Levels Of Acrolein Research Articles

Pro-inflammatory cytokines, oxidative stress and diffuse coronary reocclusions in elderly patients after coronary stenting

BackgroundThe inflammation responses and oxidative stress were closely associated with coronary heart disease. We tried to evaluate the effects of multiple stents, long stents and small-diameter stents on inflammation responses and oxidative stress in the elderly patients with long diffuse reocclusions. MethodsThe blood samples were obtained after an overnight fast and we evaluated the expression levels of soluble ST2 (sST2), acrolein (ACR), aldosterone (ALD), angiotensin II (Ang II), toll-like receptor 4 (TLR4), tumour necrosis factor-α (TNF-α), malondialdehyde (MDA) and high sensitivity C-reactive protein (hs-CRP) in the elderly patients with long diffuse reocclusions after multiple stents, long stents, small-diameter stents implanted. Results: Levels of sST2, ACR, ALD, Ang II, TLR4, TNF-α, MDA and hs-CRP were remarkably increased (P < 0.001) in the elderly patients with long diffuse reocclusions after multiple stents, long stents, small-diameter stents implanted. The multiple stents, long stents and small-diameter stents may promote inflammatory response and oxidative stress, and led to long diffuse reocclusions in the elderly patients. The multiple stents, long stents and small-diameter stents may play the key roles in long diffuse reocclusions of the elderly patients. ConclusionsThe inflammatory and oxidative stress biomarkers could be considered as potential non-invasive diagnostic, predictive, prognostic and therapeutic molecular biomarkers for long diffuse reocclusions in the elderly patients after implantations of multiple stents, long stents and small-diameter stents.

Determining the impact of flavored e-liquids on aldehyde production during Vaping

1,2-Propylene glycol and glycerin, principal components of e-liquids, can thermally degrade to form acetaldehyde, acrolein, and formaldehyde when heated in electronic nicotine delivery systems (ENDS). Recently the flavors in e-liquids were suggested to be the major source of these aldehydes. We used the same 10 ENDS devices to test 5 e-liquid formulations (four flavored & one corresponding non-flavored) and measured device mass loss and levels of acetaldehyde, acrolein, and formaldehyde (30 replicate measurements per formulation). Despite finding reasonable variability in measurements of device mass loss, two out of 10 ENDS devices tested produced outlier values for aerosol levels acetaldehyde, acrolein, and formaldehyde. After removing these devices from further analysis, acceptable variability (≤20% RSD) in aerosol levels of acetaldehyde, and formaldehyde were found. The flavored formulations tested resulted in a consistent and selective increase of 150%–200% in acetaldehyde, no increase or decrease in acrolein and depending on the flavor formulation, an increase, a decrease or no change in formaldehyde levels. Comparison of our results to the literature illustrates the need for development of a standardized ENDS testing protocol. Our results further support that device variability must be fully characterized and considered before assessing the impact of e-liquid formulations.

Involuntary Tobacco Smoking while Sailing across the Sea

Smoking is one of the most important factors for human health problems. Little is known about involuntary smoking effects in an outdoor sport environment, e.g. sailing. The aim of the study was to evaluate the extend of active and passive smoking during open air activities by measuring the sensitive markers of smoking namely acetonitrile, acrolein, and benzene levels in smokers and non-smokers during leisure sailing across the sea.

Anti-inflammatory Effect of AZD6244 on Acrolein-Induced Neuroinflammation.

