摘要
The effect of ionising radiation exposure on dementia is approached by applying the causation models of John Stuart Mill and of Sir Austin Bradford Hill to mechanism and epidemiological evidence. Since ionizing radiation is known to kill brain cells in laboratory culture and to affect hippocampal neurogenesis in animal experiments at modest doses, it is reasonable to assume that exposure to radiation must affect neurological integrity and hence dementia rates in those who are exposed. There is persuasive evidence from the epidemiological studies of a large cohort of female nuclear workers that ionising radiation exposure is associated with significant low dose region dose-dependent increases in rates of dementia. Using results from these studies, the Probability of Causation approach (PC), conventionally employed for assessing cancer risk following radiation exposure, is extended to dementia to find a risk coefficient for all ages of 60 per Sievert cumulative exposure over the range 0-100 mSv. The finding suggests that natural background external exposures to ionizing radiation are partly responsible for the development of dementia in human populations. A simple general model for dementia is proposed.
The effect of ionising radiation exposure on dementia is approached by applying the causation models of John Stuart Mill and of Sir Austin Bradford Hill to mechanism and epidemiological evidence. Since ionizing radiation is known to kill brain cells in laboratory culture and to affect hippocampal neurogenesis in animal experiments at modest doses, it is reasonable to assume that exposure to radiation must affect neurological integrity and hence dementia rates in those who are exposed. There is persuasive evidence from the epidemiological studies of a large cohort of female nuclear workers that ionising radiation exposure is associated with significant low dose region dose-dependent increases in rates of dementia. Using results from these studies, the Probability of Causation approach (PC), conventionally employed for assessing cancer risk following radiation exposure, is extended to dementia to find a risk coefficient for all ages of 60 per Sievert cumulative exposure over the range 0-100 mSv. The finding suggests that natural background external exposures to ionizing radiation are partly responsible for the development of dementia in human populations. A simple general model for dementia is proposed.
