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Acute effect of fine particulate matter on blood pressure, heart rate and related inflammation biomarkers: A panel study in healthy adults.

ABSTRACT: Epidemiological evidence of short-term fine particulate matter (PM_2.5) exposure on blood pressure (BP), heart rate (HR) and related inflammation biomarkers has been inconsistent. We aimed to explore the acute effect of PM_2.5 on BP, HR and the mediation effect of related inflammation biomarkers. A total of 32 healthy college students were recruited to perform 4 h of exposure at two sites with different PM_2.5 concentrations in Wuhan between May 2019 and June 2019. The individual levels of PM_2.5 concentration, BP and HR were measured hourly for each participant. Blood was drawn from each participant after each visit and we measured the levels of inflammation markers, including serum high-sensitivity C-reactive protein and plasma fibrinogen. Linear mixed-effect models were to explore the acute effect of PM_2.5 exposure on BP, HR, and related inflammation biomarkers. In addition, we evaluated related inflammation biomarkers as the mediator in the association of PM_2.5 and cardiovascular health indicators. The results showed that a 10 μg/m³ increment in PM_2.5 concentration was associated with an increase of 0.84 (95% CI: 0.54, 1.15) beats/min (bpm) in HR and a 3.52% (95% CI: 1.60%, 5.48%) increase in fibrinogen. The lag effect model showed that the strongest effect on HR was observed at lag 3 h of PM_2.5 exposure [1.96 bpm (95% CI: 1.19, 2.75)], but for fibrinogen, delayed exposure attenuated the association. Increased fibrinogen levels may account for 39.07% (P = 0.44) of the elevated HR by PM_2.5. Null association was observed when it comes to short-term PM_2.5 exposure and BP. Short-term exposure to PM_2.5 was associated with elevated HR and increased fibrinogen levels. But our finding was not enough to suggest that exposure to PM_2.5 might induce adverse cardiovascular effects by the pathway of inflammation.

SUBMITTER: Li Z

PROVIDER: S-EPMC8655618 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Fine particulate matter (PM2.5) released during the livestock industry endangers the respiratory health of animals. Our previous findings suggested that broilers exposed to PM2.5 exhibited lung inflammation and changes in the pulmonary microbiome. Therefore, this study was to investigate whether the pulmonary microbiota plays a causal role in the pathogenesis of PM2.5-induced lung inflammation. We first used antibiotics to establish a pulmonary microbiota intervention broiler model, which showed a significantly reduced total bacterial load in the lungs without affecting the microbiota composition or structure. Based on it, 45 AA broilers of similar body weight were randomly assigned to three groups: control (CON), PM2.5 (PM), and pulmonary microbiota intervention (ABX-PM). From 21 d of age, broilers in the ABX-PM group were intratracheally instilled with antibiotics once a day for 3 d. Meanwhile, broilers in the other two groups were simultaneously instilled with sterile saline. On 24 and 26 d of age, broilers in the PM and ABX-PM groups were intratracheally instilled with PM2.5 suspension to induce lung inflammation, and broilers in the CON group were simultaneously instilled with sterile saline. The lung histomorphology, inflammatory cytokines' expression levels, lung microbiome, and microbial growth conditions were analyzed to determine the effect of the pulmonary microbiota on PM2.5-induced lung inflammation. Broilers in the PM group showed lung histological injury, while broilers in the ABX-PM group had normal lung histomorphology. Furthermore, microbiota intervention significantly reduced mRNA expression levels of interleukin-1β, tumor necrosis factor-α, interleukin-6, interleukin-8, toll-like receptor 4 and nuclear factor kappa-B. PM2.5 induced significant changes in the β diversity and structure of the pulmonary microbiota in the PM group. However, no significant changes in microbiota structure were observed in the ABX-PM group. Moreover, the relative abundance of Enterococcus cecorum in the PM group was significantly higher than that in the CON and ABX-PM groups. And sterile bronchoalveolar lavage fluid from the PM group significantly promoted the growth of E. cecorum, indicating that PM2.5 altered the microbiota's growth condition. In conclusion, pulmonary microbiota can affect PM2.5-induced lung inflammation in broilers. PM2.5 can alter the bacterial growth environment and promote dysbiosis, potentially exacerbating inflammation.

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Acute effect of fine particulate matter on blood pressure, heart rate and related inflammation biomarkers: A panel study in healthy adults.

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