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Aims: Cardiac arrhythmias have been associated with intense solar and geomagnetic activity (SGA) and exposures to air pollution.Methods and Results: We examined whether oscillations of SGA can modify the effect of hourly exposures to air pollutants on atrial fibrillation ≥30 s (AF) risk in patients with dual-chamber implantable cardioverter-defibrillators. The effects of SGA on ambient particulate matter <2.5 µm (PM2.5), black carbon (BC), ultrafine particles (PN), and associations with AF were assessed. Measures of SGA included solar wind proton density (SW), total interplanetary magnetic field strength (IMF), and Kp index, a measure of global geomagnetic activity. Overall time lags between 0 and 24 h, periods of increased SGA (>50th percentile in IMF, SW, and Kp index) enhanced the effects of all three air pollutants on AF, while during periods of reduced SGA the associations were considerably weaker or absent. During periods of intense SW 6 h prior to an AF event, the odds ratio (OR) for PM2.5 exposure per interquartile range (IQR) of 5.6 µg/m3 was 1.7 [95% confident interval (CI) 1.3-2.3, P = 0.0001]. For periods of reduced SW, the OR for PM2.5 exposure per IQR was 1.2 (95% CI 0.9-1.5; P = 0.27). There were similar effects for PN and BC exposures. In patients with multiple AF events per hour, the associations with air pollutants during intense SGA were even greater.Conclusion: The effects of air pollutants up to 24 h before AF events were enhanced during periods of increased SGA. Our results suggest that these effects may account for variation in AF risk. [ABSTRACT FROM AUTHOR]

BACKGROUND: Diesel engine exhaust (DEE) has recently been classified as a known human carcinogen. OBJECTIVE: We derived a meta-exposure--response curve (ERC) for DEE and lung cancer mortality and estimated lifetime excess risks (ELRs) of lung cancer mortality based on assumed occupational and environmental exposure scenarios. METHODS: We conducted a meta-regression of lung cancer mortality and cumulative exposure to elemental carbon (EC), a proxy measure of DEE, based on relative risk (RR) estimates reported by three large occupational cohort studies (including two studies of workers in the trucking industry and one study of miners). Based on the derived risk function, we calculated ELRs for several lifetime occupational and environmental exposure scenarios and also calculated the fractions of annual lung cancer deaths attributable to DEE. RESULTS: We estimated a lnRR of 0.00098 (95% CI: 0.00055, 0.0014) for lung cancer mortality with each 1-µg/[m.sup.3]-year increase in cumulative EC based on a linear meta-regression model. Corresponding lnRRs for the individual studies ranged from 0.00061 to 0.0012. Estimated numbers of excess lung cancer deaths through 80 years of age for lifetime occupational exposures of 1, 10, and 25 µg/[m.sup.3] EC were 17, 200, and 689 per 10,000, respectively. For lifetime environmental exposure to 0.8 µg/[m.sup.3] EC, we estimated 21 excess lung cancer deaths per 10,000. Based on broad assumptions regarding past occupational and environmental exposures, we estimated that approximately 6% of annual lung cancer deaths may be due to DEE exposure. CONCLUSIONS: Combined data from three U.S. occupational cohort studies suggest that DEE at levels common in the workplace and in outdoor air appear to pose substantial excess lifetime risks of lung cancer, above the usually acceptable limits in the United States and Europe, which are generally set at 1/1,000 and 1/100,000 based on lifetime exposure for the occupational and general population, respectively., Introduction Recently, a working group of the International Agency for Research on Cancer (IARC) Monograph Series reviewed the scientific evidence regarding the carcinogenicity of diesel engine exhaust (DEE). The Working [...]