Clinically, high levels of acrolein (a highly reactive α, β-unsaturated aldehyde) and acrolein adducts are detected in the brain of patients with CNS neurodegenerative diseases, including Alzheimer's disease and spinal cord injury. Our previous study supports this notion by showing acrolein as a neurotoxin in a Parkinsonian animal model. In the present study, the effect of AZD6244 (an ATP non-competitive MEK1/2 inhibitor) on acrolein-induced neuroinflammation was investigated using BV-2 cells and primary cultured microglia. Our immunostaining study showed that lipopolysaccharide (LPS, an inflammation inducer as a positive control) increased co-localized immunoreactivities of phosphorylated ERK and ED-1 (a biomarker of activated microglia) in the treated BV-2 cells. Similar elevation in co-localized immunoreactivities of phosphorylated ERK and ED-1 was detected in the acrolein-treated BV-2 cells. Furthermore, Western blot assay showed increases in phosphorylated ERK in BV-2 cells subjected to LPS (1μg/mL) or acrolein (30μM); these increases were blocked by AZD6244 (10μM). At the same time, AZD6244 attenuated LPS-induced TNF-α (a pro-inflammatory cytokine) and cyclooxygenase-II (COX II, a pro-inflammatory enzyme). Consistently, AZD6244 reduced acrolein-induced elevations in COX-II mRNA and COX-II protein expression. In addition, AZD6244 inhibited acrolein-induced increases in activated caspase 1 (a biomarker of inflammasome activation) and heme oxygenase-1 (a redox-regulated chaperone protein) in BV-2 cells. Using a transwell migration assay, AZD6244 attenuated acrolein (5μM)-induced migration of BV-2 cells and primary cultured microglia. In conclusion, our study shows that acrolein is capable of inducing neuroinflammation which involved ERK activation in microglia. Furthermore, AZD6244 is capable of inhibiting acrolein-induced neuroinflammation. Our study suggests that ERK inhibition may be a neuroprotective target against acrolein-induced neuroinflammation in the CNS neurodegenerative diseases.

Human chemical signature: Investigation on the influence of human presence and selected activities on concentrations of airborne constituents

There is growing evidence that the very presence of human beings in an enclosed environment can impact air quality by affecting the concentrations of certain airborne volatile organic compounds (VOC). This influence increases considerably when humans perform different activities, such as using toiletries, or simply eating and drinking. To understand the influence of these parameters on the concentrations of selected airborne constituents, a study was performed under simulated residential conditions in an environmentally-controlled exposure room. The human subjects either simply remained for a certain time in the exposure room, or performed pre-defined activities in the room (drinking wine, doing sport, using toiletries, and preparation of a meal containing melted cheese). The impact of each activity was assessed separately using our analytical platform and exposure room under controlled environmental conditions. The results showed that prolonged human presence leads to increased levels of isoprene, TVOCs, formaldehyde and, to a lesser extent, acetaldehyde. These outcomes were further supported by results of meta-analyses of data acquired during several internal studies performed over two years. Furthermore, it was seen that the indoor concentrations of several of the selected constituents rose when the recreational and daily living activities were performed. Indeed, an increase in acetaldehyde was observed for all tested conditions, and these higher indoor levels were especially notable during wine-drinking as well as cheese meal preparation. Formaldehyde increased during the sessions involving sport, using toiletries, and cheese meal preparation. Like acetaldehyde, acrolein, crotonaldehyde and particulate matter levels rose significantly during the cheese meal preparation session. In conclusion, prolonged human residence indoors and some recreational and daily living activities caused substantial emissions of several airborne pollutants under ventilation typical for residential environments.

Side Effects of Coronary Stenting such as Severe Coronary Stenosis and Multiple Coronary Chronic Total Occlusions in Elderly Patients via Induced Proinflammatory and Prooxidative Stress.

Background Severe coronary stenosis and multiple coronary chronic total occlusions are serious side effects of coronary stent implantation in elderly patients. This research sought to investigate the side effects of coronary stenting such as severe coronary stenosis and multiple coronary chronic total occlusions in elderly patients via induced proinflammatory and prooxidative stress. Methods We evaluated the expression levels of tumor necrosis factor-α (TNF-α), toll-like receptor 4 (TLR4), acrolein (ACR), malondialdehyde (MDA), high-sensitivity C-reactive protein (hs-CRP), stromal cell-derived factor-1α (SDF-1α), superoxide dismutase 3 (SOD3), and endothelial nitric oxide synthase (eNOS) in elderly patients with severe coronary stenosis and multiple coronary chronic total occlusions. Results Levels of TNF-α, TLR4, ACR, MDA, and hs-CRP were remarkably increased (P < 0.001), and levels of SDF-1α, SOD3, and eNOS were remarkably lowered (P < 0.001) in elderly patients with severe coronary stenosis and multiple coronary chronic total occlusions. Coronary stenting induced proinflammatory and prooxidant mediator expression and inhibited anti-inflammatory/antioxidant mediators. The proinflammatory and prooxidant mediators may be involved in severe coronary stenosis and multiple coronary chronic total occlusions in elderly patients. ConclusionsSide effects such as severe coronary stenosis and multiple coronary chronic total occlusions because of coronary stenting in elderly patients were induced by proinflammatory and prooxidative stress. Circulating proinflammatory and prooxidant mediators could predict early severe coronary stenosis and multiple coronary chronic total occlusions in elderly coronary heart disease patients.

