Window-Related Energy Consumption in the US Residential and Commercial Building Stock

We present a simple spreadsheet-based tool for estimating window-related energy consumption in the United States. Using available data on the properties of the installed US window stock, we estimate that windows are responsible for 2.15 quadrillion Btu (Quads) of heating energy consumption and 1.48 Quads of cooling energy consumption annually. We develop estimates of average U-factor and SHGC for current window sales. We estimate that a complete replacement of the installed window stock with these products would result in energy savings of approximately 1.2 quads. We demonstrate that future window technologies offer energy savings potentials of up to 3.9 Quads

Spatiotemporal profiles of ultrafine particles differ from other traffic-related air pollutants : lessons from long-term measurements at fixed sites and mobile monitoring

Peer reviewe

Persistence of Primary and Secondary Pollutants in Delhi : Concentrations and Composition from 2017 through the COVID Pandemic

We assess impacts of the 2020 COVID-19 lockdown on ambient air quality in Delhi, building on over three years of real-time measurements of black carbon (BC) and nonrefractory submicrometer aerosol (NR-PM1) composition from the Delhi Aerosol Supersite and public data from the regulatory monitoring network. We performed source apportionment of organic aerosol (OA) and robust statistical analyses to differentiate lockdown-related impacts from baseline seasonal and interannual variability. The primary pollutants NOx, CO, and BC were most reduced, primarily due to lower transportation emissions. Local and regional emissions such as agricultural burning decreased during the lockdown. PM2.5 declined but remained well above WHO guidelines. Despite the lockdown, NR-PM1 changed only moderately compared to prior years. Differences in the trends of hydrocarbon-like OA and BC suggest that some sources of primary aerosol may have increased. Despite notable reductions in some primary pollutants, the lockdown restrictions led to rather small perturbations in the primary fraction of NR-PM1, with secondary aerosol continuing to dominate. Overall, our results demonstrate the impact of secondary and primary pollution on Delhi's air quality and show that large changes in emissions within Delhi alone are insufficient to bring about needed improvements in air quality.Peer reviewe

Persistence of Primary and Secondary Pollutants in Delhi : Concentrations and Composition from 2017 through the COVID Pandemic

We assess impacts of the 2020 COVID-19 lockdown on ambient air quality in Delhi, building on over three years of real-time measurements of black carbon (BC) and nonrefractory submicrometer aerosol (NR-PM1) composition from the Delhi Aerosol Supersite and public data from the regulatory monitoring network. We performed source apportionment of organic aerosol (OA) and robust statistical analyses to differentiate lockdown-related impacts from baseline seasonal and interannual variability. The primary pollutants NOx, CO, and BC were most reduced, primarily due to lower transportation emissions. Local and regional emissions such as agricultural burning decreased during the lockdown. PM2.5 declined but remained well above WHO guidelines. Despite the lockdown, NR-PM1 changed only moderately compared to prior years. Differences in the trends of hydrocarbon-like OA and BC suggest that some sources of primary aerosol may have increased. Despite notable reductions in some primary pollutants, the lockdown restrictions led to rather small perturbations in the primary fraction of NR-PM1, with secondary aerosol continuing to dominate. Overall, our results demonstrate the impact of secondary and primary pollution on Delhi's air quality and show that large changes in emissions within Delhi alone are insufficient to bring about needed improvements in air quality.Peer reviewe

Effects of Very Low Nicotine Content Cigarettes on Smoking Behavior and Biomarkers of Exposure in Menthol and Non-menthol Smokers.

