Increase In Ambient Levels Research Articles

Impact of a pollution breach at a coke oven factory on asthma control in nearby vulnerable adults

Previous studies have related sulfur dioxide (SO2) exposure to asthma exacerbations. We utilized the University of Pittsburgh Asthma Institute registry to study associations of asthma exacerbations between 2 geographically distinct populations of adults with asthma. Our objective was to examine whether asthma symptoms worsened following a significant fire event that destroyed pollution control equipment at the largest coke works in the United States. Two groups of patients with asthma, namely, those residing within 10 miles of the coke works fire (the proximal group [n= 39]) and those residing beyond that range (the control group [n= 44]), were geocoded by residential address. Concentrations of ambient air SO2 were generated by using local University of Pittsburgh Asthma Institute registry air monitoring data. Factory emissions were also evaluated. Data from a patient historical acute exposure survey and in-person follow-up data were evaluated. Inferential statistics were used to compare the groups. In the immediate postfire period (6-8 weeks), the level of emissions of SO2 from the factory emissions increased to 25 times more than the typical level. Following the pollution control breach, the proximal cohort self-reported an increase in medication use (risk ratio= 1.76; 95% CI= 1.1-2.8; P< .01) and more exacerbations. In a small subset of the follow-up cohort of those who completed the acute exposure survey only, asthma control metrics improved. Real-world exposure to a marked increase in ambient levels of SO2 from a pollution control breach was associated with worsened asthma control in patients proximal to the event, with the worsened control improving following repair of the controls. Improved spatial resolution of air pollutant measurements would enable better examination of exposures and subsequent health impacts.

Glia-Dependent Switch of Kainate Receptor Presynaptic Action

Presynaptic kainate receptors (KARs) exert a modulatory action on transmitter release. This effect can be switched from facilitation to inhibition by an increased concentration of KAR agonists. We here report that activation of presynaptic GluK1-containing KARs facilitates GABA release on oxytocin and vasopressin neurons in the supraoptic nucleus of the hypothalamus. Increase in ambient levels of glutamate associated with the physiological reduction of astrocytic coverage of oxytocin neurons in lactating rats switches this KAR-mediated facilitation to inhibition of GABAergic transmission. This effect was reproduced in both oxytocin and vasopressin neurons of virgin rats when glutamate transporters were blocked pharmacologically, thereby establishing that enhanced levels of extracellular glutamate induce the switch in KAR-mediated action. The facilitation of GABA release was inhibited with philanthotoxin, a Ca(2+)-permeable KAR antagonist, suggesting that this effect was associated with an ionotropic mode of action. Conversely, KAR-mediated inhibition was compromised in the presence of U73122, a phospholipase C inhibitor, in agreement with the involvement of a metabotropic pathway. We thus reveal that physiological astrocytic plasticity modifies the mode of action of presynaptic KARs, thereby inversing their coupling with GABA release.

The Use of a Uniquely Designed Anesthetic Scavenging Hood to Reduce Operating Room Anesthetic Gas Contamination During General Anesthesia

Numerous studies have suggested that chronic exposure to trace levels of anesthetic gas is harmful to operating room (OR) personnel. In the delivery of pediatric general anesthesia, an uncuffed endotracheal tube (ETT) is normally used which can result in considerable volatile anesthetic and nitrous oxide contamination of the OR. In this report, we present a method to reduce exposure to these anesthetic gases by means of an anesthetic scavenging hood (ASH). The ASH was used on six pediatric patients undergoing general endotracheal anesthesia via an uncuffed ETT. Measurements of all ambient gas levels were made 6 in. horizontally from the patient’s ear and 6 in. from the table surface. The application of the vacuum source to the ASH resulted in a very significant (P < 0.01, paired t-test) decrease in levels of ambient anesthetic gas, with no measurable change in ventilatory variables or changes in body temperature (P > 0.05, paired t-test). Discontinuation of the vacuum force to the ASH resulted in a marked increase in ambient levels of anesthetic gas. We conclude that the ASH is extremely effective in reducing waste anesthetic gas associated with anesthesia administered via an uncuffed ETT. The ASH may be a valuable and cost-effective addition in the OR for both reducing ambient anesthetic waste gas levels and conserving patient heat.