Comparative levels of carbonyl delivery between mass-market cigars and cigarettes

The recent 2016 deeming of cigars by the US Food and Drug Administration (FDA) has led to increased interest in cigar science, including ways to accurately measure the harmful and potentially harmful constituents (HPHCs) found within mainstream cigar smoke. At present, there are standardized methods for evaluating HPHCs in mainstream cigarette smoke but none specific to cigar analysis except for nicotine and carbon monoxide. This study sought to analyze carbonyl delivery in marketed cigars and cigarillos and compare them against levels found in cigarettes. To accomplish this the standard cigarette method, CORESTA recommended method 74 (CRM-74), was optimized for cigar smoking including an evaluation of the trapping efficiency and the stability of the carbonyl-hydrazone adducts due to the increased smoke time required for cigar collection. On a per product basis, carbonyl delivery from cigars smoked under CRM-64 conditions was found to yield similar levels of formaldehyde and greater levels of acetaldehyde, acrolein and crotonaldehyde than measured in mainstream cigarette smoke collected under conditions prescribed under ISO standard 3308. Furthermore, on a per product basis, cigarettes smoked under the ISO 20778 intense smoking regime delivered higher levels of formaldehyde, acrolein and crotonaldehyde as compared to cigars smoked under the CORESTA regime, while acetaldehyde was found to be higher in mainstream cigar smoke. Given the recent deeming, this work expands upon previously reported work, limited in scope by either number of products or analytes reported, through the analysis of carbonyl delivery found in the mainstream smoke for 12 brands of cigars and cigarillos.

Differences in exposure to toxic and/or carcinogenic volatile organic compounds between Black and White cigarette smokers.

Objective:It is unclear why Black smokers in the United States have elevated risk of some tobacco-related diseases compared to White smokers. One possible causal mechanism is differential intake of tobacco toxicants but results across studies are inconsistent. Thus, we examined racial differences in biomarkers of toxic volatile organic compounds (VOCs) present in tobacco smoke.Method:We analyzed baseline data collected from 182 Black and 184 White adult smokers who participated in a randomized clinical trial in 2013–2014 at 10 sites across the U.S. We examined differences in urinary levels of 10 VOC metabolites, total nicotine equivalents (TNE), and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), controlling for covariates such as cigarettes per day (CPD), as well as differences in VOCs per TNE to assess the extent to which tobacco exposure, and not metabolic factors, accounted for racial differences.Results:Concentration of metabolites of acrolein, acrylonitrile, ethylene oxide, and methylating agents were significantly higher in Blacks compared to Whites when controlled for covariates. Other than the metabolite of methylating agents, VOCs per TNE did not differ between Blacks and Whites. Concentrations of TNE/CPD and VOCs/CPD were significantly higher in Blacks. Menthol did not contribute to racial differences in VOC levels.Conclusion:For a given level of CPD, Black smokers likely take in higher levels of acrolein, acrylonitrile, and ethylene oxide than White smokers. Our findings are consistent with Blacks taking in more nicotine and toxicants per cigarette smoked, which may explain their elevated disease risk relative to other racial groups.

Biomarkers of Exposure and Potential Harm among Natural American Spirit Smokers.

