Radon (Rn) is a radioactive gas that decays into radiation-emitting progenies capable of inducing cellular damage once inhaled. Residential exposure to Rn is common; however, current health concerns and regulations are based only on its effects as a lung carcinogen. It is not known whether exposure to Rn decay products results in other, non-cancer, adverse health effects, as we propose in chronic obstructive pulmonary disease (COPD) patients. In this exploratory and developmental application, we will assess whether exposure to Rn decay products, as assessed using lead-210 (210Pb), the progeny with the longest half-life, enhances the toxicity (and health effects) of air pollution particles. In 170 Eastern Massachusetts COPD patients, we have previously assessed indoor-home exposures to PM2.5 and black carbon by collecting up to four 7-day samples seasonally over the period of one year. Since 210Pb is in equilibrium with alpha (?)-emitting progeny on archived PM2.5 filter samples, the measurement of total ?- radiation emitted from them will permit back-calculation of residential 210Pb levels (as a surrogate measure of Rn progeny) present at the time of sampling. Therefore, we will investigate whether exposure to Rn progeny (as210Pb) modifies (increases) the effect of PM2.5 and black carbon on: 1) plasma biomarkers of systemic inflammation (C-reactive protein and interleukin-6); 2) urinary biomarkers of oxidative damage to lipids (malondialdehyde) and DNA (8-hydroxy-2'-deoxyguanosine); and 3) pulmonary function (FEV1, FVC, and FEV1/FVC). This research design encompasses a strong and novel exposure component linked to clinically relevant and mechanistic outcomes. These are relevant to the health of COPD patients, which is a common disease affecting approximately 11% of the US population older than age 55 years.
Exposure to radon (Rn) gas is common and is associated with an increased risk of lung cancer; however, it is not known whether Rn exposure is also associated with non-cancer health effects. Our hypothesis is that Rn (through its progeny that emit radiation) increases the toxicity of inhaled indoor particles in COPD patients. We will measure Rn decay products in archived air pollution samples and assess whether they interact with particulate matter to reduce pulmonary function and cause systemic effects by increasing levels of various blood and urine markers.
