摘要：Objectives . We assessed 2 pathways through which dietary antioxidants may counter adverse effects of exposure to particulate matter less than 2.5 micrometers in diameter (PM2.5) on blood pressure (BP): main (compensatory) and modifying (protective) models. Methods . We used 2002 to 2003 data from the Detroit Healthy Environments Partnership community survey conducted with a multiethnic sample of adults (n = 347) in low- to moderate-income, predominantly Hispanic and non-Hispanic Black neighborhoods in Detroit, Michigan. We used generalized estimating equations to test the effects of ambient exposure to PM2.5 and dietary antioxidant intake on BP, with adjustment for multiple confounders. Results . Dietary antioxidant intake was inversely associated with systolic BP (b = −0.5; P < .05) and pulse pressure (b = −0.6; P < .05) in neighborhoods closest to major sources of air pollutants. Adverse effects of PM2.5 remained significant after accounting for antioxidant intakes. Exploratory analyses suggested potential modifying effects of antioxidant intake on associations between ambient PM2.5 exposure and BP. Conclusions . Interventions to improve access to antioxidant-rich foods in polluted urban areas may be protective of cardiovascular health. However, efforts to reduce PM2.5 exposure remain critical for cardiovascular health promotion. Regulatory actions reducing fine particulate matter less than 2.5 micrometers in diameter (PM2.5) are associated with improvements in life expectancy in the United States. 1,2 However, levels of PM2.5 remain high and continue to be positively associated with risk of high blood pressure (BP), a precursor for many adverse cardiovascular outcomes, including coronary heart disease, myocardial infarction, and heart failure. 3–6 In the United States overall, medical expenses associated with the nearly 1 in 3 adults with hypertension 7 are estimated at approximately $131 billion annually. 8 Cardiovascular disease is the leading cause of death in the United States and accounts for one third of the excess risk of death experienced by non-Hispanic Black in comparison with non-Hispanic White Americans. 9,10 Non-Hispanic Blacks, Hispanics, and individuals of low income in the United States are disproportionately likely to reside in communities with excess exposure to environmental hazards, including PM2.5. 11–13 Continued investigation of strategies to reduce exposure to PM2.5, and its adverse effects on BP, are essential to efforts to reduce racial and ethnic disparities in cardiovascular risk. Oxidative stress may be one molecular pathway linking PM2.5 to BP. 14–17 PM2.5 compounds, whose composition largely depends on their source (e.g., industry, transportation), typically contain organic chemicals, metals, soot, soil, dust, allergens, and acids on their surface. When inhaled, these particles, alone or through chemical reactions, may initiate the creation of reactive oxygen species (ROS), commonly referred to as free radicals, resulting in various physiological responses in lung, heart, and vascular tissue. 18 Specifically, ROS can contribute to vasoconstriction, endothelial dysfunction, and hypertrophy, among other mechanisms that can ultimately contribute to hypertension. 19 Oxidative stress may be mitigated when antioxidants absorb ROS in the airways and inhibit oxidation. 20 Antioxidants are available through dietary intake of foods or supplements (e.g., vitamins A, C, and E and selenium) and may protect against adverse effects of oxidative stress. The majority of studies addressing the effects of antioxidants on cardiovascular health have examined the modifying (protective) or main (compensatory) role of antioxidant intake from supplements, rather than from whole foods captured through dietary intakes. These effects remains unsettled, however, with several meta-analyses reporting minimal or no main effects of supplements on the incidence of major cardiovascular effects across study designs. 21,22 Romieu et al. conducted a substantial review of air pollution, oxidative stress, and various health outcomes and concluded that antioxidant supplements may modify air pollution’s adverse effects on cardiovascular health. 23 A few clinical studies have noted deleterious effects of antioxidant supplement use. 24,25 Many factors compromise or complicate comparison of these studies’ outcomes. For example, study design varies by antioxidant type, dose, duration, and the health status of study participants. 26–28 Reflecting these inconclusive findings, the American Heart Association’s scientific position recommends against antioxidant supplement use. 29 By contrast, on the basis of modest evidence of reductions in aging-related illnesses, 30 the Institute of Medicine provides recommended dietary allowances for many well-known antioxidants, including selenium (400 mg) and vitamins A (900 µg), C (90 mg), and E (15 mg). Despite the uncertainties in the evidence base, several scholars recommend direct dietary intake of antioxidants through healthy food (i.e., fruit, vegetables, whole grains) or beverage sources to mitigate the adverse effects of ROS on cardiovascular health. 30–34 Antioxidant intakes are not consistent across diverse populations. Chun et al. 31 used food consumption and supplement use data from National Health and Nutritional Examination Survey (1999–2002) 35 to estimate overall antioxidant intake in the United States, deriving antioxidant values from the US Department of Agriculture Database for the Flavonoid Content of Selected Food. 36 They concluded that overall intake appeared to be higher among women, older adults, non-Hispanic Whites, and higher-income and physically active individuals. For some antioxidants, including vitamin C and carotenes, intake appeared to be higher among nonsmokers and those who did not consume alcohol. 31 Researchers have used various clinical indicators to detect antioxidant deficiency among those with chronic illnesses, including asthma, chronic obstructive lung diseases, diabetes, and cardiovascular disease, 13,23,37,38 which have well-established disparities by race, ethnicity, and income. 39,40 The unequal distribution of exposure to PM2.5 and unequal access to antioxidant-rich foods 41 raise questions about their contributions to racial, ethnic, and socioeconomic health inequities. Residents of urban communities of color and low-income communities are more likely to experience excess exposure to PM2.5. 11,42 Emerging research also suggests racial differences in oxidative stress, with persons of color experiencing higher levels. 43–45 Access to stores that sell fresh produce, an important source of dietary antioxidants, is low in some urban communities, particularly lower-income communities composed predominantly of people of color. 46–50 Together, excess exposure to air pollutants and psychosocial stress may increase levels of oxidative stress in low-income, urban communities of color, at the same time that these communities experience reduced access to foods rich in protective antioxidants. Few studies have examined the question of whether dietary antioxidant intake (DAI) may counter the adverse effects of exposure to PM2.5 on blood pressure in a community sample. We previously reported adverse effects of PM2.5 on blood pressure 4,51 and associations between neighborhood availability of fruits and vegetables and dietary intakes of those foods. 41,50 We built on those findings to specifically examine, in data from Detroit, Michigan, the extent to which DAI is inversely associated with BP and whether it may partially compensate for or counter adverse effects of PM2.5 on BP. If higher levels of DAI inhibit oxidation through absorption of ROS, thus reducing levels of oxidative stress, adverse effects of PM2.5 on BP may be contingent on DAI levels. Thus, we also examined protective models, exploring the extent to which DAI modifies adverse effects of exposure to PM2.5 on BP. We considered the implications of our findings for understanding and intervening to reduce excess risk of cardiovascular disease among residents of predominantly non-Hispanic Black and Hispanic low- to moderate-income urban communities. Our research questions were (1) Is DAI associated with reduced BP? (2) Does DAI reduce adverse effects of PM2.5 on BP? and (3) Does DAI modify the association between PM2.5 and BP?
