The problem of noise as a potential health hazard to urban man has been raised. The literature was used to establish two premises: that cities are noisy environments, and that noise-free societies have less coronary artery disease (CAD) than do industrialized sections of the world. These differences also hold for rural and urban areas of the United States. Geographical questions concerning rate differentials for CAD have been addressed by numerous disciplines. Subsequently, social, psychological, and physical explanations have been put forth. Throughout this paper the emphasis has been placed on the physical aspects of noise exposure. The conceptual frame utilizes noise-load, overload, stress and deformation. Noise was described as a force capable of eliciting a predictable physiological response from the human organism. Noise was further conceptualized as a by-product of technology which exerts a stressor effect upon the cardiovascular system of man. The investigation, from which the data were generated, was a micro-view of physiological effects, in that the only measurement taken was heart rate change in hospitalized patients in response to noise. The heart rate was calculated under low noise conditions, and comparisons subsequently made to heart rate during noise. In addition, the noise climate for each of two coronary care units (CCU) was tabulated over a 24 hour period. Generally noise levels in the CCUs were higher than might be found in a man's own home. Only between the hours of 3:00 and four in the morning, was ambient noise equal to or below the suggested levels (45 dbA) for any sustained period of time. Conditions of noise elicited heart rate change in 30 of 37 subjects (p=.001). This finding relates to the presence of a change and does not speak to the extent or meaningfulness of that change. Patients with heart attacks responded to noise conditions (11=18, P=.01) in that 17 of the eighteen patients experienced a change in heart rate when noise was introduced. No differences could be noted for categories by site of infarctions. It was further hypothesized that the extent of heart rate response (HRR) would be a function of the gap between low noise and high noise conditions. A regression analysis showed the response to be significantly correlated with noise gap for the total population (N=37, P=.05), however the correlation was minimal (r=.4528) with slightly less than 21 per cent of the variation in HRR explained by the variation in noise gap. Those subjects more than 60 years of age (n=20), also showed a significant correlation (r=.5173) with 26 per cent of the variation in HRR explained by the variation in noise gap. The highest correlation (r=.7373) was obtained for ten persons with a past history of heart disease (r2=.5436, P=.05). The implications for site planning and structure are many, particularly for hospitals, nursing, and convalescent homes where older persons with heart disease are housed. Site planning should give attention to noise environment; and structural planning, to sound-proofing. Interviews with architects and hospital builders showed this goal to be attainable mechanically, if somewhat costly. It was agreed by those interviewed that such costs as evolve from noise-reduction or noise-proofing in hospitals would most certainly be passed on to the consumer and be reflected in his health care costs. Additional research is needed which focuses on the effects of noise on the cardiovascular system over time, using standardized criteria for cardiovascular health and cardiovascular disease. Other research might focus on larger samples of patients hospitalized with CAD, in an effort to identify an index of physiological and psychological responses to noise.