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Personal exposure to fine particulate air pollutants impacts blood pressure and heart rate variability.

ABSTRACT: Air pollution has increasingly been recognized as a major healthcare concern. Air pollution, particularly fine particulate matter (??2.5 ?m in aerodynamic diameter [PM_2.5]) has demonstrated an increase in adverse cardiovascular events. This study aimed to assess the cardiovascular response to personal exposure to different levels of PM_2.5. This prospective cohort study enrolled healthy volunteers aged ??18 years with no cardiovascular disease. Study subjects carried personal exposure monitor of PM_2.5, digital thermo-hygrometer for temperature and humidity, 24-h blood pressure monitor, and continuous electrocardiogram monitor. Measurements were repeated twice with an interval of 6-12 months. Statistical models consisted of generalized estimation equations to various repeated measures of each subject. A total of 22 subjects were enrolled in this study between July 2018 and January 2019. Measurement was performed twice in all participants, and a total of 36 data were collected except for insufficient data collection. The mean age of the study population was 41.6 years, and 95% of the subjects were females. No study subjects had hypertension or other cardiovascular diseases. The average systolic blood pressure increased with higher PM_2.5 levels with marginal significance (0.22 mmHg [95% confidential intervals -?0.04 to 0.48 mmHg] per 10 ?g/m³ of PM_2.5). All parameters for heart rate variability significantly decreased with a higher level of PM_2.5. In this study, we measured individual personal exposure to PM_2.5 by using a portable device. We found that 24-h exposure to high levels of PM_2.5 was associated with a significant decrease in heart rate variability, suggesting impaired autonomous nervous function.

SUBMITTER: Lee DH

PROVIDER: S-EPMC7538889 | biostudies-literature | 2020 Oct

REPOSITORIES: biostudies-literature

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Personal exposure to fine particulate air pollutants impacts blood pressure and heart rate variability.

Lee Dong-Hoon DH Kim Sun-Hwa SH Kang Si-Hyuck SH Kwon Oh Kyung OK Park Jin-Joo JJ Yoon Chang-Hwan CH Cho Young-Seok YS Heo Jongbae J Yi Seung-Muk SM Youn Tae-Jin TJ Chae In-Ho IH

Scientific reports 20201006 1

Air pollution has increasingly been recognized as a major healthcare concern. Air pollution, particularly fine particulate matter (≤ 2.5 μm in aerodynamic diameter [PM<sub>2.5</sub>]) has demonstrated an increase in adverse cardiovascular events. This study aimed to assess the cardiovascular response to personal exposure to different levels of PM<sub>2.5</sub>. This prospective cohort study enrolled healthy volunteers aged ≥ 18 years with no cardiovascular disease. Study subjects carried persona ...[more]