We compared biomarkers of exposure and potential harm in smokers of American Spirit (AS) to smokers of Marlboro, Newport, Camel, and Pall Mall. We conducted secondary analysis on: (1) data from a randomized clinical trial (RCT); and (2) the Population Assessment of Tobacco Use and Health (PATH) Study. Biomarkers analyzed included: total nicotine equivalents (TNE); 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol and its glucuronides (total NNAL); N'-nitrosonornicotine and its N-glucuronide (total NNN);3-hydroxypropylmercapturic acid(3-HPMA); 2-hydroxypropylmercapturic acid (2-HPMA), 3-hydroxy-1 methylpropylmercapturic acid (HMPMA); S-phenylmercapturic acid(SPMA); 2-cyanoethylmercapturic acid (CEMA); phenanthrene tetraol(PheT);1-hydroxypyrene (1-HOP);8-iso-PGF2α; white blood count(WBC); prostaglandin E metabolite(PGEM); and high sensitivity C-reactive protein(hsCRP). AS smokers did not differ in TNE but had higher TNE per cigarette compared to other brands. Total NNAL, total NNN, CEMA, and 3-HPMA were lower in AS smokers. All other biomarkers were no different in AS smokers compared to all or the majority of the other brands. Levels of total NNAL, total NNN, acrylonitrile, and acrolein were reduced in AS smokers; however, it is not known whether reductions in exposure to these toxicants contribute to reduced harm. Higher TNE per cigarette smoked in AS smokers suggests a greater addictive potential compared to other brands. Regulatory action to ensure that consumers are not misled about the risks of the AS brand are recommended.

The relationship between acrolein and oxidative stress in COPD: in systemic plasma and in local lung tissue.

PurposeCigarette smoke produces a high level of acrolein, which is thought to be pathogenically involved in the development of chronic obstructive pulmonary disease (COPD). The present study investigated the pathological role of acrolein in the development of COPD.Patients and methodsAcrolein concentration was measured in plasmas obtained from 47 patients with COPD and 18 current smokers without COPD, and in supernatants of homogenized lung tissues obtained from 10 never-smokers, 8 current smokers, and 8 patients with COPD by high-performance liquid chromatography. Oxidant status and antioxidant activity were measured using derivatives of reactive oxygen metabolite (d-ROM) and bio-antioxidant power (BAP), respectively, in the Free Radical Elective Evaluation FRAS4 system. In addition, immunohistochemistry was used to evaluate the over-presentation of acrolein in lung tissues of patients with COPD.ResultsPlasma concentrations of acrolein were significantly higher in the patients with COPD than the non-COPD smokers (P<0.001), which significantly correlated with the oxidant status in patients with COPD (R=0.69, P<0.05). Similar pathological alterations in acrolein concentrations were found in the lung tissue supernatants of patients with COPD, which significantly correlated with the oxidant status in patients with COPD. Furthermore, acrolein was strongly expressed in the lung tissues of patients with COPD.ConclusionThe increased acrolein concentrations were highly involved in the pathogenesis of COPD through interference in the balance of oxidative stress versus antioxidant potentiality.

Heated Tobacco Products: Volatile Emissions and Their Predicted Impact on Indoor Air Quality.

This study characterized emissions from IQOS, a heated tobacco product promoted as a less harmful alternative to cigarettes. Consumable tobacco plugs were analyzed by headspace GC/MS to assess the influence of heating temperature on the emission profile. Yields of major chemical constituents increased from 4.1 mg per unit at 180 °C to 6.2 mg at 200 °C, and 10.5 mg at 220 °C. The Health Canada Intense smoking regime was used to operate IQOS in an environmental chamber, quantifying 33 volatile organic compounds in mainstream and sidestream emissions. Aldehydes, nitrogenated species, and aromatic species were found, along with other harmful and potentially harmful compounds. Compared with combustion cigarettes, IQOS yields were in most cases 1-2 orders of magnitude lower. However, yields were closer to, and sometimes higher than electronic cigarettes. Predicted users' daily average intake of benzene, formaldehyde, acetaldehyde and acrolein were 39 μg, 32 μg, 2.2 mg and 71 μg, respectively. Indoor air concentrations were estimated for commonly encountered scenarios, with acrolein levels of concern (over 0.35 μg m-3) derived from IQOS used in homes and public spaces. Heated tobacco products are a weaker indoor pollution source than conventional cigarettes, but their impacts are neither negligible nor yet fully understood.

The Health Risks of Electronic Cigarette Use to Bystanders.

