Considerable investigations have been carried out to address the relationship between ambient fine particulate matter (PM₂.₅) and blood pressure (BP) in patients with hypertension. However, few studies have explored the influence of PM₂.₅ and its constituents on Trimethylamine N-oxide (TMAO), an established risk factor for hypertension and cardiovascular disease (CVD), particularly in severely air-polluted areas. To explore the potential impact of PM₂.₅ constituents on BP, plasma hormones, and TMAO, a panel study was conducted to investigate changes in BP, plasma hormones, and TMAO in response to ambient air pollution exposure in stage 1 hypertensive young adults. Linear mixed effect models were used to estimate the cumulative effects of fine particulate matters (PM₂.₅) and its constituents on BP, plasma hormones and TMAO. We found that one interquartile range (IQR) (35 μg/m³) increase in 0–1 day moving-average PM₂.₅ concentrations was statistically significantly associated with elevated systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) with estimated values of 0.13 (95% confidence interval (CI): 0.03 to 0.23) mmHg, 0.18 (95% CI: 0.08 to 0.28) mmHg, and 0.17 (95% CI: 0.09 to 0.26) mmHg, respectively. Hormone disturbance in the renin-angiotensin-aldosterone system was also associated with PM₂.₅ exposure. Elevated TMAO levels with an IQR increase for 0–4, 0–5, 0–6 moving-average concentrations of PM₂.₅ were found, and the increased values ranged from 26.28 (95% CI: 2.92 to 49.64) to 60.78 (31.95–89.61) ng/ml. More importantly, the PM₂.₅-bound metal constituents, such as manganese (Mn), titanium (Ti), and selenium (Se) showed robust associations with elevated BP and plasma TMAO levels. This study demonstrates associations between PM₂.₅ metal constituents and increased BP, changes in plasma hormones and TMAO, in stage 1 hypertensive young adults. Source control, aiming to reduce the emission of PM₂.₅-bound metals should be implemented to reduce the risk of hypertension and CVD.

Ambient particulate air pollution is a risk factor for cardiovascular and respiratory disease, yet the biological mechanisms underlying this association are not well understood. The current study aimed to investigate the mediation role of microRNAs on the association between personal PM₂.₅ exposure and blood pressure and lung function. One hundred and twenty adults (60 truck drivers and 60 office workers) aged 18–46 years were assessed on the June 15, 2008 and at follow-up (1- to 2-weeks later). MicroRNAs were extracted from the peripheral blood samples. Compared to truck drivers, there is a significant increase in FEF₂₅₋₇₅, FEV₁, and FEV₁/FVC and a decrease in PM₂.₅ in office workers (all p < 0.05). According to the Bonferroni corrected threshold p-value < 6.81 × 10⁻⁵ (0.05/734) used, personal PM₂.₅ data showed a significant positive association with miR-644 after the adjustment for age, BMI, smoking status, and habitual alcohol use. The mediation effect of miR-644 on the association between personal PM₂.₅ exposure and FEF₂₅₋₇₅ [B (95%CI) = −1.342 (−2.810, −0.113)], PEF [B (95%CI) = -1.793 (−3.926, −0.195)], and FEV₁/FVC [B (95%CI) = −0.119‰ (−0.224‰, −0.026‰)] was significant only for truck drivers after the adjustment for covariates. There were no similar associations with blood pressure. These results demonstrate microRNAs to potentially mediate association of PM₂.₅ with lung function. Subsequent studies are needed to further elucidate the potential mechanisms of action by which the mediation effect of microRNAs is achieved with this process.

Excessive exposure to light at night (LAN) has become a serious public health concern. However, little is known about the impact of indoor LAN exposure on blood pressure, particularly among young adults. We aimed to investigate the effects of bedroom individual-level LAN exposure in real-world environment on blood pressure and hypertension among vulnerable young adults, and to evaluate the possible buffering effect of physical activity. In this cross-sectional study, a total of 400 healthy young adults aged 16–22 years were included. Bedroom LAN exposure was recorded at 1-min intervals for two consecutive nights using a TES-1339 R illuminance meter. Blood pressure was measured three times (8–11 a.m. in the physical examination day) in the seated position using an Omron HEM-7121 digital sphygmomanometer. A wrist-worn triaxial accelerometer (ActiGraph GT3X-BT) was used to assess physical activity for seven consecutive days. Each 1 lx increase of bedroom LAN intensity was associated with 0.55 mmHg-increase in SBP (95% CI: 0.15, 0.95), 0.30 mmHg-increase in DBP (95% CI: 0.06, 0.54), and 0.38 mmHg-increase in MAP (95% CI: 0.12, 0.65). Higher levels of LAN exposure were associated with increased risk of hypertension (LAN ≥ 3lx vs. LAN < 3lx: OR = 3.30, 95%CI = 1.19–9.19; LAN ≥ 5lx vs. LAN < 5lx: OR = 3.87, 95%CI = 1.37–10.98). However, these detrimental effects of bedroom LAN exposure on blood pressure and hypertension were not observed among young adults with high MVPA (≥2 h/day) level. MVPA can alleviate negative effects of bedroom LAN exposure on blood pressure and hypertension. Maintaining bedroom settings darkness at night may be an important strategy for reducing the risk of hypertension. Furthermore, for individuals living with high levels of indoor LAN exposure, regular physical activity may be a good option for preventing cardiovascular disease and hypertension.

