Indoor radon survey in Greenland and dose assessment.

Indoor radon and its decay products are the primary sources of the population's exposure to background ionizing radiation. Radon decay products are one of the leading causes of lung cancer, with a higher lung cancer risk for smokers due to the synergistic effects of radon decay products and cigarette smoking. A total of 459 year-long radon measurements in 257 detached and semi-detached residential homes in southwest and south Greenland were carried out, and a dose assessment for adults was performed. The annual arithmetic and geometric means of indoor radon concentrations was 10.5 ± 0.2 Bq m-3 and 8.0 ± 2.3 Bq m-3 in Nuuk, 139.0 ± 1.0 Bq m-3 and 97.3 ± 2.1 Bq m-3 in Narsaq, and 42.1 ± 0.7 Bq m-3 and 22.0 ± 3.1 Bq m-3 in Qaqortoq. Arithmetic and geometric mean radon concentration of 79.0 Bq m-3 and 50.3 Bq m-3 were estimated for adult, person-weighted living in south Greenland. The total number of detached and semi-detached residential homes where indoor radon is exceeding 100 Bq m-3, 200 Bq m-3, and 300 Bq m-3 is 37 homes (15.0%), 13 homes (5.2%), and 8 homes (3.2%), respectively. A positive correlation between indoor air radon concentrations and underlying geology was observed. The indoor radon contribution to the annual inhalation effective dose to an average adult was 0.5 mSv in Nuuk, 6.5 mSv in Narsaq, 2.0 mSv in Qaqortoq, and 4.0 mSv for south Greenland adult person weighted. The estimated annual average effective dose to adults in Narsaq is higher than the world's average annual effective dose of 1.3 mSv due to inhalation of indoor radon. Cost-efficient mitigation methods exist to reduce radon in existing buildings, and to prevent radon entry into new buildings.

Modeling the absorbed dose to the common carotid arteries following radioiodine treatment of benign thyroid disease.

INTRODUCTION: External fractionated radiotherapy of cancer increases the risk of cardio- and cerebrovascular events, but less attention has been paid to the potential side effects on the arteries following internal radiotherapy with radioactive iodine (RAI), i.e. 131-iodine. About 279 per million citizens in the western countries are treated each year with RAI for benign thyroid disorders (about 140,000 a year in the EU), stressing that it is of clinical importance to be aware of even rare radiation-induced side effects. In order to induce or accelerate atherosclerosis, the dose to the carotid arteries has to exceed 2 Gy which is the known lower limit of ionizing radiation to affect the endothelial cells and thereby to induce atherosclerosis. OBJECTIVE: To estimate the radiation dose to the carotid arteries following RAI therapy of benign thyroid disorders. METHODS: Assuming that the lobes of the thyroid gland are ellipsoid, that the carotid artery runs through a part of the lobes, that there is a homogeneous distribution of RAI in the lobes, and that the 24 h RAI uptake in the thyroid is 35 % of the (131)I orally administrated, we used integrated modules for bioassay analysis and Monte Carlo simulations to calculate the dose in Gy/GBq of administrated RAI. RESULTS: The average radiation dose along the arteries is 4-55 Gy/GBq of the (131)I orally administrated with a maximum dose of approximately 25-85 Gy/GBq. The maximum absorbed dose rate to the artery is 4.2 Gy/day per GBq (131)I orally administrated. CONCLUSION: The calculated radiation dose to the carotid arteries after RAI therapy of benign thyroid disorder clearly exceeds the 2 Gy known to affect the endothelial cells and properly induce atherosclerosis. This simulation indicates a relation between the deposited dose in the arteries following RAI treatment and an increased risk of atherosclerosis and subsequent cerebrovascular events such as stroke.