PM2.5 increases mouse blood pressure by activating toll-like receptor 3

Zhang, Jinna; Chen, Rucheng; Zhang, Guoqing; Wang, Yixuan; Peng, Jing; Hu, Renjie; Li, Ran; Gu, Weijia; Zhang, Lu; Sun, Qinghua; Liu, Cuiqing

doi:10.1016/j.ecoenv.2022.113368

Cited by 14 publications

(2 citation statements)

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“…We have previously reported that exposure to noise alone increased systolic and diastolic blood pressure via stimulating the release of neurohormones and by activating the HPA-axis [ 41 , 42 ]. Single exposure to PM2.5 increases blood pressure in mice by activating Toll-like receptor 3 [ 73 ]. All three exposure groups showed significant increases in both systolic and diastolic blood pressures, but with no additive effects in the setting of co-exposure.…”

Section: Discussionmentioning

confidence: 99%

Co-exposure to urban particulate matter and aircraft noise adversely impacts the cerebro-pulmonary-cardiovascular axis in mice

Kuntic¹,

Kuntic²,

Krishnankutty

et al. 2023

Redox Biology

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Section: Discussionmentioning

confidence: 99%

Co-exposure to urban particulate matter and aircraft noise adversely impacts the cerebro-pulmonary-cardiovascular axis in mice

Kuntic¹,

Kuntic²,

Krishnankutty

et al. 2023

Redox Biology

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“…In addition, abundant epidemiological evidence suggests that long-or shortterm exposure to high concentrations of ambient PM2.5 has increased the risk of hypertension in the past decade [9][10][11][12][13][14]. Possible reasons include the following: (a) the impact of PM2.5 exposure on vascular dysfunction and remodeling [15][16][17]; (b) possible systemic inflammation, oxidative stress, and altered neuroendocrine factors caused by PM2.5 exposure [18,19]; and (c) other unclear drivers.…”

Section: Introductionmentioning

confidence: 99%

Mediating effect of body fat percentage in the association between ambient particulate matter exposure and hypertension: a subset analysis of China hypertension survey

Xue,

Li,

et al. 2023

BMC Public Health

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Background Hypertension caused by air pollution exposure is a growing concern in China. The association between air pollutant exposure and hypertension has been found to be potentiated by obesity, however, little is known about the processes mediating this association. This study investigated the association between fine particulate matter (aerodynamic equivalent diameter ≤ 2.5 microns, PM2.5) exposure and the prevalence of hypertension in a representative population in southern China and tested whether obesity mediated this association. Methods A total of 14,308 adults from 48 communities/villages in southern China were selected from January 2015 to December 2015 using a stratified multistage random sampling method. Hourly PM2.5 measurements were collected from the China National Environmental Monitoring Centre. Restricted cubic splines were used to analyze the nonlinear dose-response relationship between PM2.5 exposure and hypertension risk. The mediating effect mechanism of obesity on PM2.5-associated hypertension was tested in a causal inference framework following the approach proposed by Imai and Keele. Results A total of 20.7% (2966/14,308) of participants in the present study were diagnosed with hypertension. Nonlinear exposure-response analysis revealed that exposure to an annual mean PM2.5 concentration above 41.8 µg/m3 was associated with increased hypertension risk at an incremental gradient. 9.1% of the hypertension burden could be attributed to exposure to elevated annual average concentrations of PM2.5. It is noteworthy that an increased body fat percentage positively mediated 59.3% of the association between PM2.5 exposure and hypertension risk, whereas body mass index mediated 34.3% of this association. Conclusions This study suggests that a significant portion of the estimated effect of exposure to PM2.5 on the risk of hypertension appears to be attributed to its effect on alterations in body composition and the development of obesity. These findings could inform intersectoral actions in future studies to protect populations with excessive fine particle exposure from developing hypertension.

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