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Short-term effects of particle gamma radiation activities on pulmonary function in COPD patients.

ABSTRACT: BACKGROUND: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 (PR?)] is associated with reduced pulmonary function in chronic obstructive pulmonary disease (COPD) patients. OBJECTIVE:We hypothesize that the inhalation of gamma radiation emitted from ambient air particles may be associated with reduced pulmonary function in individuals with COPD. METHODS:In 125 patients with COPD from Eastern Massachusetts who had up to 4 seasonal one-week assessments of particulate matter ?2.5??m (PM2.5), black carbon (BC), and sulfur followed by spirometry. The US EPA continuously monitors ambient gamma (?) radiation including ? released from radionuclides attached to particulate matter that is recorded as 9 ?-energy spectra classes (i?=?3-9) in counts per minute (CPM?) in the Boston area (USA). We analyzed the associations between ambient and indoor PR?i (up to one week) and pre and post-bronchodilator (BD) forced expiratory volume in 1?s (FEV1) and with forced vital capacity (FVC) using mixed-effects regression models. We estimated indoor PR?i using the ratio of the indoor-to-outdoor sulfur in PM2.5 as a proxy for infiltration of ambient radionuclide-associated particles. RESULTS:Overall, exposures to ambient and indoor PR?i were associated with a similar decrease in pre- and post-BD FEV1 and FVC. For example, ambient PR?3 exposure averaged from the day of pulmonary function testing through the previous 3 days [IQR of 55.1?counts per minute (CPM?)] was associated with a decrease in pre-BD FEV1 of 21.0?ml (95%CI: -38.5 to -3.0?ml; p?

SUBMITTER: Vieira CLZ

PROVIDER: S-EPMC6609300 | biostudies-literature | 2019 Aug

REPOSITORIES: biostudies-literature

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Project description:BackgroundWe hypothesized that particulate matter (PM) gamma activity (gamma radiation associated with PM) is associated with systemic effects.ObjectiveExamine short-term relationships between ambient and indoor exposures to PM gamma activities with systemic inflammation and endothelial activation in chronic obstructive pulmonary disease (COPD) patients.MethodsIn 85 COPD patients from Eastern Massachusetts, USA from 2012 to 2014, plasma C-reactive protein (CRP), interleukin-6 (IL-6), and soluble vascular cell adhesion molecule-1 (sVCAM-1) were measured seasonally up to four times. We used US EPA RadNet data measuring ambient gamma radiation attached to PM adjusted for background radiation, and estimated in-home gamma radiation exposures using the ratio of in-home-to-ambient sulfur in PM2.5. Linear mixed-effects regression models were used to determine associations between moving averages of PM gamma activities through the week before phlebotomy with these biomarkers. We explored ambient and indoor PM2.5, black carbon (BC), and NO2 as confounders.ResultsAmbient and indoor PM gamma activities measured as energy spectra classes 3 through 9 were positively associated with CRP and IL-6. For example, averaged from phlebotomy day through previous 6 days, each IQR increase in indoor PM gamma activity for each spectra class, was associated with an CRP increase ranging from 7.45% (95%CI: 2.77, 12.4) to 13.4% (95%CI: 5.82, 21.4) and for ambient exposures were associated with an increase of 8.75% (95%CI: -0.57, 18.95) to 14.8% (95%CI: 4.5, 26.0). Indoor exposures were associated with IL-6 increase of 3.56% (95%CI: 0.31, 6.91) to 6.46% (95%CI:1.33, 11.85) and ambient exposures were associated with an increase of 0.03% (95%CI: -6.37, 6.87) to 3.50% (95%CI: -3.15, 10.61). There were no positive associations with sVCAM-1. Sensitivity analyses using two-pollutant models showed similar effects.ConclusionsOur results demonstrate that short-term exposures to environmental PM gamma radiation activities were associated with systemic inflammation in COPD patients.

Project description:BACKGROUND:Exposure to ultrafine particles (UFP, particles with aerodynamic diameter?<?100?nm) is associated with reduced lung function and airway inflammation in individuals with asthma. Recently, elevated UFP number concentrations (PN) from aircraft landing and takeoff activity were identified downwind of the Los Angeles International Airport (LAX) but little is known about the health impacts of airport-related UFP exposure. METHODS:We conducted a randomized crossover study of 22 non-smoking adults with mild to moderate asthma in Nov-Dec 2014 and May-Jul 2015 to investigate short-term effects of exposure to LAX airport-related UFPs. Participants conducted scripted, mild walking activity on two occasions in public parks inside (exposure) and outside (control) of the high UFP zone. Spirometry, multiple flow exhaled nitric oxide, and circulating inflammatory cytokines were measured before and after exposure. Personal UFP PN and lung deposited surface area (LDSA) and stationary UFP PN, black carbon (BC), particle-bound PAHs (PB-PAH), ozone (O3), carbon dioxide (CO2) and particulate matter (PM2.5) mass were measured. Source apportionment analysis was conducted to distinguish aircraft from roadway traffic related UFP sources. Health models investigated within-subject changes in outcomes as a function of pollutants and source factors. RESULTS:A high two-hour walking period average contrast of ~34,000?particles·cm-3 was achieved with mean (std) PN concentrations of 53,342 (25,529) and 19,557 (11,131)?particles·cm-3 and mean (std) particle size of 28.7 (9.5) and 33.2 (11.5) at the exposure and control site, respectively. Principal components analysis differentiated airport UFPs (PN), roadway traffic (BC, PB-PAH), PM mass (PM2.5, PM10), and secondary photochemistry (O3) sources. A standard deviation increase in the 'Airport UFPs' factor was significantly associated with IL-6, a circulating marker of inflammation (single-pollutant model: 0.21, 95% CI?=?0.08-0.34; multi-pollutant model: 0.18, 0.04-0.32). The 'Traffic' factor was significantly associated with lower Forced Expiratory Volume in 1?s (FEV1) (single-pollutant model: -1.52, -2.28 to -0.77) and elevated sTNFrII (single-pollutant model: 36.47; 6.03-66.91; multi-pollutant model: 64.38; 6.30-122.46). No consistent associations were observed with exhaled nitric oxide. CONCLUSIONS:To our knowledge, our study is the first to demonstrate increased acute systemic inflammation following exposure to airport-related UFPs. Health effects associated with roadway traffic exposure were distinct. This study emphasizes the importance of multi-pollutant measurements and modeling techniques to disentangle sources of UFPs contributing to the complex urban air pollution mixture and to evaluate population health risks.

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Short-term effects of particle gamma radiation activities on pulmonary function in COPD patients.

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