This works aimed to assess the health risks of e-cigarette use to bystanders. The exhaled breath of 17 volunteers was collected while they were vaping, and the levels of nicotine, propylene glycol, glycerol, formaldehyde, acetaldehyde, acrolein, tobacco-specific nitrosamines (TSNAs), and heavy metals were analyzed. Increased levels of nicotine, propylene glycol, TSNAs and copper were found in the exhaled breath of the volunteers. From these measurements, bystander exposure was estimated for two different scenarios: (1) A non-ventilated car with two e-cigarette users and (2) a ventilated office with one e-cigarette user. Our results show that bystanders may experience irritation of the respiratory tract as a result of exposure to propylene glycol and glycerol. Systemic effects of nicotine should also be expected if nicotine-containing e-liquid is used, including palpitations, and an increase of the systolic blood pressure. Furthermore, due to the presence of TSNAs in some e-liquids, an increased risk of tumors could not be excluded for the ‘car’ scenario. While e-cigarette use can clearly have effects on the health of bystanders, the risks depend on the rate of ventilation, dimensions of the room, and vaping behavior of the e-cigarette user. The presence of TSNAs in e-liquids can be avoided, which will prevent the most serious effect identified (increased risk of tumors).

Tetramethylrhodamine is an essential scaffold of azide probe in detecting cellular acrolein.

Tetramethylrhodamine (TAMRA)-phenyl azide is a chemical probe used to detect intracellular acrolein directly in live cells. Herein, we demonstrated that TAMRA is the optimum fluorophore for the probe. TAMRA-phenyl azide was used to reveal that high levels of acrolein are generated in a variety of breast cancer cells, regardless of the tumor subtype. These findings corroborate the analysis presented in our previous report, in which TAMRA-phenyl azide was used to label breast cancer tissues resected from breast cancer patients. Because high levels of acrolein were generated in all cancer cell types, we believe that acrolein detection may be useful as a general method for labeling cancerous tissues.

Gut microbial transformation of the dietary mutagen MeIQx may reduce exposure levels without altering intestinal transport

The mutagen and probable human carcinogen 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx) is metabolized in the colon to 9-hydroxyl-2,7-dimethyl-7,9,10,11-tetrahydropyrimido[2′,1′:2,3]imidazo[4,5-f]quinoxaline (MeIQx-M1) by conjugation with microbially generated acrolein. However, whether this microbiota-controlled process alters systemic exposure and hepatotoxicity of MeIQx remains unclear. The physiological relevance of this microbial transformation on the systemic exposure of MeIQx was investigated using an in vitro-in vivo extrapolation approach. To address whether microbial transformation influences intestinal transport of MeIQx, the intestinal uptake of MeIQx and its metabolite MeIQx-M1 was quantified using Ussing chambers mounted with different intestinal segments from male Fischer 344 rats. Up to 0.4% of both MeIQx and MeIQx-M1 were transported from the mucosal side to the serosal side of intestinal tissue within 90 min, suggesting that the intestinal uptake of both compounds is similar. With the uptake rates of both compounds, physiologically based pharmacokinetic (PBPK) modeling of the fate of MeIQx in the human body including microbial transformation of MeIQx was performed. Results indicate for the first time that high levels of microbe-derived acrolein would be required to significantly reduce systemic exposure of MeIQx in humans. Finally, neither MeIQx nor MeIQx-M1 were cytotoxic towards human liver HepaRG cells at dietary or higher concentrations of MeIQx. In summary, these findings suggest that gut microbial transformation of heterocyclic amines has the potential to influence systemic human exposure to some extent, but may require significant gut microbial production of acrolein and that further investigations are needed to understand physiological levels of acrolein and competing biotransformation pathways.

Understanding skin absorption of common aldehyde vapours from exposure during hazardous material incidents.

