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.

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.

People with chronic obstructive pulmonary disease, cardiovascular disease, or hypertension have a high risk of developing severe coronavirus disease 2019 (COVID-19) and of COVID-19 mortality. However, the association between long-term exposure to air pollutants, which increases cardiopulmonary damage, and vulnerability to COVID-19 has not yet been fully established. We collected data of confirmed COVID-19 cases during the first wave of the epidemic in mainland China. We fitted a generalized linear model using city-level COVID-19 cases and severe cases as the outcome, and long-term average air pollutant levels as the exposure. Our analysis was adjusted using several variables, including a mobile phone dataset, covering human movement from Wuhan before the travel ban and movements within each city during the period of the emergency response. Other variables included smoking prevalence, climate data, socioeconomic data, education level, and number of hospital beds for 324 cities in China. After adjusting for human mobility and socioeconomic factors, we found an increase of 37.8% (95% confidence interval [CI]: 23.8%–52.0%), 32.3% (95% CI: 22.5%–42.4%), and 14.2% (7.9%–20.5%) in the number of COVID-19 cases for every 10-μg/m³ increase in long-term exposure to NO₂, PM₂.₅, and PM₁₀, respectively. However, when stratifying the data according to population size, the association became non-significant. The present results are derived from a large, newly compiled and geocoded repository of population and epidemiological data relevant to COVID-19. The findings suggested that air pollution may be related to population vulnerability to COVID-19 infection, although the extent to which this relationship is confounded by city population density needs further exploration.

We used real-world exposure scenarios to evaluate the effect of six ambient air pollutant (PM₂.₅, PM₁₀, NO₂, SO₂, CO, and O₃) exposure on renal function among older adults without chronic kidney disease (CKD). We recruited 169 older adults without CKD in Beijing, China, for a longitudinal study from 2016 to 2018. The Modification of Diet in Renal Disease (MDRD) and the Chronic Kidney Disease Epidemiology Collaboration (EPI) equations were employed to derive the estimated glomerular filtration rate (eGFR). A linear mixed-effects model with random intercepts for participants was employed to determine the effects of air pollutants on renal function evaluated on the basis of eGFR and urinary albumin/creatinine ratio at different exposure windows (1-, 2-, 3-, 5-, 7-, 14-, 28-, 45-, and 60-days moving averages). An interquartile range (IQR) increase in NO₂ for was associated with significant decreases of in eGFR (MDRD equation) [percentage changes: −4.49 (95% confidence interval: −8.44, −0.37), −5.51 (−10.43, −0.33), −2.26 (−4.38, −0.08), −3.71 (−6.67, −0.65), −5.44 (−9.58, −1.11), −5.50 (−10.24, −0.51), −6.15 (−10.73, −1.33), and −6.34 (−11.17, −1.25) for 1-, 2-, 5-, 7-, 14-, 28-, 45-, and 60-days moving averages, respectively] and in eGFR (EPI equation) [percentage changes: −5.04 (−7.09, −2.94), −6.25 (−8.81, −3.62), −5.16 (−7.34, −2.92), −5.10 (−7.85, −2.28), −5.83 (−8.23, −3.36), −6.04 (−8.55, −3.47) for 1-, 2-, 14-, 28-, 45-, and 60-days moving averages, respectively]. In two-pollutant model, only the association of NO₂ exposure with eGFR remained robust after adjustment for any other pollutant. This association was stronger for individuals with hypertension for the EPI equation or BMI <25 kg/m² for the MDRD equation at lags 1 and 1–2. Our findings suggest that NO₂ exposure is associated with eGFR reduction among older adults without CKD for short (1-, 2-days) and medium (14-, 28-, 45-, 60-days) term exposure periods; thus, NO₂ exposure may contribute to renal impairment.

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.

