Radon decay product particle radioactivity and oxidative stress biomarkers in patients with COPD.

Radon decay products include α-radiation emitting radionuclides that attach to airborne particles that have potential to promote oxidative tissue damage after inhalation. To assess associations between α-particle radioactivity (α-PR) with urinary biomarkers of oxidative tissue damage, 140 patients with chronic obstructive pulmonary disease (COPD) had up to four 1-week seasonal assessments (N = 413) of indoor (home) and ambient (central site) PM2.5 and black carbon (BC). Following environmental sampling, urine samples were analyzed for total and free malondialdehyde (MDA), biomarkers of lipid oxidation, and 8-hydroxyl-2'-deoxyguanosine (8-OHdG), a biomarker of DNA oxidative damage. Particle radioactivity was measured as α-activity on PM2.5 filter samples. Linear mixed-effects regression models adjusted for urinary creatinine and other personal characteristics were used to assess associations. Indoor α-PR was associated with an increase in 8-OhdG (8.53%; 95% CI: 3.12, 14.23); total MDA (5.59%; 95% CI: 0.20, 11.71); and free MDA (2.17%; 95% CI: 2.75, 7.35) per interquartile range (IQR) of α-PR [median 1.25 mBq/m3; IQR 0.64], similar adjusting for PM2.5 or BC. The ratio of indoor/ambient α-PR was positively associated with each biomarker and associations with ambient α-PR were positive but weaker than with indoor concentrations. These findings are consistent with a contribution of radon decay products as measured by α-PR to oxidative stress in patients with COPD, with a greater contribution of indoor radon decay products.

Particle radioactivity from radon decay products and reduced pulmonary function among chronic obstructive pulmonary disease patients.

BACKGROUND: Radon (222Rn) decay products can attach to particles in the air, be inhaled, and potentially cause airway damage. RESEARCH QUESTION: Is short-term exposure to particle radioactivity (PR) attributable to radon decay products emitted from particulate matter ≤2.5 µm in diameter (PM2.5) associated with pulmonary function in chronic obstructive pulmonary disease (COPD) patients? STUDY DESIGN AND METHODS: In this cohort study, 142 elderly, predominantly male patients with COPD from Eastern Massachusetts each had up to 4 one-week long seasonal assessments of indoor (home) and ambient (central site) PR and PM2.5 over the course of a year (467 assessments). Ambient and indoor PR were measured as α-activity on archived PM2.5 filter samples. Ratios of indoor/ambient PR were calculated, with higher ratios representing PR from an indoor source of radon decay. We also considered a measure of outside air infiltration that could dilute the concentrations of indoor radon decay products, the indoor/ambient ratio of sulfur concentrations in PM2.5 filter samples. Spirometry pre- and post-bronchodilator (BD) forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC) were conducted following sampling. Generalized additive mixed models were adjusted for meteorologic variables, seasonality, and individual-level determinants of pulmonary function. We additionally adjusted for indoor PM2.5 and black carbon (BC). RESULTS: PR exposure metrics indicating radon decay product exposure from an indoor source were associated with a reduction in FEV1 and FVC. Patients in homes with high indoor PR (≥median) and low air infiltration (

Development of rapid methods for assessing doses from internally deposited radionuclides.

During the initial phases of the National Institute for Occupational Safety and Health Radiation Dose Reconstruction Program, all calculations of organ doses due to internally deposited radionuclides were performed using the Integrated Modules for Bioassay Analysis program. However, limitations associated with this program, including the need to calculate separate internal dose assessments for each radionuclide, created inefficiencies in the processing of claims. As a result, the National Institute for Occupational Safety and Health developed and introduced a suite of tools to expedite the process. The first of these was the Chronic Annual Dose Workbook program. This innovative tool permits a dose reconstructor to calculate, in a single step, an organ dose that involves up to 255 separate intakes in any combination of radionuclides, intake modes, and absorption types. In addition, the program enables dose reconstructors to determine the specific radionuclide characteristics that will deliver the highest organ dose for a specific intake. Furthermore, the results are displayed in a format that is compatible with the Interactive RadioEpidemiological Program, which is used by the U.S. Department of Labor in establishing the probability of causation. The value of the probability of causation, in combination with other information, subsequently enables the U.S. Department of Labor to render a decision on compensability. These developments have played a major role in enabling the dose reconstruction teams to meet the claim processing goals with increased efficiency and accuracy.