The most common disposal method in the United States for municipal solid waste (MSW) is burial in landfills. Until recently, air emissions from these landfills were not regulated. Under the New Source Performance Standards and Emission Guidelines for MSW landfills, MSW operators are required to determine the nonmethane organic gas generation rate of their landfill through modeling and/or measurements. This paper summarizes speciated nonmethane organic compound (NMOC) measurement data collected during an intensive, short-term field program. Over 250 separate landfill gas samples were collected from emission sources at the Fresh Kills landfill in New York City and analyzed for approximately 150 different analytes. The average total NMOC value for the landfill was 438 ppmv (as hexane) versus the regulatory default value of 4000 ppmv (as hexane). Over 70 individual volatile organic compounds (VOCs) were detected and quantified in the landfill gas samples. The typical gas composition for this landfill was determined as well as estimates of the spatial, temporal, and measurement variability in the gas composition. The data for NMOC show that the gas composition within the landfill is equivalent to the composition of the gas exiting the landfill through passive vents and through the soil cover.

The results of an API‐sponsored pilot‐scale subsurface venting system study are presented. The purpose of this study was to evaluate the effectiveness of forced venting techniques in controlling and removing hydrocarbon vapors from a subsurface formation. Both qualitative and quantitative sampling and analytical procedures were developed to measure hydrocarbon vapors extracted from the soil. Vapor recovery and equivalent liquid product recovery rates were measured at each test cell evacuation rate. Two identical test cells were installed. Each cell contained 16 vapor monitoring probes spaced at distances from 4 to 44 feet from a vapor extraction (vacuum) well. Each cell was also configured with two air inlet wells to allow atmospheric air to enter the subsurface formation. The vapor monitoring probes were installed at three discrete elevations above the capillary zone. In situ vapor samples were obtained periodically from these probes to measure changes in vapor concentration and composition while extracting vapors from the vacuum well at three different flow rates (18.5 scfm, 22.5 scfm and 39.8 scfm). In situ vapor samples were analyzed using a portable gas chromatograph to quantify and speciate the vapors. Vacuum levels were also measured at each vapor sampling probe and at the vacuum well. The soil venting techniques evaluated during this study offer an alternative approach for controlling and eliminating spilled or leaked hydrocarbons from sand or gravel formations of high porosity and moderate permeability. These techniques may also be used to augment conventional liquid recovery methods. The data collected during this study will be useful in optimizing subsurface venting systems for removing and controlling hydrocarbon vapors in soil. Study results indicate pulsed venting techniques may offer a cost‐effective means of controlling or eliminating hydrocarbon vapors in soil.

BackgroundSmoking has significant negative impact on periodontal health and treatment outcomes. The molecular effects of smoking on oral immune homeostasis have not been fully elucidated. The present study aimed to provide a comprehensive assessment of smoking‐associated gene expression changes in healthy palatal mucosa and to identify potentially implicated immunologic pathways.MethodsPalatal biopsies, in the form of connective tissue grafts, were obtained from periodontally healthy smokers and non‐smokers. Smoking status was biochemically verified (exhaled air CO and serum cotinine). Tissue samples were processed for next generation sequencing, quantitative real‐time polymerase chain reaction (qPCR), and immunohistochemistry. Gene set enrichment/pathway analysis and correlation analysis between gene expression and serum cotinine levels were also performed.ResultsAnalysis of palatal tissues from 12 non‐smokers and 10 smokers identified 830 significantly (P <0.05) differentially expressed genes (DEGs), 249 with fold change (FC) >2. Most increased in expression (≥5‐FC) were CYP1A1, CYP1B1, and USP17L9P; most decreased (≥6‐FC) were IL36A, DEFB4A, DEFB4B, SPRR2F, CCL20, KLK6, and ADH4. 203 DEGs (FC >2) were significantly correlated with serum cotinine levels. Significant enrichment pathways for cotinine‐associated genes include antimicrobial humoral response, regulation of humoral response and various metabolic processes. qPCR and immunohistochemistry confirmed gene and protein expression of selected DEGs.ConclusionsSmoking has a significant effect on the transcriptome of normal human palatal mucosa and seems to target genes important for innate immune defenses, which may prove to be one of the key mechanisms by which tobacco smoking leads to increased periodontitis susceptibility.