Data (N = 10644) for US adults aged ≥20 years for 2003–2016 from National Health and Nutrition Examination Survey were analyzed to evaluate the impact of co-occurrence of obesity with diabetes, anemia, albuminuria, and hypertension on concentrations of five perfluoroalkyl acids (PFAA), namely, perfluorooctanoic acid (PFOA), perfluorooctane sulfonic acid (PFOS), perfluorodecanoic acid (PFDA), perfluorohexane sulfonic acid (PFHxS), and perfluorononanoic acid (PFNA). For the total population, males, and females, co-occurrence of obesity with hypertension, albuminuria, anemia, and diabetes was found to be associated with lower adjusted geometric means (AGM) than nonobese for every PFAA. For example for females, for PFOS, AGMs for obese with no diseases, hypertension, albuminuria, anemia, and diabetes were 8.2, 10.8, 5.8, 4.6, and 7.7 ng/mL respectively. In comparison, for PFOS, for nonobese females, AGMs for those with no diseases, hypertension, albuminuria, anemia, and diabetes were found to be 8.9, 13.4, 7.7, 6.0, and 10.2 ng/mL respectively. This implies obesity is associated with higher excretion rates. Females, in general, had lower AGMs than males for both obese and nonobese for every PFAA for every disease group. For example, percent ratios of obese females to males AGMs for PFOA were 66.7%, 87.1%, 88.2%, 70.6%, and 90% for those with no diseases, hypertension, albuminuria, anemia, and diabetes respectively. The ratios of obese to nonobese AGMs for females were lower than males for every PFAA for those with no diseases and hypertension only. For example, for PFOA for those with no diseases, obese to nonobese AGM ratios were 87% for females and 100% for males. Thus, additional excretion of certain PFAAs due to obesity is higher in females than males for those with no diseases and hypertension only.

Metabolic syndrome is an important risk factor for non-communicable diseases, particularly type 2 diabetes, coronary heart disease, and stroke. Long-term exposure to greenspace could be protective of metabolic syndrome, but evidence for such an association is lacking. Accordingly, we investigated the association between long-term exposure to greenspace and risk of metabolic syndrome.The present longitudinal study was based on data from four clinical examinations between 1997 and 2013 in 6076 participants of the Whitehall II study, UK (aged 45–69 years at baseline). Long-term exposure to greenspace was assessed by satellite-based indices of greenspace including Normalized Difference Vegetation Index (NDVI) and Vegetation Continuous Field (VCF) averaged across buffers of 500 and 1000 m surrounding the participants’ residential location at each follow-up. The ascertainment of metabolic syndrome was based on the World Health Organization (WHO) definition. Hazard ratios for metabolic syndrome were estimated using Cox proportional hazards regression models, controlling for age, sex, ethnicity, lifestyle factors, and socioeconomic status.Higher residential surrounding greenspace was associated with lower risk of metabolic syndrome. An interquartile range increase in NDVI and VCF in the 500 m buffer was associated with 13% (95% confidence interval (CI): 1%, 23%) and 14% (95% CI: 5%, 22%) lower risk of metabolic syndrome, respectively. Greater exposure to greenspace was also associated with each individual component of metabolic syndrome, including a lower risk of high levels of fasting glucose, large waist circumference, high triglyceride levels, low HDL cholesterol, and hypertension. The association between residential surrounding greenspace and metabolic syndrome may have been mediated by physical activity and exposure to air pollution.The findings of the present study suggest that middle-aged and older adults living in greener neighbourhoods are at lower risk of metabolic syndrome than those living in neighbourhoods with less greenspace.

Multiple cross-sectional studies indicated an association between hypertension and road traffic noise and they were recently synthetized in a WHO systematic evidence review. However, recent years have seen a growing body of high-quality, large-scale research, which is missing from the WHO review. Therefore, we aimed to close that gap by conducting an updated systematic review and meta-analysis on the exposure-response relationship between residential road traffic noise and the risk of hypertension in adults. Studies were identified by searching MEDLINE, EMBASE, the Internet, conference proceedings, reference lists, and expert archives in English, Russian, and Spanish through August 5, 2017. The risk of bias for each extracted estimate and the overall quality of evidence were evaluated using a list of predefined safeguards against bias related to different study characteristics and the Grading of Recommendations Assessment, Development and Evaluation system, respectively. The inverse variance heterogeneity (IVhet) model was used for meta-analysis. The possibility of publication bias was evaluated by funnel and Doi plots, and asymmetry in these was tested with Egger's test and the Luis Furuya-Kanamori index, respectively. Sensitivity analyses included leave-one-out meta-analysis, subgroup meta-analysis with meta-regressions, and non-linear exposure-response meta-analysis. Based on seven cohort and two case-control studies (n = 5 514 555; 14 estimates; Lden range ≈ 25–90 dB(A)), we found “low” evidence of RR per 10 dB(A) = 1.018 (95% CI: 0.984, 1.053), moderate heterogeneity (I2 = 46%), and no publication bias. In the subgroup of cohort studies, we found “moderate” evidence of RR per 10 dB(A) = 1.018 (95% CI: 0.987, 1.049), I2 = 31%, and no publication bias. In conclusion, residential road traffic noise was associated with higher risk of hypertension in adults, but the risk was lower than previously reported in the systematic review literature.