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.

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.

Exposure to fine particulate matter (PM₂.₅) was associated with altered heart rate variability (HRV). However, whether blood pressure (BP) control and angiotensin II receptor blocker (ARB) treatment modifies the associations was seldom addressed. Therefore, we conducted a 3-phase panel study among 282 hypertensive subjects aged 35–74 years in four cities of China to address this issue. Real-time personal PM₂.₅ sampling and 24-h ambulatory electrocardiogram monitoring were performed repeatedly in 3 different seasons. Linear mixed-effects models were fitted overall and by control status of BP and ARB treatment to assess the associations between short-term PM₂.₅ exposure and HRV. The average hourly PM₂.₅ concentrations (Mean ± SD) ranged from 19.3 ± 18.2 μg/m³ to 99.4 ± 76.9 μg/m³ across study phases and cities. Generally, PM₂.₅ exposure was associated with decreased hourly and 24-h HRV. However, these adverse impacts were attenuated among patients with controlled BP (<140/90 mmHg). For each 10 μg/m³ increment in moving average of previous 2 days' (MA2d) PM₂.₅ exposure, 24-h SDNN (standard deviation of NN intervals) and rMSSD (root mean square of successive RR interval differences) decreased by 0.89% (95% CI: 0.19%–1.59%) and 2.98% (95% CI: 1.04%–4.89%) among patients with uncontrolled BP (≥140/90 mmHg), whereas no obvious declines were observed among those with controlled BP (Pdᵢffₑᵣₑₙcₑ = 0.007 and 0.022, respectively). Furthermore, ARB treatment alleviated or eliminated PM₂.₅-associated declines in hourly and 24-h HRV among those with uncontrolled BP. For instance, 24-h SDNN decreased by 1.31% (95% CI: 0.54%–2.07%) with a 10 μg/m³ increment in lag 2 days’ PM₂.₅ exposure in ARB nonusers, whereas no obvious changes were observed in ARB users (Pdᵢffₑᵣₑₙcₑ = 0.021). In conclusion, although PM₂.₅ exposure would decrease HRV, better BP control and ARB treatment could attenuate these adverse impacts, which provides supporting evidence for alleviating autonomic dysfunction of hypertension patients living in areas with high-level PM₂.₅.

Exposure to traffic-related air pollution (TRAP) may enhance the risk of cardiovascular disease. However, the short-term effects of TRAP components on the cardiovascular system are not well understood. We conducted a randomized, double-blinded, crossover intervention study in which 39 healthy university students spent 2 h next to a busy road. Participants wore a powered air-purifying respirator (PAPR) or an N95 mask. PAPRs were equipped with a filter for particulate matter (PM), a PM and volatile organic compounds (VOCs) filter or a sham filter. Participants were blinded to PAPR filter type and underwent randomized exposures four times, once for each intervention mode. Blood pressure (BP), heart rate (HR) and heart rate variability (HRV) were measured before, during and for 6 h after the roadside exposure. Linear mixed-effect models were used to evaluate the effects of the interventions relative to baseline controlling for other covariates. All HRV measures increased during and following exposure for all intervention modes. Some HRV measures (SDNN and rMSSD during exposure and SDNN after exposure) were marginally affected by PM filtration. Wearing the N95 mask affected VLF power and rMSSD responses to traffic exposure differently than the PAPR interventions. Both systolic and diastolic BP increased slightly during exposure, but then were generally lower than baseline after exposure for the sham and filter interventions. HR, which fell during exposure and mostly remained lower than baseline after exposure, was lower yet with all filter interventions compared to the sham mode following exposure. Therefore, short-term exposure to traffic acutely affects HRV, BP and HR, but N95 mask and PAPR interventions generally show little efficacy in reducing these effects. Removing the PM component of TRAP has some limited effects on HRV responses to exposure but exaggerates the traffic-related decrease in HR. HRV findings from N95 mask interventions need to be interpreted cautiously.

