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April 9, 2019 1857 Jefferson Luis Vieira, MD, PhD Edimar Alcides Bocchi, MD, PhD To the Editor: Based on data from the UK Biobank Population cohort, Aung et al1 provided a significant contribution to the literature on long-term relationships between exposure to inhaled particulate matter with an aerodynamic diameter <2.5 μm (PM2.5) and heart failure (HF). The authors examined cardiovascular magnetic resonance in a cohort of 3920 asymptomatic individuals who lived near UK National Health Service assessment centers after a median exposure length of 5.2 years. After adjustment for covariates, they found that each interquartile increment in PM2.5 concentration was associated with larger biventricular volume, predominantly left ventricular end-diastolic and end-systolic volumes and right ventricular end-diastolic volume. However, we believe that some points should be revisited. First, although large sample sizes have a number of strengths, studies must be representative of the population to which the results will be generalized. According to Kloog et al,2 the absence of spatially resolved daily PM2.5 concentration data limits studies to the proximity of monitoring sites, which may not be representative of the population as a whole. In the present case, studied individuals were living within a median distance to the nearest major road of 356 meters. Surprisingly, although distance from the major roads was associated with lower left ventricular mass, there was no significant relationship between traffic intensity and any of the cardiac morpho-functional phenotypes. Second, although the authors adjusted for all covariates, we noted that 28.3%, 38.7%, and 44,8% of the individuals had a past medical history of hypertension, smoking (either current or previous), and regular alcohol use, respectively. These risk factors are highly prevalent in the general population and well associated with HF. We consider that to better represent a sample “with no prevalent cardiovascular disease,” as stressed, those individuals should have been either excluded from the analysis or analyzed separately. For instance, the medications used in the management of hypertension and HF are often similar, and 20.1% of the study individuals were receiving some antihypertensive medication. This may have significance, because drugs like β-blockers and angiotensin-converting enzyme inhibitors have independent efficacy in attenuating the early and late phases of remodeling. Third, the authors did not consider vascular impairment as a mechanism involved in their results because systolic and diastolic components of blood pressure and presence of hypertension do not appear to mediate the association between air pollution and cardiac parameters. We have recently shown that short-term exposure to PM2.5 is associated with endothelial dysfunction, B-type natriuretic peptide increase, and exercise impairment in patients with HF, without changes in systemic blood pressure.3,4 Cao et al5 previously reported that endothelial or arterial stiffness might impact left ventricular hypertrophy. Also, it is widely recognized that endothelial © 2019 American Heart Association, Inc. LETTER TO THE EDITOR