Exhalation of alternative tobacco product aerosols differs from cigarette smoke-and may lead to alternative health risks.

BACKGROUND: Variation in alternative tobacco product (ATP) constituents, heating potential, and consumer behaviors have made it difficult to characterize their health risks. To date, most toxicity studies of ATPs have used established cigarette endpoints to inform study design. Furthermore, to assess where ATPs fall on the tobacco harm continuum, with cigarettes representing maximum potential risk, studies have tended to compare the relative biological responses to ATPs against those due to cigarettes. OBJECTIVES: 1) To characterize the exhalation profiles of two popular ATPs: electronic cigarettes (e-cigarettes) and hookah waterpipes (hookah) and 2) to determine if ATP exhalation patterns were representative of cigarette exhalation patterns. METHODS: Exhalation patterns were recorded (mouth only, nose only, or both mouth and nose) among individuals observed in the New York City tri-state area using a recognizable tobacco product (cigarette, e-cigarette, or hookah). Cigarette smokers and e-cigarette vapers were observed on city streets; water-pipe smokers were observed inside Manhattan hookah bars. RESULTS: E-cigarette vapers practiced exclusive nasal exhalation at far higher rates than did cigarette smokers (19.5% vs 4.9%). Among vapers, e-cigarette device type was also significantly associated with exhalation profile. Overall, cigarette smokers exhaled from their nose approximately half to one-third as often as ATP users (hookah and e-cigarettes, respectively). CONCLUSIONS: Nasal exhalation of tobacco emissions appears to be a shared characteristic across several types of ATPs. It is therefore plausible that ATP-specific consumer behaviors may foster unique upper respiratory health consequences that have not been observed in smokers. Thus, product-specific behaviors should inform the prioritization of biological endpoints used in studies evaluating ATP toxicity and health effects.

PM2.5 Concentration and Composition in Subway Systems in the Northeastern United States.

OBJECTIVES: 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: We report real-time and gravimetric PM2.5 concentrations and particle composition from area samples collected in the subways of Philadelphia, Pennsylvania; Boston, Massachusetts; New York City, New York/New Jersey (NYC/NJ); and Washington, District of Columbia. A total of 71 stations across 12 transit lines were monitored during morning and evening rush hours. RESULTS: We observed variable and high PM2.5 concentrations for on-train and on-platform measurements during morning (from 0600 hours to 1000 hours) and evening (from 1500 hours to 1900 hours) rush hour across cities. Mean real-time PM2.5 concentrations in underground stations were 779±249, 548±207, 341±147, 327±136, and 112±46.7 µg/m3 for the PATH-NYC/NJ; MTA-NYC; Washington, DC; Boston; and Philadelphia transit systems, respectively. In contrast, the mean real-time ambient PM2.5 concentration taken above ground outside the subway stations of PATH-NYC/NJ; MTA-NYC; Washington, DC; Boston; and Philadelphia were 20.8±9.3, 24.1±9.3, 12.01±7.8, 10.0±2.7, and 12.6±12.6 µg/m3, respectively. Stations serviced by the PATH-NYC/NJ system had the highest mean gravimetric PM2.5 concentration, 1,020 µg/m3, ever reported for a subway system, including two 1-h gravimetric PM2.5 values of approximately 1,700 µg/m3 during rush hour at one PATH-NYC/NJ subway station. Iron and total carbon accounted for approximately 80% of the PM2.5 mass in a targeted subset of systems and stations. DISCUSSION: Our results document that there is an elevation in the PM2.5 concentrations across subway systems in the major urban centers of Northeastern United States during rush hours. Concentrations in some subway stations suggest that transit workers and commuters may be at increased risk according to U.S. federal environmental and occupational guidelines, depending on duration of exposure. This concern is highest for the PM2.5 concentrations encountered in the PATH-NYC/NJ transit system. Further research is urgently needed to identify the sources of PM2.5 and factors that contribute to high levels in individual stations and lines and to assess their potential health impacts on workers and/or commuters. https://doi.org/10.1289/EHP7202.

Microglial activation and responses to vasculature that result from an acute LPS exposure.

Bacterial cell wall endotoxins, i.e. lipopolysaccharides (LPS), are some of the original compounds shown to evoke the classic signs of systemic inflammation/innate immune response and neuroinflammation. The term neuroinflammation often is used to infer the elaboration of proinflammatory mediators by microglia elicited by neuronal targeted activity. However, it also is possible that the microglia are responding to vasculature through several signaling mechanisms. Microglial activation relative to the vasculature in the hippocampus and parietal cortex was determined after an acute exposure of a single subcutaneous injection of 2 mg/kg LPS. Antibodies to allograft inflammatory factor (Aif1, a.k.a. Iba1) were used to track and quantify morphological changes in microglia. Immunostaining of platelet/endothelial cell adhesion molecule 1 (Pecam1, a.k.a. Cd31) was used to visualize vasculature in the forebrain and glial acidic fibrillary protein (GFAP) to visualize astrocytes. Neuroinflammation and other aspects of neurotoxicity were evaluated histologically at 3 h, 6 h, 12 h, 24 h, 3 d and 14 d following LPS exposure. LPS did not cause neurodegeneration as determined by Fluoro Jade C labeling. Also, there were no signs of mouse IgG leakage from brain vasculature due to LPS. Some changes in microglia size occurred at 6 h, but by 12 h microglial activation had begun with the combined soma and proximal processes size increasing significantly (1.5-fold). At 24 h, almost all the microglia soma and proximal processes in the hippocampus, parietal cortex, and thalamus were closely associated with the vasculature and had increased almost 2.0-fold in size. In many areas where microglia were juxtaposed to vasculature, astrocytic endfeet appeared to be displaced. The microglial activation had subsided slightly by 3 d with microglial size 1.6-fold that of control. We hypothesize that acute LPS activation can result in vascular mediated microglial responses through several mechanisms: 1) binding to Cd14 and Tlr4 receptors on microglia processes residing on vasculature; 2) damaging vasculature and causing the release of cytokines; and 3) possibly astrocytic endfeet damage resulting in cytokine release. These acute responses may serve as an adaptive mechanism to exposure to circulating LPS where the microglia surround the vasculature. This could further prevent the pathogen(s) circulating in blood from entering the brain. However, diverting microglial interactions away from synaptic remodeling and other types of microglial interactions with neurons may have adverse effects on neuronal function.