We aimed to explore the effects of mixtures of lead and various metals on blood pressure (BP) and the odds of pre-hypertension (systolic blood pressure (SBP) 120–139 mmHg, and/or diastolic blood pressure (DBP) 80–89 mmHg) and hypertension (SBP/DBP ≥140/90 mmHg) among Chinese adults in a cross-sectional study. This study included 11,037 adults aged 18 years or older from the 2017–2018 China National Human Biomonitoring. Average BP and 13 metals (lead, antimony, arsenic, cadmium, mercury, thallium, chromium, cobalt, molybdenum, manganese, nickel, selenium, and tin) in blood and urine were measured and lifestyle and demographic data were collected. Weighted multiple linear regressions were used to estimate associations of metals with BP in both single and multiple metal models. Weighted quantile sum (WQS) regression was performed to assess the relationship between metal mixture levels and BP. In the single metal model, after adjusting for potential confounding factors, the blood lead levels in the highest quartile were associated with the greater odds of both pre-hypertension (odds ratio (OR): 1.56, 95% CI: 1.22–1.99) and hypertension (OR:1.75, 95% CI: 1.28–2.40) when compared with the lowest quartile. We also found that blood arsenic levels were associated with increased odds of pre-hypertension (OR:1.31, 95% CI:1.00–1.74), while urinary molybdenum levels were associated with lower odds of hypertension (OR:0.68, 95% CI:0.50–0.93). No significant associations were found for the other 10 metals. WQS regression analysis showed that metal mixture levels in blood were significantly associated with higher SBP (β = 1.56, P < 0.05) and DBP (β = 1.56, P < 0.05), with the largest contributor being lead (49.9% and 66.8%, respectively). The finding suggests that exposure to mixtures of metals as measured in blood were positively associated with BP, and that lead exposure may play a critical role in hypertension development.

Metals may affect adversely cardiovascular system, but epidemiological evidence on the associations of priority-controlled metals including antimony (Sb), arsenic (As), cadmium, lead, and thallium with children's blood pressure (BP) was scarce and inconsistent. We conducted two panel studies with 3 surveys across 3 seasons among 144 and 142 children aged 4–12 years in Guangzhou and Weinan, respectively. During each seasonal survey, urine samples were collected for 4 consecutive days and BP was measured on the 4th day. We obtained 786 BP values and urinary metals measurements at least once within 4 days, while 773, 596, 612, and 754 urinary metals measurements were effective on the health examination day (Lag 0), and the 1ˢᵗ, 2ⁿᵈ, and 3ʳᵈ day preceding BP measurement (Lag 1, lag 2 and lag 3), respectively. We used linear mixed-effect models, generalized estimating equations and multiple informant models to assess the associations of individual metal at each lag day and accumulated lag day (4 days averaged, lag 0–3) with BP and hypertension, and Bayesian Kernel Machine Regression to evaluate the relations of metals mixture at lag 0–3 and BP outcomes. We found Sb was positively and consistently related to systolic BP (SBP), mean arterial pressure (MAP), and odds of having hypertension within 4 days, which were the strongest at lag 0 and declined over time. And such relationships at lag 0–3 showed in a dose-response manner. Meanwhile, Sb was the only contributor to the relations of mixture with SBP, MAP, and odds of having hypertension. Also, synergistic interaction between Sb and As was significant. In addition, modification effect of passive smoking status on the association of Sb and SBP was more evident in passive smokers. Accordingly, urinary Sb was consistently and dose-responsively associated with increased BP and hypertension, of which Sb was the major contributor among children.

