CuI-amidobis(phosphine) catalyzed C(sp3)-C(sp3) direct homo- and hetero-coupling of unactivated alkanes via C(sp3)-H activation.

Herein, we present a CuI-dimer, [CuI{Ph2PC6H4C(O)NC6H4PPh2-o}]2, which catalyzed direct C(sp3)-H homocoupling of benzyl and cycloalkane derivatives with excellent yields and regio-selectivity. The method is very simple and tolerates various functionalities. Synergistic metal-ligand cooperativity was observed in Cu-N bond cleavage and protonation of nitrogen, and facilitates a bifunctional pathway, minimising the free energy corrugation for catalytic intermediates.

Copper(I) Complexes of Amide Functionalized Bisphosphine: Proximity Enhanced Metal-Ligand Cooperativity and Its Catalytic Advantage in C(sp3)-H Bond Activation of Unactivated Cycloalkanes in Dehydrogenative Carboxylation Reactions.

The reactions of amide functionalized bisphosphine, o-Ph2PC6H4C-(O)N(H)C6H4PPh2-o (1) (BalaHariPhos), with copper salts is described. Treatment of 1 with CuX in a 1:1 molar ratio yielded chelate complexes of the type [CuX{(o-Ph2PC6H4C(O)N(H)C6H4PPh2-o)}-κ2-P,P] (X = Cl, 2; Br, 3; and I, 4), which on subsequent treatment with KOtBu resulted in a dimeric complex [Cu(o-Ph2PC6H4C(O)(N)C6H4PPh2-o)]2 (5). Interestingly, complexes 2-4 showed weak N-H···Cu interactions. These weak H-bonding interactions are studied in detail both experimentally and computationally. Also, CuI complexes 2-5 were employed in the oxidative dehydrogenative carboxylation (ODC) of unactivated cycloalkanes in the presence of carboxylic acids to form the corresponding allylic esters. Among complexes 2-5, halide-free dimeric CuI complex 5 showed excellent metal-ligand cooperativity in the oxidative dehydrogenative carboxylation (ODC) in the presence of carboxylic acids to form the corresponding allylic esters through C(sp3)-H bond activation of unactivated cycloalkanes. Mechanistic details of the catalytic process were established by isolating the precatalyst [Cu{(o-Ph2PC6H4C(O)(NH)C6H4PPh2-o)-κ2-P,P}(OOCPh)] (6) and fully characterized by mass spectrometry, NMR data, and single-crystal X-ray analysis. Density functional theory-based calculations further provided a quantitative understanding of the energetics of a series of H atom transfer steps occurring in the catalytic cycle.

RuII complexes of 1,2,3-triazole appended tertiary phosphines, [P(Ph){(o-C6H4)(1,2,3-N3C(Ph)CH}2] and [P(Ph){o-C6H4(CCH)-(1,2,3-N3-Ph)}2]: highly active catalysts for transfer hydrogenation of carbonyl/nitro compounds and for α-alkylation of ketones.

The synthesis of two new 1,2,3-triazole appended monophosphines [P(Ph){(o-C6H4)(1,2,3-N3C(Ph)CH}2] (1) and [P(Ph){o-C6H4(CCH)(1,2,3-N3-Ph)}2] (2) and their RuII complexes is described. The reactions of 1 and 2 with [Ru(PPh3)3Cl2] in a 1 : 1 molar ratio produced cationic complexes 3 and 4, respectively. Both the complexes showed very high catalytic activity towards transfer hydrogenation, nitro reduction, and α-alkylation reactions and afforded the corresponding products in good to excellent yields. The free energy of ß-hydride elimination from the respective Ru-alkoxide intermediates, a key mechanistic step common to all the three catalytic pathways, was calculated to be close to ergoneutral by density functional theory-based calculations, which is posited to rationalize the catalytic activity of 3. The reduction of aromatic nitro compounds was found to be highly chemoselective and produced the corresponding amines as major products even in the presence of a carbonyl group. The triazolyl-N2 coordinated RuII-NPN complex 3 showed better catalytic activity compared to the triazolyl-N3 coordinated complex 4.

Cause and Age-specific premature mortality attributable to PM2.5 Exposure: An analysis for Million-Plus Indian cities.

In India, a majority population is exposed to high levels of ambient PM2.5 resulting in adverse health outcomes. Epidemiological studies have associated diseases such as Ischemic Heart Disease (IHD), Cerebrovascular Disease (Stroke), Chronic Obstructive Pulmonary Disease (COPD), Lower Respiratory Infection (LRI), and Lung Cancer (LNC) to long-term PM2.5 exposure resulting in premature mortality. In the present work, the Integrated Exposure Response (IER) model is used to estimate such premature deaths for the year 2016 in 29 million-plus Indian cities. The city-specific registered deaths data along with information of percent share of cause-specific deaths in the total deaths and measured ambient PM2.5 concentrations are used to estimate cause-specific baseline mortality in a city. The premature mortality attributable to PM2.5 exposure is estimated from this baseline mortality. The premature mortality burden attributable to PM2.5 exposure in these cities is 114,700 (104,100-125,500) deaths from the five causes (IHD, Stroke, COPD, LRI, and LNC). IHD is the leading cause of death accounting for 58% of PM2.5 related premature deaths, followed by Stroke (22%), COPD (14%), LRI (4%), and LNC (2%) in these 29 cities. The estimated number of PM2.5 related deaths in productive age group (25 - 50 years) is quite low compared to older people, but the percentage share of these deaths in the cumulative cause-specific baseline deaths is higher for productive age group. Thus, the productive population is considerably at a higher risk of mortality due to PM2.5 exposure. There is approximately 18% and 70% reduction in premature mortality if these cities can attain National Ambient Air Quality Standards (NAAQS) (40 µg/m3) and the World Health Organization (WHO) guidelines (10 µg/m3) of annual PM2.5, respectively. The estimates of air pollution related mortality at the city level could assist in city-specific policy formulation for better air pollution control.