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. 2018 Sep-Oct;30(11-12):439-447.
doi: 10.1080/08958378.2018.1551443. Epub 2019 Jan 15.

Pulmonary exposure to peat smoke extracts in rats decreases expiratory time and increases left heart end systolic volume

Leslie C Thompson  1 , Yong Ho Kim  1   2 , Brandi L Martin  3 , Allen D Ledbetter  1 , Janice A Dye  1 , Mehdi S Hazari  1 , M Ian Gilmour  1 , Aimen K Farraj  1
Affiliations

Pulmonary exposure to peat smoke extracts in rats decreases expiratory time and increases left heart end systolic volume

Leslie C Thompson et al. Inhal Toxicol. 2018 Sep-Oct.

Abstract

Exposure to wildland fire-related particulate matter (PM) causes adverse health outcomes. However, the impacts of specific biomass sources remain unclear. The purpose of this study was to investigate cardiopulmonary responses in rats following exposure to PM extracts collected from peat fire smoke. We hypothesized that peat smoke PM would dose-dependently alter cardiopulmonary function. Male Sprague-Dawley rats (n = 8/group) were exposed to 35 µg (Lo PM) or 350 µg (Hi PM) of peat smoke PM extracts suspended in saline, or saline alone (Vehicle) via oropharyngeal aspiration (OA). Ventilatory expiration times, measured in whole-body plethysmographs immediately after OA, were the lowest in Hi PM exposed subjects at 6 min into recovery (p = .01 vs. Lo PM, p = .08 vs. Vehicle) and resolved shortly afterwards. The next day, we evaluated cardiovascular function in the same subjects via cardiac ultrasound under isoflurane anesthesia. Compared to Vehicle, Hi PM had 45% higher end systolic volume (p = .03) and 17% higher pulmonary artery blood flow acceleration/ejection time ratios, and both endpoints expressed significant increasing linear trends by dose (p = .01 and .02, respectively). In addition, linear trend analyses across doses detected an increase for end diastolic volume and decreases for ejection fraction and fractional shortening. These data suggest that exposure to peat smoke constituents modulates regulation of ventricular ejection and filling volumes, which could be related to altered blood flow in the pulmonary circulation. Moreover, early pulmonary responses to peat smoke PM point to irritant/autonomic mechanisms as potential drivers of later cardiovascular responses.

Keywords: Wildfire; biomass; echocardiography; heart function; particulate matter; peat; pulmonary irritation; smoke; ultrasound; wildland fire.

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Figures

Figure 1.
Figure 1.. Ventilatory changes minutes after exposure to peat smoke PM.
(A) One-minute averages of expiratory time during the 12 minutes of ventilatory assessment. (B) Average expiratory time at 6 minutes. (C) One-minute averages of relaxation time during the 12 minutes of ventilatory assessment. (D) Average relaxation time at 6 minutes. (E) One-minute averages of breathing frequency during the 12 minutes of ventilatory assessment. (F) Average breathing frequency at 6 minutes. A, C, and E are mean ± SEM of one-minute averages tested by Repeated Measures ANOVA with Bonferroni’s post-test. B, D, and F were tested by One Way ANOVA with Tukey’s and linear trend analysis post-tests. p-values less than 0.1 are provided for clarity.
Figure 2.
Figure 2.. Changes in left ventricular volume regulation one day after exposure to peat smoke PM.
(A) End systolic volume. (B) End diastolic volume. (C) Ejection fraction. (D) Fractional shortening. Data were tested by One Way ANOVA with Tukey’s and linear trend analysis post-tests. p-values less than 0.1 are provided for clarity.
Figure 3.
Figure 3.. Changes in pulmonary artery hemodynamics one day after exposure to peat smoke PM.
Data were tested by One Way ANOVA with Tukey’s post-test.
See this image and copyright information in PMC

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