Background: The mechanism for spread of SARS-CoV-2 has been attributed to large particles produced by coughing and sneezing. There is controversy whether smaller airborne particles may transport SARS-CoV-2. Smaller particles, particularly fine particulate matter (≤ 2.5 µm in diameter), can remain airborne for longer periods than larger particles and after inhalation will penetrate deeply into the lungs. Little is known about the size distribution and location of airborne SARS-CoV-2 RNA.Methods: As a measure of hospital-related exposure, air samples of three particle sizes (> 10.0 µm, 10.0-2.5 µm, and ≤ 2.5 µm) were collected in a Boston, Massachusetts (USA) hospital from April to May 2020 (N = 90 size-fractionated samples). Locations included outside negative-pressure COVID-19 wards, a hospital ward not directly involved in COVID-19 patient care, and the emergency department.Results: SARS-CoV-2 RNA was present in 9% of samples and in all size fractions at concentrations of 5 to 51 copies m-3. Locations outside COVID-19 wards had the fewest positive samples. A non-COVID-19 ward had the highest number of positive samples, likely reflecting staff congregation. The probability of a positive sample was positively associated (r = 0.95, p < 0.01) with the number of COVID-19 patients in the hospital. The number of COVID-19 patients in the hospital was positively associated (r = 0.99, p < 0.01) with the number of new daily cases in Massachusetts.Conclusions: More frequent detection of positive samples in non-COVID-19 than COVID-19 hospital areas indicates effectiveness of COVID-ward hospital controls in controlling air concentrations and suggests the potential for disease spread in areas without the strictest precautions. The positive associations regarding the probability of a positive sample, COVID-19 cases in the hospital, and cases in Massachusetts suggests that hospital air sample positivity was related to community burden. SARS-CoV-2 RNA with fine particulate matter supports the possibility of airborne transmission over distances greater than six feet. The findings support guidelines that limit exposure to airborne particles including fine particles capable of longer distance transport and greater lung penetration. [ABSTRACT FROM AUTHOR]

Background: Particulate matter (PM) air pollution has been associated with decreased pulmonary function, but the exposure-response relationship in chronic obstructive pulmonary disease (COPD) patients is uncertain, and most studies have only focused on exposures to ambient pollution. Objectives: We aimed to assess associations between pulmonary function and indoor and ambient PM [less than or equal to] 2.5 [micro]m ([PM.sub.2.5]) and black carbon (BC). Methods: Between November 2012 and December 2014, 125 patients with COPD (mean age, 73.4 y) who were not currently smoking and without known indoor BC sources were recruited. Indoor BC and [PM.sub.2.5] were measured in each home for a week in each season, up to four times a year, followed by in-person spirometry pre- and post-bronchodilator. Ambient exposures were available from a central site monitor. Multivariable adjusted mixed effects regression models were used to assess associations scaled per interquartile range (IQR) of exposure. Results: There were 367 study visits; the median (IQR) indoor BC and [PM.sub.2.5] were 0.19 (0.22) [micro]g/[m.sup.3] and 6.67 (5.80) [micro]g/[m.sup.3], respectively. Increasing indoor exposures to BC were associated with decreases in pre-bronchodilator forced expiratory volume in 1 s ([FEV.sub.1]) and forced vital capacity (FVC), and [FEV.sub.1] /FVC. For example, in multivariable adjusted models, each IQR increase in indoor BC from the weekly integrated filter was associated with a 17.87 mL [95% confidence interval (CI): -33.76, -1.98] decrease in pre-bronchodilator [FEV.sub.1]. Increases in indoor [PM.sub.2.5] were associated with decreases in [FEV.sub.1] and FVC of smaller magnitude than those for indoor BC; however, the results were less precise. Ambient BC was not associated with pre-bronchodilator pulmonary function, ambient [PM.sub.2.5] was only associated with decreases in FVC and increases in [FEV.sub.1]/FVC, and neither indoor nor ambient BC or [PM.sub.2.5] were associated with post-bronchodilator pulmonary function. Conclusions: Low-level exposures to indoor BC and [PM.sub.2.5], but not ambient exposures, were consistently associated with decreases in prebronchodilator pulmonary function. There was no association between exposures and post-bronchodilator pulmonary function. https://doi.org/10.1289/EHP3668, Introduction Chronic obstructive pulmonary disease (COPD) is a common disease that results in considerable morbidity and mortality. According to the most recent Global Burden of Disease estimates, 174.5 million individuals [...]