Particulate-filtering respirators (PFRs) have been recommended as a practical personal-level intervention to protect individuals from the health effects of particulate matter exposure. However, the cardiovascular benefits of PFRs including improvements in key surrogate endpoints remain unclear. We performed a systematic review and meta-analysis of randomized studies (wearing versus not wearing PFRs) reporting the effects on blood pressure (BP) and heart rate variability (HRV). The search was performed on January 3, 2022 to identify published papers until this date. We queried three English databases, including PubMed, Web of Science Core Collection and Scopus. Of 527 articles identified, eight trials enrolling 312 participants (mean age ± standard deviation: 36 ± 19.8; 132 female) met our inclusion criteria for analyses. Study participants wore PFRs from 2 to 48 h during intervention periods. Wearing PFRs was associated with a non-significant pooled mean difference of −0.78 mmHg (95% confidence interval [CI]: −2.06, 0.50) and −0.49 mmHg (95%CI: −1.37, 0.38) in systolic and diastolic BP (SBP and DBP). There was a marginally significant reduction of mean arterial pressure (MAP) by nearly 1.1 mmHg (95%CI: −2.13, 0.01). The use of PFRs was associated with a significant increase of 38.92 ms² (95%CI: 1.07, 76.77) in pooled mean high frequency (power in the high frequency band (0.15–0.4 Hz)) and a reduction in the low (power in the low frequency band (0.04–0.15Hz))-to-high frequency ratio [−0.14 (95%CI: −0.27, 0.00)]. Other HRV indices were not significantly changed. Our meta-analysis demonstrates modest or non-significant improvements in BP and many HRV parameters from wearing PFRs over brief periods. However, these findings are limited by the small number of trials as well as variations in experimental designs and durations. Given the mounting global public health threat posed by air pollution, larger-scale trials are warranted to elucidate more conclusively the potential health benefits of PFRs.

People use a particulate respirator in order to reduce exposure to ambient fine particulate matter (PM₂.₅). Acute exposure to PM₂.₅ is known to increase blood pressure. However, systematic reviews or meta-analyses on blood pressure-related benefits of using a particulate respirator is lacking. Therefore, we reviewed randomized crossover intervention studies on blood pressure-related effects of particulate matter respirator use. We conducted a literature review of articles found on Embase, Medline, and Cochrane library on August 31, 2020. The study outcomes were systolic and diastolic blood pressure and mean arterial pressure. A random-effect model was used in the meta-analysis. Subgroup analyses, based on age (adult < 60 years, elderly ≥ 60 years), personal PM₂.₅ exposure levels (High: ≥ 25 μg/m³, Low: < 25 μg/m³), and types of monitoring methods (ambulatory and resting blood pressure) were conducted. We identified 297 references, and seven studies were included in our systematic review. None of the studies used a sham respirator as control and complete allocation concealment and blinding were impossible. The use of a particulate respirator was associated with a −1.23 mmHg (95% confidence interval (CI): −2.53, 0.07) change in systolic blood pressure and a −1.57 mmHg (95% CI: −3.85, 0.71) change in mean arterial pressure. There were significant heterogeneities and possibilities for publication bias. The subgroup analyses revealed that studies involving elderly individuals, those conducted in high PM₂.₅ personal exposure, and those in which resting blood pressure was monitored demonstrated a larger decrease in blood pressure resulting from respirator use. Further intervention studies with a large sample size and subjects with diverse characteristics and different personal PM₂.₅ levels may add the evidence to current literature.

Numerous studies have established that acute or chronic exposure to environmental pollutants like particulate matter (PM) leads to the development of accelerated aging related pathologies including pulmonary and cardiovascular diseases, and thus air pollution is one of the major global threats to human health. Air pollutant particulate matter 2.5 (PM₂.₅)-induced cellular dysfunction impairs tissue homeostasis and causes vascular and cardiopulmonary damage. To test a hypothesis that elevated plasminogen activator inhibitor-1 (PAI-1) levels play a pivotal role in air pollutant-induced cardiopulmonary pathologies, we examined the efficacy of a drug-like novel inhibitor of PAI-1, TM5614, in treating PM₂.₅-induced vascular and cardiopulmonary pathologies. Results from biochemical, histological, and immunohistochemical studies revealed that PM₂.₅ increases the circulating levels of PAI-1 and thrombin and that TM5614 treatment completely abrogates these effects in plasma. PM₂.₅ significantly augments the levels of pro-inflammatory cytokine interleukin-6 (IL-6) in bronchoalveolar lavage fluid (BALF), and this also can be reversed by TM5614, indicating its efficacy in amelioration of PM₂.₅-induced increases in inflammatory and pro-thrombotic factors. TM5614 reduces PM₂.₅-induced increased levels of inflammatory markers cluster of differentiation 107 b (Mac3) and phospho-signal transducer and activator of transcription-3 (pSTAT3), adhesion molecule vascular cell adhesion molecule 1 (VCAM1), and apoptotic marker cleaved caspase 3. Longer exposure to PM₂.₅ induces pulmonary and cardiac thrombosis, but TM5614 significantly ameliorates PM₂.₅-induced vascular thrombosis. TM5614 also reduces PM₂.₅-induced increased blood pressure and heart weight. In vitro cell culture studies revealed that PM₂.₅ induces the levels of PAI-1, type I collagen, fibronectin (Millipore), and sterol regulatory element binding protein-1 and 2 (SREBP-1 and SREBP-2), transcription factors that mediate profibrogenic signaling, in cardiac fibroblasts. TM5614 abrogated that stimulation, indicating that it may block PM₂.₅-induced PAI-1 and profibrogenic signaling through suppression of SREBP-1 and 2. Furthermore, TM5614 blocked PM₂.₅-mediated suppression of nuclear factor erythroid related factor 2 (Nrf2), a major antioxidant regulator, in cardiac fibroblasts. Pharmacological inhibition of PAI-1 with TM5614 is a promising therapeutic approach to control air pollutant PM₂.₅-induced cardiopulmonary and vascular pathologies.

