5) on atrial fibrillation/flutter (AF) predictors, including P-wa

5) on atrial fibrillation/flutter (AF) predictors, including P-wave duration, PR interval duration, and P-wave complexity, were investigated in a community-dwelling sample of 106 nonsmokers. Individual-level 24-h beat-to-beat electrocardiogram (ECG) data were visually examined. After identifying and removing artifacts and arrhythmic beats, the 30-min averages of the AF predictors were calculated. A personal PM2.5 monitor was used to measure individual-level, real-time PM2.5 exposures

during the same 24-h Selleckchem CUDC-907 period, and corresponding 30-min average PM2.5 concentration were calculated. Under a linear mixed-effects modeling framework, distributed lag models were used to estimate regression coefficients (s) associating PM2.5 with AF predictors. Most of the adverse effects on AF predictors occurred within 1.5-2 h after PM2.5 exposure. The multivariable adjusted s per 10-g/m3 rise in PM 2.5 at lag 1 and lag 2 were significantly associated with P-wave complexity. PM2.5 exposure was also significantly associated with prolonged PR duration at lag 3 and lag 4. Higher PM2.5 was found to be associated with increases in P-wave Topoisomerase inhibitor complexity and PR duration. Maximal effects were observed within 2 h. These findings suggest that PM2.5 adversely affects AF predictors; thus, PM2.5 may be indicative of greater susceptibility to AF.”
“Inhalation

exposure to particulates such as cigarette smoke and coal dust is known to contribute to the development of chronic lung disease. The purpose of this study was to estimate the amount of elemental carbon (EC) deposits from autopsied lung samples from cigarette smokers, miners, and control subjects and explore the relationship between EC level, exposure history, and the extent of

chronic lung disease. The samples comprised three subgroups representing never smokers (8), chronic cigarette smokers (26), and coal miners (6). Following the dissolution of lung tissue, the extracted EC residue was quantified using a thermal-optical transmission (TOT) carbon analyzer. Mean EC levels in the lungs of the control group were 56.68 +/- 24.86 (SD) g/g dry lung weight. Respective mean EC values in lung samples from the smokers and coal miners were 449.56 +/- 320.3 AICAR order g/g and 6678.2 +/- 6162 g/g. These values were significantly higher than those obtained from the never-smoker group. EC levels in the lung and pack-years of cigarette smoking correlated significantly, as did EC levels and the severity of small airway disease. This study provides one of the first quantitative assessments of EC in human lungs from populations at high relative risk for the development of chronic lung disease.”
“Arsenic (As) is a known carcinogen commonly found in drinking water. An emerging body of evidence suggests that exposure to inorganic As may be associated with nonmalignant respiratory disease.

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