IntroductionBecause 30% of cigarettes sold in the United States are characterized as menthol cigarettes, it is important to understand how menthol preference may affect the impact of a nicotine reduction policy.MethodsIn a recent trial, non-treatment-seeking smokers were randomly assigned to receive very low nicotine cigarettes (VLNC; 0.4 mg nicotine/g tobacco) or normal nicotine cigarettes (NNC; 15.5 mg/g) for 20 weeks. On the basis of preference, participants received menthol or non-menthol cigarettes. We conducted multivariable regression analyses to examine whether menthol preference moderated the effects of nicotine content on cigarettes per day (CPD), breath carbon monoxide (CO), urinary total nicotine equivalents (TNE), urinary 2-cyanoethylmercapturic acid (CEMA), and abstinence.ResultsAt baseline, menthol smokers (n = 346) reported smoking fewer CPD (14.9 vs. 19.2) and had lower TNE (52.8 vs. 71.6 nmol/mg) and CO (17.7 vs. 20.5 ppm) levels than non-menthol smokers (n = 406; ps < .05). At week 20, significant interactions indicated that menthol smokers had smaller treatment effects than non-menthol smokers for CPD (-6.4 vs. -9.3), TNE (ratio of geometric means, 0.22 vs. 0.10) and CEMA (ratio, 0.56 vs. 0.37; ps < .05), and trended toward a smaller treatment effect for CO (-4.5 vs. -7.3 ppm; p = .06). Odds ratios for abstinence at week 20 were 1.88 (95% confidence interval [CI] = 0.8 to 4.4) for menthol and 9.11 (95% CI = 3.3 to 25.2) for non-menthol VLNC smokers (p = .02) relative to the NNC condition.ConclusionsAlthough menthol smokers experienced reductions in smoking, toxicant exposure, and increases in quitting when using VLNC cigarettes, the magnitude of change was smaller than that observed for non-menthol smokers.ImplicationsResults of this analysis suggest that smokers of menthol cigarettes may respond to a nicotine reduction policy with smaller reductions in smoking rates and toxicant exposure than would smokers of non-menthol cigarettes

Expression of nampt in hippocampal and cortical excitatory neurons is critical for cognitive function

Nicotinamide adenine dinucleotide (NAD(+)) is an enzyme cofactor or cosubstrate in many essential biological pathways. To date, the primary source of neuronal NAD(+) has been unclear. NAD(+) can be synthesized from several different precursors, among which nicotinamide is the substrate predominantly used in mammals. The rate-limiting step in the NAD(+) biosynthetic pathway from nicotinamide is performed by nicotinamide phosphoribosyltransferase (Nampt). Here, we tested the hypothesis that neurons use intracellular Nampt-mediated NAD(+) biosynthesis by generating and evaluating mice lacking Nampt in forebrain excitatory neurons (CaMKIIαNampt(−/−) mice). CaMKIIαNampt(−/−) mice showed hippocampal and cortical atrophy, astrogliosis, microgliosis, and abnormal CA1 dendritic morphology by 2–3 months of age. Importantly, these histological changes occurred with altered intrahippocampal connectivity and abnormal behavior; including hyperactivity, some defects in motor skills, memory impairment, and reduced anxiety, but in the absence of impaired sensory processes or long-term potentiation of the Schaffer collateral pathway. These results clearly demonstrate that forebrain excitatory neurons mainly use intracellular Nampt-mediated NAD(+) biosynthesis to mediate their survival and function. Studying this particular NAD(+) biosynthetic pathway in these neurons provides critical insight into their vulnerability to pathophysiological stimuli and the development of therapeutic and preventive interventions for their preservation

Role of Bile Acids in Liver Injury and Regeneration following Acetaminophen Overdose

Bile acids play a critical role in liver injury and regeneration, but their role in acetaminophen (APAP)–induced liver injury is not known. We tested the effect of bile acid modulation on APAP hepatotoxicity using C57BL/6 mice, which were fed a normal diet, a 2% cholestyramine (CSA)–containing diet for bile acid depletion, or a 0.2% cholic acid (CA)–containing diet for 1 week before treatment with 400 mg/kg APAP. CSA-mediated bile acid depletion resulted in significantly higher liver injury and delayed regeneration after APAP treatment. In contrast, 0.2% CA supplementation in the diet resulted in a moderate delay in progression of liver injury and significantly higher liver regeneration after APAP treatment. Either CSA-mediated bile acid depletion or CA supplementation did not affect hepatic CYP2E1 levels or glutathione depletion after APAP treatment. CSA-fed mice exhibited significantly higher activation of c-Jun N-terminal protein kinases and a significant decrease in intestinal fibroblast growth factor 15 mRNA after APAP treatment. In contrast, mice fed a 0.2% CA diet had significantly lower c-Jun N-terminal protein kinase activation and 12-fold higher fibroblast growth factor 15 mRNA in the intestines. Liver regeneration after APAP treatment was significantly faster in CA diet–fed mice after APAP administration secondary to rapid cyclin D1 induction. Taken together, these data indicate that bile acids play a critical role in both initiation and recovery of APAP-induced liver injury