€: ~11- CM le Recently Benditt has shown (40) that the human atherosclerotic plaque is a monoclonal proliferation of a mutated cell of the artery wall, and thus an arterial tumor. Elkeles (41-43) iias observed anomalously high concen- trations of alpha activity at the calcified plaque sites. In addition atherosclerosis plaques normally occur in the main and abdominal aortasand the coronary arteries, but rarely in the pulmonary arteries “#2744 | This distribution suggests a respiratory origin for the mutagenic agent. Attempts to reproduce arterial Jesions in animals by chemical, mechanical and nutritional means have not produced plaques similar- to those of atherosclerosis in man (40) | However atherosclerotic plaques have been -directiy induced in human arteries by intensive irradiation with X-rays and radium “45) , There ts a high incidence of early coronaries among cigarette smokers, with a mortality rate for males who smoke two packs or more daiiy that is 2 to 2.5 times that of non-smokers but at a mean age of death some 10 to 16 years earlier (4&5, all these reasons it is proposed that inhaled insoluble alpha emitting emoke particles are very likely to be the mutagenic agent which gives rise to atherosclerosis in cigarette smokers. If this is the case, similar increased risk of early coronaries are to be expected for other groups of individuals who are occupationally or envirormentally exposed to the inhalation of insoluble alpha emitting particles of respirable size. Attention should be addressed to industrial and combustion product aerosols which contain uranium oxide, thorium oxide and lead-210, as well as to plutonium oxide from nuclear industry, nuclear accidentsand fallout from atmospheric nuclear tests. The first snd most obvious place to look for such effects is past and present plutonium workers. among Very significant increases in the incidence of early corcnaries as well as lung cancers and cancers at other sites is observed among cigarette emokers (46) with insoluble alpha emitting A1