PMID: 33024194

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Project description:Importance:Fine particulate matter (smaller than 2.5 ?m) (PM2.5) air pollution is a major global risk factor for cardiovascular (CV) morbidity and mortality. Few studies have tested the benefits of portable air filtration systems in urban settings in the United States. Objective:To investigate the effectiveness of air filtration at reducing personal exposures to PM2.5 and mitigating related CV health effects among older adults in a typical US urban location. Design, Setting, and Participants:This randomized, double-blind crossover intervention study was conducted from October 21, 2014, through November 4, 2016, in a low-income senior residential building in Detroit, Michigan. Forty nonsmoking older adults were enrolled, with daily CV health outcome and PM2.5 exposure measurements. Interventions:Participants were exposed to the following three 3-day scenarios separated by 1-week washout periods: unfiltered air (sham filtration), low-efficiency (LE) high-efficiency particulate arrestance (HEPA)-type filtered air, and high-efficiency (HE) true-HEPA filtered air using filtration systems in their bedroom and living room. Main Outcomes and Measures:The primary outcome was brachial blood pressure (BP). Secondary outcomes included aortic hemodynamics, pulse-wave velocity, and heart rate variability. Exposures to PM2.5 were measured in the participants' residences and by personal monitoring. Results:The 40 participants had a mean (SD) age of 67?(8) years (62% men). Personal PM2.5 exposures were significantly reduced by air filtration from a mean (SD) of 15.5 (10.9) ?g/m3 with sham filtration to 10.9 (7.4) ?g/m3 with LE fitration and 7.4 (3.3) ?g/m3 with HE filtration. Compared with sham filtration, any filtration for 3 days decreased brachial systolic and diastolic BP by 3.2 mm Hg (95% CI, -6.1 to -0.2 mm Hg) and 1.5 mm Hg (95% CI, -3.3 to 0.2 mm Hg), respectively. A continuous decrease occurred in systolic and diastolic BP during the 3-day period of LE filtration, with a mean of 3.4 mm Hg (95% CI, -6.8 to -0.1 mm Hg) and 2.2 mm Hg (95% CI, -4.2 to -0.3 mm Hg), respectively. For HE filtration, systolic and diastolic BP decreased by 2.9 mm Hg (95% CI, -6.2 to 0.5 mm Hg) and 0.8 mm Hg (95% CI, -2.8 to 1.2 mm Hg), respectively. Most secondary outcomes were not significantly improved. Conclusions and Relevance:Results of this study showed that short-term use of portable air filtration systems reduced personal PM2.5 exposures and systolic BP among older adults living in a typical US urban location. The use of these relatively inexpensive systems is potentially cardioprotective against PM2.5 exposures and warrants further research. Trial Registration:ClinicalTrials.gov identifier: NCT03334565.

Project description:BackgroundThe adverse effects of particulate air pollution on heart rate variability (HRV) have been reported. However, it remains unclear whether they differ by the weight status as well as between wake and sleep.MethodsA repeated-measure study was conducted in 97 young adults in Beijing, China, and they were classified by body mass index (BMI) as normal-weight (BMI, 18.5-24.0 kg/m2) and obese (BMI ≥ 28.0 kg/m2) groups. Personal exposures to fine particulate matter (PM2.5) and black carbon (BC) were measured with portable exposure monitors, and the ambient PM2.5/BC concentrations were obtained from the fixed monitoring sites near the subjects' residences. HRV and heart rate (HR) were monitored by 24-h Holter electrocardiography. The study period was divided into waking and sleeping hours according to time-activity diaries. Linear mixed-effects models were used to investigate the effects of PM2.5/BC on HRV and HR in both groups during wake and sleep.ResultsThe effects of short-term exposure to PM2.5/BC on HRV were more pronounced among obese participants. In the normal-weight group, the positive association between personal PM2.5/BC exposure and high-frequency power (HF) as well as the ratio of low-frequency power to high-frequency power (LF/HF) was observed during wakefulness. In the obese group, personal PM2.5/BC exposure was negatively associated with HF but positively associated with LF/HF during wakefulness, whereas it was negatively correlated to total power and standard deviation of all NN intervals (SDNN) during sleep. An interquartile range (IQR) increase in BC at 2-h moving average was associated with 37.64% (95% confidence interval [CI]: 25.03, 51.51%) increases in LF/HF during wakefulness and associated with 6.28% (95% CI: - 17.26, 6.15%) decreases in SDNN during sleep in obese individuals, and the interaction terms between BC and obesity in LF/HF and SDNN were both statistically significant (p < 0.05). The results also suggested that the effects of PM2.5/BC exposure on several HRV indices and HR differed in magnitude or direction between wake and sleep.ConclusionsShort-term exposure to PM2.5/BC is associated with HRV and HR, especially in obese individuals. The circadian rhythm of HRV should be considered in future studies when HRV is applied.