The toxic release of aldehyde vapours during a hazardous material (HAZMAT) incident primarily results in respiratory concerns for the unprotected public. However, skin absorption may be an important concurrent exposure route that is poorly understood for this scenario. This study provides experimental data on the skin absorption properties of common aldehydes used in industry, including acetaldehyde, acrolein, benzaldehyde and formaldehyde, in gaseous or vapour form using an adapted in vitro technique. Two of the four tested aldehydes were found to penetrate the skin in appreciable amounts following 30-min exposure at HAZMAT relevant atmospheric concentrations: acetaldehyde (5.29 ± 3.24 µg/cm2) and formaldehyde (3.45 ± 2.58 µg/cm2). Whereas only low levels of acrolein (0.480 ± 0.417 µg/cm2) and benzaldehyde (1.46 ± 0.393 µg/cm2) skin penetration was noted. The aldehydes demonstrated differing levels of interaction with fabric. Formaldehyde and acetaldehyde adsorbed strongly to denim, whereas benzaldehyde and acrolein displayed no sink properties. However, denim was shown to be an initial protective barrier and reduced penetration outcomes for all aldehydes. This study provides important information to assist first responders and confirms the relevance of using physicochemical properties (e.g. solubility, molecular weight, partition coefficient) to predict skin permeation potential in the absence of empirical data during HAZMAT incidents involving different types of aldehydes.

Exposure risk to carbonyl compounds and furfuryl alcohol through the consumption of sparkling wines

ABSTRACT: The goals of this study were to verify the occurrence of furfuryl alcohol (FA) and carbonyl compounds (acetaldehyde, acrolein, ethyl carbamate (EC), formaldehyde and furfural) in sparkling wines and to evaluate, for the first time, whether the consumption of the samples under study could represent risk to consumers health. These compounds are electrophilic; and therefore, may covalently bind to DNA, which may result in mutagenicity. EC and formaldehyde were present at low levels (&lt;1μg L-1) in all samples. Acetaldehyde, furfural and acrolein were also found in low levels (&lt;1.5, 1.4 and 1.0μg L-1, respectively) in 57, 71 and 76% of samples. In the other samples, levels of acetaldehyde, furfural and acrolein ranged from 5.2 to 54.8, 10.5 to 41.0 and 20.3 to 36.7μg L-1, respectively. Furfuryl alcohol was also reported in all samples in levels from 10.4 to 33.5μg L-1. Acrolein was the only compound reported at levels sufficient to represent risk to health, which occurred in 24% of the samples. A study focused on the origin of acrolein deserves attention, investigating the influence of the concentration of precursors and the role of fermentation in the formation of this aldehyde, besides the evaluation of possible environmental contamination of grapes during cultivation.

Potential Prognostic, Diagnostic and Therapeutic Markers for In-stent Reocclusion in Advanced Age Patients After Coronary Stenting.

Oxidative stress and inflammatory response played important roles in advanced atherosclerosis. We tried to confirm clinical diagnostic significance of the assessments of oxidative stress and inflammatory response status with in-stent reocclusion in 283 advanced age patients (80～90 years) after coronary stenting. We analyzed levels of circulating superoxide dismutase 3 (SOD3), nitric oxide (NO), endothelial nitric oxide synthase (eNOS), malondialdehyde (MDA), acrolein（ACR）, and paraoxonase-1 （PON-1）in advanced age patients with in-stent restenosis and reocclusion after coronary stenting. Levels of SOD3, eNOS, NO and PON-1 were lowered (P<0.001) and levels of MDA and ACR were increased (P<0.001). The assessments of the biomarkers of oxidative stress and inflammatory response (levels of MDA and ACR) and anti-oxidant biomarkers (levels of eNOS, NO, SOD3 and PON-1) could be considered as potential prognostic and diagnostic indicators of in-stent reocclusion in advanced age patients after coronary stenting.

Ambient Particulate Matter and Acrolein Co-Exposure Increases Myocardial Dyssynchrony in Mice via TRPA1.

