Composition of e-cigarette aerosols: A review and risk assessment of selected compounds.

The potential harms and benefits of e-cigarettes, or electronic nicotine delivery systems (ENDS), have received significant attention from public health and regulatory communities. Such products may provide a reduced risk means of nicotine delivery for combustible cigarette smokers while being inappropriately appealing to nicotine naive youth. Numerous authors have examined the chemical complexity of aerosols from various open- and closed-system ENDS. This body of literature is reviewed here, with the risks of ENDS aerosol exposure among users evaluated with a margin of exposure (MoE) approach for two non-carcinogens (methylglyoxal, butyraldehyde) and a cancer risk analysis for the carcinogen N-nitrosonornicotine (NNN). We identified 96 relevant papers, including 17, 13, and 5 reporting data for methylglyoxal, butyraldehyde, and NNN, respectively. Using low-end (minimum aerosol concentration, low ENDS use) and high-end (maximum aerosol concentration, high ENDS use) assumptions, estimated doses for methylglyoxal (1.78 × 10-3-135 µg/kg-bw/day) and butyraldehyde (1.9 × 10-4-66.54 µg/kg-bw/day) corresponded to MoEs of 227-17,200,000 and 271-280,000,000, respectively, using identified points of departure (PoDs). Doses of 9.90 × 10-6-1.99 × 10-4 µg/kg-bw/day NNN corresponded to 1.4-28 surplus cancers per 100,000 ENDS users, relative to a NNN-attributable surplus of 7440 per 100,000 cigarette smokers. It was concluded that methylglyoxal and butyraldehyde in ENDS aerosols, while not innocuous, did not present a significant risk of irritant effects among ENDS users. The carcinogenic risks of NNN in ENDS aerosols were reduced, but not eliminated, relative to concentrations reported in combustible cigarette smoke.

Post-transcriptional regulation in attaching and effacing pathogens: integration of environmental cues and the impact on gene expression and host interactions.

To establish infection, enteric pathogens integrate environmental cues to navigate the gastrointestinal tract and precisely control expression of virulence determinants. Emerging data indicate that post-transcriptional and post-translational gene regulation plays a key role in virulence regulation and pathogen adaptation to the host environment. Here, we highlight recent studies that reveal how physiologically relevant signals initiate post-transcriptional and post-translational regulatory circuits and the impact on virulence gene expression in the attaching and effacing pathogens, enteropathogenic Escherichia coli, enterohemorrhagic E. coli O157:H7, and Citrobacter rodentium.