConclusionGovernments should reject TTC partnerships through MoUs and instead ratify and implement the FCTC and the Protocol to effectively address illicit trade in tobacco products.

IntroductionNigeria ratified the WHO Framework Convention on Tobacco Control (FCTC) in 2005. Tobacco control advocates in Nigeria achieved some success in countering tobacco industry interference to implement the FCTC.MethodsWe triangulated interviews with key informants from local and international organisations who worked in Nigeria with documentation of the legislative process and Nigerian newspaper articles. Data were analysed and interpreted using the Policy Dystopia Model and WHO categories of tobacco industry interference that had been developed mostly based on experience in high-income countries.ResultsAs in high-income countries, the tobacco industry continued to oppose tobacco control policies after Nigeria ratified the FCTC, including weakening Nigeria’s 2015 National Tobacco Control Act. Both tobacco control advocates and industry used discursive (argument-based) and instrumental (activity-based) strategies. The industry argued self-regulation and the economic importance of tobacco. They exploited legislative procedures, used front groups and third parties to push for pro-industry changes. Advocates, with help from international organisations, mobilised prominent Nigerians and the public. Advocates pre-empted and countered the industry through traditional and social media, monitoring and exposing tobacco industry activities, and by actively engaging lawmakers and citizens during the legislative process.ConclusionThe Policy Dystopia Model and WHO categories of industry interference provide a helpful framework for understanding tobacco control debates in low/middle-income countries (LMICs) as in high-income countries. One difference in LMIC is the important role of international tobacco control advocates in supporting national tobacco control advocates. This partnership is important in pushing for FCTC-compliant legislation and countering industry activities in LMIC.

RationaleCigarette smoke exposure is associated with an increased risk of the acute respiratory distress syndrome (ARDS); however, the mechanisms underlying this relationship remain largely unknown.ObjectiveTo assess pathways of lung injury and inflammation in smokers and non-smokers with and without lipopolysaccharide (LPS) inhalation using established biomarkers.MethodsWe measured plasma and bronchoalveolar lavage (BAL) biomarkers of inflammation and lung injury in smokers and non-smokers in two distinct cohorts of healthy volunteers, one unstimulated (n=20) and one undergoing 50 μg LPS inhalation (n=30).Measurements and main resultsAfter LPS inhalation, cigarette smokers had increased alveolar-capillary membrane permeability as measured by BAL total protein, compared with non-smokers (median 274 vs 208 μg/mL, p=0.04). Smokers had exaggerated inflammation compared with non-smokers, with increased BAL interleukin-1β (p=0.002), neutrophils (p=0.02), plasma interleukin-8 (p=0.003), and plasma matrix metalloproteinase-8 (p=0.006). Alveolar epithelial injury after LPS was more severe in smokers than non-smokers, with increased plasma (p=0.04) and decreased BAL (p=0.02) surfactant protein D. Finally, smokers had decreased BAL vascular endothelial growth factor (VEGF) (p<0.0001) with increased soluble VEGF receptor-1 (p=0.0001).ConclusionsCigarette smoke exposure may predispose to ARDS through an abnormal response to a ‘second hit,’ with increased alveolar-capillary membrane permeability, exaggerated inflammation, increased epithelial injury and endothelial dysfunction. LPS inhalation may serve as a useful experimental model for evaluation of the acute pulmonary effects of existing and new tobacco products.

TikTok is a microvideo social media platform currently experiencing rapid growth and with 60% of its monthly users between the ages of 16 and 24 years. Increased exposure to e-cigarette content on social media may influence patterns of use, including the risk of overconsumption and possible nicotine poisoning, when users engage in trending challenges online. However, there is limited research assessing the characteristics of nicotine poisoning-related content posted on social media. We aimed to assess the characteristics of content on TikTok that is associated with a popular nicotine poisoning-related hashtag. We collected TikTok posts associated with the hashtag #nicsick, using a Python programming package (Selenium) and used an inductive coding approach to analyze video content and characteristics of interest. Videos were manually annotated to generate a codebook of the nicotine sickness-related themes. Statistical analysis was used to compare user engagement characteristics and video length in content with and without active nicotine sickness TikTok topics. A total of 132 TikTok videos associated with the hashtag #nicsick were manually coded, with 52.3% (69/132) identified as discussing firsthand and secondhand reports of suspected nicotine poisoning symptoms and experiences. More than one-third of nicotine poisoning-related content (26/69, 37.68%) portrayed active vaping by users, which included content with vaping behavior such as vaping tricks and overconsumption, and 43% (30/69) of recorded users self-reported experiencing nicotine sickness, poisoning, or adverse events such as vomiting following nicotine consumption. The average follower count of users posting content related to nicotine sickness was significantly higher than that for users posting content unrelated to nicotine sickness (W=2350.5, P=.03). TikTok users openly discuss experiences, both firsthand and secondhand, with nicotine adverse events via the #nicsick hashtag including reports of overconsumption resulting in sickness. These study results suggest that there is a need to assess the utility of digital surveillance on emerging social media platforms for vaping adverse events, particularly on sites popular among youth and young adults. As vaping product use-patterns continue to evolve, digital adverse event detection likely represents an important tool to supplement traditional methods of public health surveillance (such as poison control center prevalence numbers).

Background Sarcopenia is characterized by the loss of skeletal muscle mass and strength and is associated with poor prognosis in patients with chronic obstructive pulmonary disease (COPD). Cigarette smoke (CS) exposure, a major cause for COPD, induces mitochondrial damage, which has been implicated in sarcopenia pathogenesis. The current study sought to examine the involvement of insufficient Parkin‐mediated mitophagy, a mitochondrion‐selective autophagy, in the mechanisms by which dysfunctional mitochondria accumulate with excessive reactive oxygen species (ROS) production in the development of COPD‐related sarcopenia. Methods The involvement of Parkin‐mediated mitophagy was examined using in vitro models of myotube formation, in vivo CS‐exposure model using Parkin−/− mice, and human muscle samples from patients with COPD‐related sarcopenia. Results Cigarette smoke extract (CSE) induced myotube atrophy with concomitant 30% reduction in Parkin expression levels (P < 0.05). Parkin‐mediated mitophagy regulated myotube atrophy by modulating mitochondrial damage and mitochondrial ROS production. Increased mitochondrial ROS was responsible for myotube atrophy by activating Muscle Ring Finger 1 (MuRF‐1)‐mediated myosin heavy chain (MHC) degradation. Parkin−/− mice with prolonged CS exposure showed enhanced limb muscle atrophy with a 31.7% reduction in limb muscle weights (P < 0.01) and 2.3 times greater MuRF‐1 expression (P < 0.01) compared with wild‐type mice with concomitant accumulation of damaged mitochondria and oxidative modifications in 4HNE expression. Patients with COPD‐related sarcopenia exhibited significantly reduced Parkin but increased MuRF‐1 protein levels (35% lower and 2.5 times greater protein levels compared with control patients, P < 0.01 and P < 0.05, respectively) and damaged mitochondria accumulation demonstrated in muscles. Electric pulse stimulation‐induced muscle contraction prevented CSE‐induced MHC reduction by maintaining Parkin levels in myotubes. Conclusions Taken together, COPD‐related sarcopenia can be attributed to insufficient Parkin‐mediated mitophagy and increased mitochondrial ROS causing enhanced muscle atrophy through MuRF‐1 activation, which may be at least partly preventable through optimal physical exercise.