Air pollution is a complex mixture of particulate matter and gases linked to adverse clinical outcomes. As such, studying responses to individual pollutants does not account for the potential biological responses resulting from the interaction of various constituents within an ambient air shed. We previously reported that exposure to high levels of the gaseous pollutant acrolein perturbs myocardial synchrony. Here, we examined the effects of repeated, intermittent co-exposure to low levels of concentrated ambient particulates (CAPs) and acrolein on myocardial synchrony and the role of transient receptor potential cation channel A1 (TRPA1), which we previously linked to air pollution-induced sensitization to triggered cardiac arrhythmia. Female B6129 and Trpa1-/- mice (n = 6/group) were exposed to filtered air (FA), CAPs (46 µg/m3 of PM2.5), Acrolein (0.42 ppm), or CAPs+Acrolein for 3 h/day, 2 days/week for 4 weeks. Cardiac ultrasound was conducted to assess cardiac synchronicity and function before and after the first exposure and after the final exposure. Heart rate variability (HRV), an indicator of autonomic tone, was assessed after the final exposure. Strain delay (time between peak strain in adjacent cardiac wall segments), an index of myocardial dyssynchrony, increased by 5-fold after the final CAPs+Acrolein exposure in B6129 mice compared with FA, CAPs, or Acrolein-exposed B6129 mice, and CAPs+Acrolein-exposed Trpa1-/- mice. Only exposure to acrolein alone increased the HRV high frequency domain (5-fold) in B6129 mice, but not in Trpa1-/- mice. Thus, repeated inhalation of pollutant mixtures may increase risk for cardiac responses compared with single or multiple exposures to individual pollutants through TRPA1 activation.

E-cigarettes expose mouths to reactive carbonyls

As e-cigarette use skyrockets, so too do studies of their chemistry. The handheld devices generate vapors from nicotine-containing liquids, and most work has focused on the stages of that transformation. Fewer studies have examined the chemistry occurring inside e-cigarette users’ mouths, but Silvia Balbo surmised her team’s mass spectrometry technique could provide insight. The technique analyzes reactive carbonyl compounds appearing in mouths after alcohol exposure, and the glycerol or propylene glycol in e-cigarette liquids generate similar compounds. Balbo and postdoctoral researcher Romel Dator, who presented the work at last week’s ACS meeting, recruited five users and collected saliva before and after 15-minute vaping sessions at their University of Minnesota Masonic Cancer Center clinic. After vaping, levels of acrolein and methylglyoxal in users’ saliva increased by as much as 50 times. To examine potential damage by these compounds to DNA, users swished a saline mouthwash to provide oral cells. Compared to

'Real-world' compensatory behaviour with low nicotine concentration e-liquid: subjective effects and nicotine, acrolein and formaldehyde exposure.

AimsTo compare the effects of (i) high versus low nicotine concentration e‐liquid, (ii) fixed versus adjustable power and (iii) the interaction between the two on: (a) vaping behaviour, (b) subjective effects, (c) nicotine intake and (d) exposure to acrolein and formaldehyde in e‐cigarette users vaping in their everyday setting.DesignCounterbalanced, repeated measures with four conditions: (i) low nicotine (6 mg/ml)/fixed power; (ii) low nicotine/adjustable power; (iii) high nicotine (18 mg/ml)/fixed power; and (iv) high nicotine/adjustable power.SettingLondon and the South East, England.ParticipantsTwenty experienced e‐cigarette users (recruited between September 2016 and February 2017) vaped ad libitum using an eVic Supreme™ with a ‘Nautilus Aspire’ tank over 4 weeks (1 week per condition).MeasurementsPuffing patterns [daily puff number (PN), puff duration (PD), interpuff interval (IPI)], ml of e‐liquid consumed, changes to power (where permitted) and subjective effects (urge to vape, nicotine withdrawal symptoms) were measured in each condition. Nicotine intake was measured via salivary cotinine. 3‐Hydroxypropylmercapturic acid (3‐HPMA), a metabolite of the toxicant acrolein, and formate, a metabolite of the carcinogen formaldehyde, were measured in urine.FindingsThere was a significant nicotine concentration × power interaction for PD (P < 0.01). PD was longer with low nicotine/fixed power compared with (i) high nicotine/fixed power (P < 0.001) and (ii) low nicotine/adjustable power (P < 0.01). PN and liquid consumed were higher in the low versus high nicotine condition (main effect of nicotine, P < 0.05). Urge to vape and withdrawal symptoms were lower, and nicotine intake was higher, in the high nicotine condition (main effects of nicotine: P < 0.01). While acrolein levels did not differ, there was a significant nicotine × power interaction for formaldehyde (P < 0.05).ConclusionsUse of a lower nicotine concentration e‐liquid may be associated with compensatory behaviour (e.g. higher number and duration of puffs) and increases in negative affect, urge to vape and formaldehyde exposure.