Search

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]

It is not known whether environmental gamma radiation measured in US cities has detectable adverse health effects. We assessed whether short-term exposure to gamma radiation emitted from ambient air particles [gamma particle activity (PRγ)] is associated with reduced pulmonary function in chronic obstructive pulmonary disease (COPD) patients. We hypothesize that the inhalation of gamma radiation emitted from ambient air particles may be associated with reduced pulmonary function in individuals with COPD. In 125 patients with COPD from Eastern Massachusetts who had up to 4 seasonal one-week assessments of particulate matter ≤2.5 μm (PM 2.5), black carbon (BC), and sulfur followed by spirometry. The US EPA continuously monitors ambient gamma (γ) radiation including γ released from radionuclides attached to particulate matter that is recorded as 9 γ-energy spectra classes (i = 3–9) in counts per minute (CPMγ) in the Boston area (USA). We analyzed the associations between ambient and indoor PRγ i (up to one week) and pre and post-bronchodilator (BD) forced expiratory volume in 1 s (FEV 1) and with forced vital capacity (FVC) using mixed-effects regression models. We estimated indoor PRγ i using the ratio of the indoor-to-outdoor sulfur in PM 2.5 as a proxy for infiltration of ambient radionuclide-associated particles. Overall, exposures to ambient and indoor PRγ i were associated with a similar decrease in pre- and post-BD FEV 1 and FVC. For example, ambient PRγ 3 exposure averaged from the day of pulmonary function testing through the previous 3 days [IQR of 55.1 counts per minute (CPMγ)] was associated with a decrease in pre-BD FEV 1 of 21.0 ml (95%CI: −38.5 to −3.0 ml; p < 0.01) and pre-BD FVC of 27.5 ml [95% confidence interval (CI): −50.7 to −5.0 ml; p < 0.01] with similar effects adjusting for indoor and outdoor BC and PM 2.5. Our results show that short-term ambient and indoor exposures to environmental gamma radiation associated with particulate matter are associated with reduced pre- and post-BD pulmonary function in patients with COPD. • The effects of ambient particle gamma activity (gamma radiation released from particulate matter) on pulmonary function has not been previously described in the literature. • Short-term exposures to environmental gamma radiation from ambient and indoor particles is associated with reduced pre- and post-bronchodilator pulmonary function in patients with COPD. • Low-level of environmental ionizing radiation released from particulates potentially affect the health of these chronically ill individuals. [ABSTRACT FROM AUTHOR]

Little is known about personal characteristics and systemic responses to particulate pollution in patients with COPD. Assess whether diabetes, obesity, statins and non-steroidal anti-inflammatory medications (NSAIDs) modify associations between indoor black carbon (BC) and fine particulate matter ≤2.5 μm in diameter (PM 2.5) on systemic inflammation and endothelial activation. 144 individuals with COPD without current smoking and without major in-home combustion sources were recruited at Veterans Affairs Boston Healthcare System. PM 2.5 and BC were measured in each participant's home seasonally for a week (up to 4 times; 482 observations) and plasma biomarkers of systemic inflammation [C-reactive protein (CRP); interleukin-6 (IL-6)] and endothelial activation [soluble vascular adhesion molecule-1 (sVCAM-1)] measured. Linear mixed effects regression with a random intercept was used, and effect modification assessed with multiplicative interaction terms and stratum specific estimates. Median (25%ile, 75%ile) indoor BC and PM 2.5 were 0.6 (0.5,0.7) μg/m3 and 6.8 (4.8,10.4) μg/m3, respectively. Although p-values for effect modification were not statistically significant, there were positive associations (%-increase/interquartile range; 95% CI) between CRP and BC greater among non-statin (18.8%; 3.6–36.3) than statin users (11.1%; 2.1–20.9). There were also positive associations greater among non-statin users between PM 2.5 and CRP. For IL-6, associations with BC and PM 2.5 were also greater among non-statin users. Associations between CRP and BC were greater (20.3%; 4.5–38.5) in persons with diabetes than without diabetes (10.3%; 0.92–20.6) with similar effects of PM 2.5. There were no consistent associations that differed based on obesity. Effect modification was not observed for NSAID use, or with any factor considered with sVCAM-1. Associations between indoor BC and PM 2.5 and CRP were greater in patients with diabetes and those not taking statins, and with IL-6 if not taking statins. These results suggest that these characteristics may modify the systemic response to indoor BC and PM 2.5 in persons with COPD. • Greater associations between in-home BC and PM2.5 with CRP in non-statin users. •Greater associations between in-home BC and PM2.5 with CRP and IL-6 in diabetics. •NSAID use and BMI ≥ 30 did not modify BC and PM2.5 and biomarker associations. •COPD patients not using statins or with diabetes may be more susceptible to BC/PM. [ABSTRACT FROM AUTHOR]