Ethnic Differences in Cardiovascular Responses to Laboratory Stress: A Comparison Between Asian and White Americans Biing-Jiun Shen, Laura R. Stroud, and Raymond Niaura Compared to other ethnic groups, Asian Americans show significantly lower rates of cardiovascular disease (CVD). We tested the hypothesis that Asian Americans would show reduced cardiovascular responses to laboratory stressors than Caucasians. Forty-three Asians (18 men, 25 women) and 77 Caucasians (36 men, 41 women) with a mean age of 24 years (SD = 3.93) participated in a stress reactivity protocol consist- ing of four tasks (speech, serial subtraction, mirror tracing, handgrip) while heart rate (HR), systolic blood pressure (SBP), and diastolic blood pressure (DBP) were measured. Asian Americans demonstrated overall lower reactivity across tasks for SBP F(1,117 = 7.48, p < .01) and a trend toward lower HR response F(1,117 = 3.18, p < .10). A significant ethnicity by task interaction was observed for HR reactivity F(3,351 = 2.94, p < .05) such that Caucasians showed greater responses for the sub- traction task. Keywords: Asian American, Caucasian American, cardiovascular reactivity, ethnic differences Asian Americans are one of the fastest growing eth- nic groups in the U.S., accounting for 4.2 percent of the population and between 11 and 33 percent in certain metropolitan areas, such as New York, Los Angeles, and San Francisco (U.S. Bureau of Census, 2002). Ac- cording to the projections, their population growth is expected to reach approximately 15 million in 2010 (U.S. Bureau of Census, 2000). Despite their population growth, little is known about the health and medical issues among Asian Americans. Limited research suggests that Asian Americans show a distinct health and disease profile from other ethnic groups (Kuo & Porter, 1998; Zane, Takeuchi, & Young, 1994) with lower age-adjusted cardiovascular disease (CVD) mortality rates (95.6 per 100,000) than African Americans (240.2), Caucasians (154.1), and Latinos (109.3) (CDC, 2001). They also show lower prevalence rates of hypertension (16.3%) compared to Caucasian (23%) and African (30.9%) Americans (American Heart Association, 2001). How- ever, research on the ethnic differences in CVD primar- ily focuses on African Americans, and rarely moves beyond documenting the differences in mortality across groups, highlighting only one piece of the full picture of ethnic variations in CVD. One proposed mechanism underlying the develop- ment of CVD is increased cardiovascular reactivity to stress. Exaggerated cardiovascular responses to labo- ratory stressors have been associated with increased risk for hypertension (e.g., Everson, Kaplan, Goldberg, & Salonen, 1996), atherosclerosis (e.g., Barnett, Spence, Manuck, & Jennings, 1997), ischemia (Krantz et al., 1991), and possibly recurrent CVD (Manuck, Olsson, Hjemdahl, & Rehnqvist, 1992). Compared to Caucasians, African Americans demonstrated greater and more prolonged cardiovas- cular responses to laboratory stressors as well as higher prevalence of CVD (Barnes et al., 2000). Car- diovascular hyperreactivity is, therefore, proposed as a potential mechanism underlying African Ameri- cans’ greater CVD risk (Anderson, 1989; Anderson, McNeilly, & Myers, 1991). To our knowledge, no studies have directly compared cardiovascular stress responses between Asian and Caucasian Americans except one that examined Asian Indian and Caucasian college students (Stoney, Hughes, Kuntz, West, & Thornton, 2002). Although East Asians (e.g. Chinese, Korean) are the largest Asian groups in the US, we 181 International Journal of Behavioral Medicine 2004, Vol. 11, No. 3, 181–186 Copyright © 2004 by Lawrence Erlbaum Associates, Inc. Biing-Jiun Shen, Department of Psychology, University of Mi- ami, Miami, Florida, USA; Laura R. Stroud and Raymond Niaura, Centers for Behavioral and Preventive Medicine, Brown Medical School, and The Miriam Hospital, Providence, Rhode Island, USA. Laura Stroud was supported by a Career Development Award from the National Institute of Mental Health (K23 MH65443-01), a Faculty Scholar Grant from the Tobacco Etiology Network of the Robert Wood Johnson Foundation, and a Junior Investigator Award from the National Alliance for Research on Schizophrenia and De- pression (NARSAD). We would like to extend gratitude to Jeanne McCaffery for her comments on this article and to Jenelle Krishnamoorthy for her assistance during the preparation of the manuscript for this article. Correspondence concerning this article should be addressed to Biing-Jiun Shen, University of Miami, Department of Psychology, P.O. Box 248185, Coral Gables, Florida, 33124-2070, USA. E-mail: bshen@miami.edu