MicroRNAs (miRNAs) are a class of small, non-coding RNAs with a post-transcriptional regulatory function on gene expression and cell processes, including proliferation, apoptosis and differentiation. In recent decades, miRNAs have attracted increasing interest to explore the role of epigenetics in response to air pollution. Air pollution, which always contains kinds of particulate matters, are able to reach respiratory tract and blood circulation and then causing epigenetics changes. In addition, extensive studies have illustrated that miRNAs serve as a bridge between particulate matter exposure and health-related effects, like inflammatory cytokines, blood pressure, vascular condition and lung function. The purpose of this review is to summarize the present knowledge about the expression of miRNAs in response to particulate matter exposure. Epidemiological and experimental studies were reviewed in two parts according to the size and source of particles. In this review, we also discussed various functions of the altered miRNAs and predicted potential biological mechanism participated in particulate matter-induced health effects. More rigorous studies are worth conducting to understand contribution of particulate matter on miRNAs alteration and the etiology between environmental exposure and disease development.

Epidemiological studies have investigated the associations of bisphenol A (BPA) exposure with hypertension risk or blood pressure levels, but findings are inconsistent. Furthermore, the association between its alternatives bisphenol S and F (BPS and BPF) and hypertension risk are not yet known. We conducted a cross-sectional study in 1437 eligible participants without hypertension-related diseases, with complete data about blood pressure levels, hypertension diagnosis, and urinary bisphenols concentrations. Multivariable logistic and linear models were respectively applied to examine the associations of urinary bisphenols concentrations with hypertension risk and blood pressure levels. The dose-response relationship was explored by the restricted cubic spline model. Compared with the reference group of BPA, individuals in the middle and high exposure group had an adjusted odds ratio (OR) of 1.30 and 1.40 for hypertension, had a 3.08 and 2.82 mm Hg higher systolic blood pressure (SBP) levels, respectively, with an inverted “U” shaped dose-response relationship. Compared with the reference group of BPS, individuals in the second and third tertile had an adjusted OR of 1.49 and 1.48 for hypertension, had a 2.61 and 3.89 mm Hg increased levels of SBP, respectively, with a monotonic curve. No significant associations of BPF exposure with hypertension risk or blood pressure levels were found. BPA and BPS exposure were suggested to be associated with increased hypertension risk and blood pressure levels, with different dose-response relationships. Our findings have important implications for public health but require confirmation in prospective studies.

Ambient fine particulate matter (PM2.5) pollution has been implicated in the development of hypertensive disorders of pregnancy. However, evidence on the effects of PM2.5-derived chemical constituents on gestational blood pressure (BP) is limited, and the potential mechanisms underlying the association remain unclear. In this study, we repeated three consecutive 72-h personal air sampling and BP measurements in 215 pregnant women for 590 visits during pregnancy. Individual PM2.5 exposure level was assessed by gravimetric method and 28 PM2.5 chemical constituents were analyzed by ED-XRF method. Plasma biomarkers of endothelial function and inflammation were measured using multiplexed immunoassays. Robust multiple linear regression models were used to estimate the associations among personal PM2.5 exposure and chemical constituents, BP changes (compared with pre-pregnancy BP) and plasma biomarkers. Mediation analyses were performed to evaluate underlying potential pathways. Result showed that exposure to PM2.5 was significantly associated with increases in systolic blood pressure (SBP), diastolic blood pressure (DBP) and mean arterial pressure (MAP) in the early second trimester. Meanwhile, elevated concentration of lead (Pb) constituent in PM2.5 was significant associated with increases in DBP and MAP after adjusting for PM2.5 total mass. PM2.5 and Pb constituent also presented positive associations with plasma biomarkers of endothelial function (ET-1, E-selectin, ICAM-1) and inflammation (IL-1β, IL-6, TNFα) significantly. After multiple adjustment, elevated ET-1 and IL-6 were significantly correlated with increased gestational BP, and respectively mediated 1.24%–25.06% and 7.01%–10.69% of the increased BP due to PM2.5 and Pb constituent exposure. In conclusion, our results suggested that personal exposure to PM2.5 and Pb constituent were significantly associated with increased BP during pregnancy, and the early second trimester might be the sensitive window of PM2.5 exposure. The endothelial dysfunction and elevated inflammation partially mediated the effect of PM2.5 and Pb constituent on BP during pregnancy.