cAMP signaling is known to have significant effects on cell growth, either inhibitory or stimulatory depending on the cell type. Study of cAMP-induced growth inhibition in mammalian somatic cells has focused mainly on the combined role of protein kinase A (PKA) and mitogen-activated protein (MAP) kinases in regulation of progression through the G1 phase of the cell cycle. Here we show that cAMP signaling regulates histone H3 phosphorylation in a cell cycle-dependent fashion, increasing it in quiescent cells but dramatically reducing it in cycling cells. The latter is due to a rapid and dramatic loss of mitotic histone H3 phosphorylation caused by a disruption in G2 progression, as evidenced by the inhibition of mitotic entry and decreased activity of the CyclinB/Cdk1 kinase. The inhibition of G2 progression induced through cAMP signaling is dependent on expression of the catalytic subunit of PKA and is highly sensitive to intracellular cAMP concentration. The mechanism by which G2 progression is inhibited is independent of both DNA damage and MAP kinase signaling. Our results suggest that cAMP signaling activates a G2 checkpoint by a unique mechanism and provide new insight into normal cellular regulation of G2 progression.

In 2010, the Illinois Department of Transportation began implementing the flashing yellow arrow (FYA) at intersections operating with protected–permissive left-turn (PPLT) control. Research was conducted to evaluate the safety-effectiveness of FYAs at 86 intersections and 164 approaches in central Illinois. The effectiveness evaluation was performed with 3 years of before-and-after FYA installation crash data and the empirical Bayes method. In the before condition, the left-turn signals operated with a circular green display indicating the permissive interval of PPLT control using a five-section signal head. In the after condition, the FYA replaced the circular green display for the permissive interval of PPLT with a four-section signal head. Supplemental traffic signs were mounted on the mast arm adjacent to the left-turn signal at over half of the FYA installations. The results of the comprehensive safety evaluation of the FYA for PPLT control are presented. Analyses were also performed to assess the effects of the FYA supplemental signs and the effects of the FYA overall on two subsets of at-fault drivers: older drivers (age 65+) and younger drivers (age 16 to 21). The resulting mean crash modification factors for the targeted crash types ranged from 0.589 to 0.714. The findings of this research support the continued use of FYAs for PPLT control to improve safety at signalized intersections in central Illinois.

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Amyloidosis is a disease of abnormal extracellular deposition of proteins within tissues, commonly affecting solid organs such as the heart, liver, and kidneys. Less commonly, amyloidosis may affect the proximal tracheobronchial tree. Clinical symptoms are vague and may include shortness of breath, stridor, hoarseness. Pulmonary function testing at the time of diagnosis usually reveals an obstructive pattern. Diagnosis is difficult, and patients with tracheobronchial amyloidosis are frequently misdiagnosed with asthma or chronic obstructive pulmonary disease. Early changes in pulmonary function testing in patients with tracheobronchial amyloidosis have not been described. We present a case of a firefighter who with obstructive symptomatology who was subsequently diagnosed with proximal tracheobronchial amyloidosis. As a component of his occupational health surveillance, yearly examinations and pulmonary function testing had been performed. Serial pulmonary function testing dating back fourteen years prior to diagnosis reveal an early decrease in peak expiratory flow. Over time and in retrospect, progressive blunting of the expiratory limb of his flow-volume loops is identified beginning ten years prior to presentation. These changes significantly predated his clinical symptomatology and may be useful for early identification of patients with tracheobronchial amyloidosis. The relationship between chronic smoke inhalation and the development of tracheobronchial amyloidosis is unclear.