Exposure to air pollution has been linked to elevated blood pressure (BP) and hypertension, but most research has focused on short-term (hours, days, or months) exposures at relatively low concentrations. We examined the associations between long-term (3-year average) concentrations of outdoor PM₂.₅ and household air pollution (HAP) from cooking with solid fuels with BP and hypertension in the Prospective Urban and Rural Epidemiology (PURE) study. Outdoor PM₂.₅ exposures were estimated at year of enrollment for 137,809 adults aged 35–70 years from 640 urban and rural communities in 21 countries using satellite and ground-based methods. Primary use of solid fuel for cooking was used as an indicator of HAP exposure, with analyses restricted to rural participants (n = 43,313) in 27 study centers in 10 countries. BP was measured following a standardized procedure and associations with air pollution examined with mixed-effect regression models, after adjustment for a comprehensive set of potential confounding factors. Baseline outdoor PM₂.₅ exposure ranged from 3 to 97 μg/m³ across study communities and was associated with an increased odds ratio (OR) of 1.04 (95% CI: 1.01, 1.07) for hypertension, per 10 μg/m³ increase in concentration. This association demonstrated non-linearity and was strongest for the fourth (PM₂.₅ > 62 μg/m³) compared to the first (PM₂.₅ < 14 μg/m³) quartiles (OR = 1.36, 95% CI: 1.10, 1.69). Similar non-linear patterns were observed for systolic BP (β = 2.15 mmHg, 95% CI: −0.59, 4.89) and diastolic BP (β = 1.35, 95% CI: −0.20, 2.89), while there was no overall increase in ORs across the full exposure distribution. Individuals who used solid fuels for cooking had lower BP measures compared to clean fuel users (e.g. 34% of solid fuels users compared to 42% of clean fuel users had hypertension), and even in fully adjusted models had slightly decreased odds of hypertension (OR = 0.93; 95% CI: 0.88, 0.99) and reductions in systolic (−0.51 mmHg; 95% CI: −0.99, −0.03) and diastolic (−0.46 mmHg; 95% CI: −0.75, −0.18) BP. In this large international multi-center study, chronic exposures to outdoor PM₂.₅ was associated with increased BP and hypertension while there were small inverse associations with HAP.

Epidemiological studies and animal experiments have suggested that exposure to Di-(2-ethylhexyl) phthalate (DEHP) is strongly associated with an increase in blood pressure. However, the mechanisms that result in the detrimental effects of DEHP exposure on blood pressure are unclear. In our study, mice were orally exposed to DEHP dosages of 0.1, 1, 10 mg/kg/day for 6 weeks. The results showed that DEHP could induce a significant increase in systolic blood pressure (SBP) and heart rate, and a significant thickening of the ventricular wall. To explore the underlying mechanism, we measured the level of: angiotensin converting enzyme (ACE); bradykinin B2 receptor (BK2R); endothelial nitric oxide synthase (eNOS); bradykinin and Ca²⁺ in cardiac cytoplasm as well as in serum nitric oxide (NO). The results suggested that DEHP could induce an increase in ACE levels, and a decrease in bradykinin levels. Moreover, BK2R, Ca²⁺, eNOS and NO decreased when mice were exposed to 10 mg/kg/day DEHP. Interestingly, 5 mg/kg/day angiotensin converting enzyme inhibitor (ACEI) treatment inhibited the increase in blood pressure, and inhibited the decrease in the levels of BK2R, Ca²⁺, eNOS, and NO, that were induced by DEHP exposure. Our results suggest that DEHP might increase blood pressure by activating ACE expression, and inhibiting the bradykinin-NO pathway.