The effects of exposure to some environmental chemicals on blood pressure have been determined, but the association between non-occupational exposure to perfluoroalkyl substances (PFASs) and blood pressure in adolescents remains unknown. The association between blood pressure and PFAS concentrations was studied by analysing data from 2251 participants filtered from the population enrolled in the National Health and Nutrition Examination Survey (NHANES) from 2003 to 2012. After adjusting for age, sex, race, BMI, cotinine level, dietary intake of calcium, caloric intake, sodium consumption, potassium consumption and sampling year, we estimated the coefficients (betas) and 95% confidence intervals (CIs) for the relationship between PFAS concentrations and blood pressure with multiple linear regression models. Potential non-linear relationships were assessed with restricted cubic spline models. Blood levels of perfluorooctane sulfonic acid (PFOS) had a strong positive association with diastolic blood pressure (DBP) in adolescents in the linear model, while the result was not significant in the non-linear model. No significant association was observed between the concentration of any other PFASs and blood pressure. According to the fully adjusted linear regression model (P = 0.041), the mean DBP values in boys in the higher PFOS quintile were 2.70% greater than the mean DBP values of boys in the lowest PFOS quintile. Furthermore, serum PFOS concentrations predominantly affected blood pressure in male adolescents compared with female adolescents. These results provide epidemiological evidence of PFOS-related increases in DBP. Further research is needed to address related issues.

Metal pollution is a severe environmental issue in China, which has been recently linked with the risk of hypertension. However, relevant epidemiological studies are limited. The present exploratory study was conducted to assess the associations of environmental exposure to metals with the odds of hypertension as well as blood pressure (BP) levels using urine samples in a Chinese general population. From May 2016 to April 2017, a total of 823 eligible participants were consecutively enrolled in our study in Wuhan, China. Hypertension was defined as systolic BP (SBP) of ≥140 mmHg or diastolic BP (DBP) of ≥90 mmHg, a self-reported physician diagnosis, or current use of antihypertensive medication. We used urine samples as biomarkers to reflect the levels of environmental exposure to 20 metals. Multivariable regression models were applied to assess the potential association. Multi-metal models were conducted to investigate the impacts of co-exposure to various metals. Based on the results from various models, positive trends for increased odds of hypertension with increasing quartiles of vanadium (V), iron (Fe), zinc (Zn) and selenium (Se) were suggested. Compared with those in the lowest quartiles, participants in the highest quartiles of V, Fe, Zn and Se had a 4.4-fold, 4.9-fold, 4.2-fold and 2.5-fold increased odds of having hypertension, respectively. High urinary Hg level was found to increase the levels of DBP. Individuals in the highest group of Hg were found to have a 4.3 mmHg higher level of DBP. Our findings suggest that environmental exposure to V, Fe, Zn, Se and Hg might increase the risk of hypertension or elevate the levels of BP. These findings warrant further prospective studies in a larger population.

The effect of ambient air pollution exposure on childhood hypertension has emerged as a concern in China, and previous studies suggested pet ownership is associated with lower blood pressure (BP). However, limited information exists on the interactive effects pet ownership and air pollution exposure has on hypertension. We investigated the interactions between exposure to pet ownership and air pollutants on hypertension in Chinese children. 9354 students in twenty-four elementary and middle schools (aged 5–17 years) in Northeastern China were evaluated during 2012–2013. Four-year average concentrations of particulate matter with aerodynamic diameter of ≤10 μm (PM10), SO2, NO2, and O3, were collected in the 24 districts from 2009 to 2012. Hypertension was defined as average diastolic or systolic BP (three time measurements) in the 95th percentile or higher based on height, age, and sex. To examine effects, two-level regression analysis was used, controlling covariates. Consistent interactions between exposure to pet and air pollutants were observed. Compared to children exposed to pet, those not exposed exhibited consistently stronger effects of air pollution. The highest odds ratios (ORs) per 30.6 μg/m3 increase in PM10 were 1.79 (95%confidence interval [95%CI]: 1.29–2.50) in children without current pet exposure compared to 1.24 (95%CI: 0.85–1.82) in children with current pet exposure. As for BP, only O3 had an interaction for all exposure to pet ownership types, and showed lower BP in children exposed to pet. The increases in mean diastolic BP per 46.3 μg/m3 increase in O3 were 0.60 mmHg (95%CI: 0.21, 0.48) in children without pet exposure in utero compared with 0.34 mmHg (95%CI: 0.21, 0.48) in their counterparts. When stratified by age, pet exposure was more protective among younger children. In conclusion, in this large population-based cohort, pet ownership is associated with smaller associations between air pollution and hypertension in children, suggesting pet ownership reduces susceptibility to the health effects of pollutants.