This paper reviews the possible association between cardiovascular disease and occupational and environmental agents. The effects ofcarbon monoxide, fibrogenic dusts, carbon disulphide, heavy metals, noise, radiation, heat, cold, solvents and fluorocarbons are discussed. New directions for investigation are suggested.There has been a growing awareness of the relationship between the quality of the environment and the incidence of human disease, particularly in relation to chemical carcinogenesis and lung disease. In contrast, studies of the aetiology of coronary arteriosclerotic heart disease (CAHD) have not usually been concerned with exposure to environmental toxins. Those studies which have examined cardiovascular disease in relation to occupation have largely been concerned with the effect of sedentary as opposed to active work (Morris, 1959;Karvonen et al., 1961;Pell and D'Alonzo, 1963;Paffenbarger and Hale, 1975;Baxter et al., 1976;Menotti and Puddu, 1976) or the psychological stress of the work (Jenkins, 1976 The information presented in the following discussion will explore possible environmental risk factors and, in the process, new means of intervention may be suggested. The inconclusiveness of much of the data, rather than indicating an absence of effect, underlines the need for further study.The discussion of cardiovascular disease will be mainly limited to possible environmental aetiological factors of CAHD. By inference one might assume that many of these same factors would be important in the incidence of cerebrovascular disease. Included in the discussion of CAHD will be agents that cause arrhythmias or vasospasm. Although these two physiological responses are not necessarily related to arteriosclerosis it is impossible, without good autopsy data, to separate sudden death caused by these mechanisms from sudden death secondary to myocardial infarcts of atherosclerotic origin. Agents having a direct effect on myocardial tissue will also be reviewed. Environmental causes of congenital heart disease will not be discussed.The Table lists of men in the workplace, where one finds the highest exposure to the agents in the Table, may contribute, to some extent, to the known differences in incidence of heart disease between the sexes. Carbon monoxide may be an important factor in the strong association between cigarette smoking and CAHD. Carbon disulphide-exposed workers may have more CAHD because of increased blood pressure and/or cholesterol levels. Certain heavy metals may increase the incidence of CAHD by their toxic renal effect which may subsequently cause hypertension.The monoclonal theory ofarteriosclerosis (Benditt, 1977) suggests a possible mechanism for environmental agents. Cells in aortic atherosclerotic plaques from women heterozygous for X-linked glucosephosphate dehydrogenase deficiency were examined at autopsy for their clonal origin. The cells in fibrous plaques were found to be of monoclonal origin, compared with cells in normal intima (Benditt and Benditt, 1973 (Benditt, 1977)...