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Article Abstract

Background: Recent studies have related high pollen concentrations to increased cardiovascular morbidity and mortality, yet very little research concerns pre-clinical cardiovascular health, including effects on blood pressure (BP). The EPOCHAL panel study investigated the exposure-response relationship between ambient pollen exposure and systolic and diastolic BP in adults.

Methods: BP was measured in 302 adults with and in 94 without pollen allergy during the pollen season, on approximately 16 days per person (6253 observations). Average individually-relevant pollen exposure in the 96 h prior to each BP measurement was calculated by summing up the averages of all ambient pollen concentrations to which the individual was found to be sensitized in a skin prick test, and which originated from seven highly allergenic pollen types (hazel, alder, birch, ash, grasses, mugwort and ragweed). Generalized additive mixed models were used to study the association between mean individually-relevant pollen exposure in the last 96 h and BP, adjusting for individual and environmental time-varying covariates. Effect modification by pollen allergy status, sex and BMI was evaluated.

Results: Positive non-linear associations between individually-relevant pollen exposure and both systolic and diastolic BP were found in the allergic but not in the non-allergic group. BP increased sharply for exposures from zero to 60/80 pollen/m (diastolic/systolic BP), followed by a tempered further increase at higher concentrations. Increases of 2.00 mmHg [95% confidence interval (CI): 0.80-3.19] in systolic and 1.51 mmHg [95% CI: 0.58-2.45] in diastolic BP were associated with 96-h average pollen exposure of 400 pollen/m, compared to no exposure. Obesity and female sex were associated with larger BP increases.

Conclusions: The finding that short-term pollen concentration is associated with increased systolic and diastolic BP in persons with pollen allergy strengthens the evidence that pollen may cause systemic health effects and trigger cardiovascular events.

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http://dx.doi.org/10.1016/j.envres.2024.119224DOI Listing

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