Modification of the Association Between PM2.5 and Heart Rate by β-Blocker Usage Among Heart Failure Patients
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Fine particulate matter (PM2.5) is associated with cardiovascular morbidity, particularly among individuals with pre-existing conditions such as heart failure (HF). Medications may modify the association between PM2.5 and health risks, particularly those that act on the same physiologic pathways as PM2.5. Using electronic health records (EHRs) from 26,653 HF patients observed from 2014-2016 we examined if associations between heart rate (HR) and PM2.5 were modified by beta-blocker medication usage. Daily PM2.5 was modeled using ensemble machine learning models and matched based on the patient’s primary residence. Linear mixed models were adjusted for age, sex, race, smoking status, temperature, relative humidity, census sociodemographic variables, and a cubic spline term for time since start. Associations were stratified on β-blocker medication usage and examined for the day of measurement and up to 4 days prior as well as the 5-day moving average. A multiplicative interaction was used to model the interaction between PM2.5 and HR. We also utilized data from an in vivo toxicological study to compare to our epidemiological study. Results are per 10 µg/m3 increase in PM2.5. Associations across lags were consistent, so we will report only the 5-day moving averages. When no β-blocker prescription was noted in the health record, we observed a positive association between PM2.5 and HR (0.87, CI = 0.74, 1.00) with the opposite direction of association seen when β-blockers had been prescribed (-0.17, CI = -0.24, -0.11; interaction P = 1.47x10-23). Additionally, we found that rats treated with β-blockers experienced a smaller increase in HR (β = 13.0, 95% CI: 1.83, 24.12) in comparison to controls (β = 30.1, 95% CI: 17.79, 42.33) when exposed to PM2.5 similarly to humans. Medication usage likely has interactions with short-term PM2.5 and should be accounted for when possible and potentially explored for its ability to modify PM2.5-related health risks.