Project description:OBJECTIVE:Air pollution is a leading preventable risk factor for cardiovascular diseases. Previous studies mostly relied on concentrations at residence, which might not represent personal exposure. Personal air pollution exposure has a greater variability compared with levels of ambient air pollution, facilitating evaluation of exposure-response functions and vascular pathophysiology. We aimed to evaluate the association between predicted annual personal exposure to PM2.5 and black carbon (BC) and three vascular damage markers in peri-urban South India. METHODS:We analyzed the third wave of the APCAPS cohort (2010-2012), which recruited participants from 28 villages. We used predicted personal exposure to PM2.5 and BC derived from 610 participant-days of 24 h average gravimetric PM2.5 and BC measurements and predictors related to usual time-activity. Outcomes included carotid intima-media thickness (CIMT), carotid-femoral pulse wave velocity (cf-PWV) and augmentation index (AIx). We fit linear mixed models, adjusting for potential confounders and accounting for the clustered data structure. We evaluated nonlinear associations using generalized additive mixed models. RESULTS:Of the 3017 participants (mean age 38 years), 1453 (48%) were women. The average PM2.5 exposure was 51 µg/m3 (range 13-85) for men, and 61 µg/m3 (range 40-120) for women, while the average BC was 4 µg/m3 (range 3-7) for men and 8 µg/m3 (range 3-22) for women. A 10 ?g/m3 increase of PM2.5 was positively associated with CIMT (0.026 mm, 95% CI 0.014, 0.037), cf-PWV (0.069 m/s, 95% CI 0.008, 0.131) and AIx (0.8%, 95% CI 0.3, 1.3) among men. The exposure-response function for PM2.5 and AIx among men showed non-linearity, particularly within the exposure range dominated by tobacco smoking and occupational exposures. Both PM2.5 and BC were positively associated with AIx among women (0.6%, 95% CI 0.2, 1.0, per 10 ?g/m3 PM2.5; 0.5%, 95% CI 0.1, 0.8, per 2 ?g/m3 BC). CONCLUSIONS:Personal exposure to particulate matter was associated with vascular damage in a peri-urban population in South India. Personal exposure to particulate matter appears to have gender-specific effects on the type of vascular damage, potentially reflecting differences in sources of personal exposure by gender.

Project description:Epidemiological evidence indicates that exposures to fine particulate matter air pollution (PM2.5) contribute to global burden of disease, primarily as a result of increased risk of cardiovascular morbidity and mortality. However, mechanisms by which PM2.5 exposure induces cardiovascular injury remain unclear. PM2.5-induced endothelial dysfunction and systemic inflammation have been implicated, but direct evidence is lacking.To examine whether acute exposure to PM2.5 is associated with endothelial injury and systemic inflammation.Blood was collected from healthy, nonsmoking, young adults during 3 study periods that included episodes of elevated PM2.5 levels. Microparticles and immune cells in blood were measured by flow cytometry, and plasma cytokine/growth factors were measured using multiplexing laser beads. PM2.5 exposure was associated with the elevated levels of endothelial microparticles (annexin V+/CD41-/CD31+), including subtypes expressing arterial-, venous-, and lung-specific markers, but not microparticles expressing CD62+. These changes were accompanied by suppressed circulating levels of proangiogenic growth factors (EGF [epidermal growth factor], sCD40L [soluble CD40 ligand], PDGF [platelet-derived growth factor], RANTES [regulated on activation, normal T-cell-expressed and secreted], GRO? [growth-regulated protein ?], and VEGF [vascular endothelial growth factor]), and an increase in the levels of antiangiogenic (TNF? [tumor necrosis factor ?], IP-10 [interferon ?-induced protein 10]), and proinflammatory cytokines (MCP-1 [monocyte chemoattractant protein 1], MIP-1?/? [macrophage inflammatory protein 1?/?], IL-6 [interleukin 6], and IL-1? [interleukin 1?]), and markers of endothelial adhesion (sICAM-1 [soluble intercellular adhesion molecule 1] and sVCAM-1 [soluble vascular cellular adhesion molecule 1]). PM2.5 exposure was also associated with an inflammatory response characterized by elevated levels of circulating CD14+, CD16+, CD4+, and CD8+, but not CD19+ cells.Episodic PM2.5 exposures are associated with increased endothelial cell apoptosis, an antiangiogenic plasma profile, and elevated levels of circulating monocytes and T, but not B, lymphocytes. These changes could contribute to the pathogenic sequelae of atherogenesis and acute coronary events.

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Personal exposure to fine particulate air pollutants impacts blood pressure and heart rate variability.

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Personal exposure to fine particulate air pollutants impacts blood pressure and heart rate variability.

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