TRPA1 and Sympathetic Activation Contribute to Increased Risk of Triggered Cardiac Arrhythmias in Hypertensive Rats Exposed to Diesel Exhaust

Background: Diesel exhaust (DE), which is emitted from on- and off-road sources, is a complex mixture of toxic gaseous and particulate components that leads to triggered adverse cardiovascular effects such as arrhythmias

An Autonomic Link Between Inhaled Diesel Exhaust and Impaired Cardiac Performance: Insight From Treadmill and Dobutamine Challenges in Heart Failure–Prone Rats

Cardiac disease exacerbation is associated with short-term exposure to vehicular emissions. Diesel exhaust (DE) might impair cardiac performance in part through perturbing efferent sympathetic and parasympathetic autonomic nervous system (ANS) input to the heart. We hypothesized that acute changes in ANS balance mediate decreased cardiac performance upon DE inhalation. Young adult heart failure–prone rats were implanted with radiotelemeters to measure heart rate (HR), HR variability (HRV), blood pressure (BP), core body temperature, and pre-ejection period (PEP, a contractility index). Animals pretreated with sympathetic antagonist (atenolol), parasympathetic antagonist (atropine), or saline were exposed to DE (500 µg/m3 fine particulate matter, 4h) or filtered air and then treadmill exercise challenged. At 1 day postexposure, separate rats were catheterized for left ventricular pressure (LVP), contractility, and lusitropy and assessed for autonomic influence using the sympathoagonist dobutamine and surgical vagotomy. During DE exposure, atenolol inhibited increases in HR, BP, and contractility, but not body temperature, suggesting a role for sympathetic dominance. During treadmill recovery at 4h post-DE exposure, HR and HRV indicated parasympathetic dominance in saline- and atenolol-pretreated groups that atropine inhibited. Conversely, at treadmill recovery 21h post-DE exposure, HRV and PEP indicated sympathetic dominance and subsequently diminished contractility that only atenolol inhibited. LVP at 1 day postexposure indicated that DE impaired contractility and lusitropy while abolishing parasympathetic-regulated cardiac responses to dobutamine. This is the first evidence that air pollutant inhalation both causes time-dependent oscillations between sympathetic and parasympathetic dominance and decreases cardiac performance via aberrant sympathetic dominance

Characterization of Size-Fractionated Airborne Particles Inside an Electronic Waste Recycling Facility and Acute Toxicity Testing in Mice

Disposal of electronic waste (e-waste) in landfills, incinerators, or at rudimentary recycling sites can lead to the release of toxic chemicals into the environment and increased health risks. Developing e-waste recycling technologies at commercial facilities can reduce the release of toxic chemicals and efficiently recover valuable materials. While these e-waste operations represent a vast improvement over previous approaches, little is known about environmental releases, workplace exposures, and potential health impacts. In this study, airborne particulate matter (PM) was measured at various locations within a modern U.S.-based e-waste recycling facility that utilized mechanical processing. In addition, composite size fractionated PM (coarse, fine and ultrafine) samples were collected, extracted, chemically analyzed, and given by oropharyngeal aspiration to mice or cultured with lung slices for lung toxicity tests. Indoor total PM concentrations measured during the study ranged from 220 to 1200 μg/m³. In general, the coarse PM (2.5–10 μm) was 3–4 times more abundant than fine/ultrafine PM (<2.5 μm). The coarse PM contained higher levels of Ni, Pb, and Zn (up to 6.8 times) compared to the fine (0.1–2.5 μm) and ultrafine (<0.1 μm) PM. Compared to coarse PM measurements from a regional near-roadway study, Pb and Ni were enriched 170 and 20 times, respectively, in the indoor PM, with other significant enrichments (>10 times) observed for Zn and Sb, modest enrichments (>5 times) for Cu and Sr, and minor enrichments (>2 times) for Cr, Cd, Mn, Ca, Fe, and Ba. Negligible enrichment (<2 times) or depletion (<1 time) were observed for Al, Mg, Ti, Si, and V. The coarse PM fraction elicited significant pro-inflammatory responses in the mouse lung at 24 h postexposure compared to the fine and ultrafine PM, and similar toxicity outcomes were observed in the lung slice model. We conclude that exposure to coarse PM from the facility caused substantial inflammation in the mouse lung and enrichment of these metals compared to levels normally present in the ambient PM could be of potential health concern