Although road traffic noise is the most important source of environmental noise emission in large cities, little is known about health burden. The present study was conducted to estimate the burden of diseases attributed to traffic noise in the metropolis of Tehran in 2017. Using noise maps provided by the municipality of Tehran, we calculated population exposure distribution in term of Ldₙ and Lₙᵢgₕₜ and the number of DALYs lost due to ischemic heart disease, hypertension, high sleep disturbance, annoyance and stroke endpoints based on the World Health Organization Environmental Noise Guidelines for the European Region. We applied published dose-response functions to estimate the traffic noise burden for high sleep disturbance and annoyance. We estimated 61,284 DALYs or 697 DALYs per 100,000 population attributed to traffic noise in Tehran for the reference year 2017. Highly sleep disturbance with a share of 58.74% of the DALYs was recognized as the most important contributor of disease burden, and noise annoyance with a share of 23.12% was ranked next. Ischemic heart disease (11.71%), stroke (5.12%), and hypertension (1.31%) were ranked third to fourth, respectively, in terms of the burden of disease caused by environmental noise. A considerable fraction of the population of Tehran lives in areas with an environmental noise higher than the standard level. The findings showed that traffic noise pollution is an important environmental risk factor in Tehran imposes the greatest burden on the community, mainly through highly sleep disturbance and noise annoyance endpoints.

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.

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.

Recent studies suggested that long-term exposure to fine particulate matter (PM₂.₅) was related to a higher risk of dementia incidence or hospitalizations in western populations, but the evidence is limited in Asian cities. Here we explored the link between long-term PM₂.₅ exposure and dementia incidence in the Hong Kong population and whether it varied by population sub-group. We utilized a Hong Kong Chinese cohort of 66,820 people aged ≥65 years who were voluntarily enrolled during 1998–2001 and were followed up to 2011. Prevalent dementia cases were excluded based on the face-to-face interview at baseline. We ascertained the first occurrence of hospitalization for all-cause dementia and major subtypes during the follow-up period. We assessed PM₂.₅ concentrations using a satellite data-based model with a 1 × 1 km² resolution on the residential address. Cox proportional hazards models were adopted to estimate associations of annual mean PM₂.₅ exposure with dementia incidence, adjusting for potential confounders. We identified 1183 incident cases of all-cause dementia during the follow-up period, of which 655 (55.4%) were cases of Alzheimer’s disease, and 334 (28.2%) were those of vascular dementia. We found a positive association between annual mean PM₂.₅ exposure and all-cause dementia incidence in the fully adjusted model. The estimated hazard ratio was 1.06 (95% confidence interval (CI): 1.00, 1.13) per every 3.8 μg/m³ increase in annual mean PM₂.₅ exposure. And the estimated HRs for Alzheimer’s disease and vascular dementia were 1.03 (95% CI: 0.94, 1.12) and 1.09 (95% CI: 0.98, 1.22), respectively. We did not find effect modifications by age, sex, BMI, hypertension, diabetes, or heart disease on the associations. Results suggest that long-term exposure to PM₂.₅ is associated with a higher risk of dementia incidence in the Asian population.

Data from National Health and Nutrition Examination Survey for 2003–2014 for US children aged 6–11 years (N = 2097), adolescents aged 12–19 ears (N = 2642), and adults aged ≥ 20 years (N = 9170) were analyzed to investigate the effects of dietary, demographic, disease, lifestyle, and other factors on concentrations of nine metabolites of polycyclic aromatic hydrocarbons (PAH) in urine. PAHs analyzed were: 1-hydroxynaphthalene, 2-hydroxynaphthalene, 2-hydroxyfluorene, 3-hydroxyfluorene, 9-hydroxyfluorene, 1-hydroxyphenanthrene, 2-hydroxyphenanthrene, 3-hydroxyphenanthrene, and 1-hydroxypyrene. Adults with diabetes were found to have higher adjusted levels of 1-hydroxynaphthalene (4139 vs. 3622 ng/L, p < 0.01) than nondiabetics. Adults with albuminuria had higher adjusted levels of 1-hydroxynaphthalene (4140 vs.3621 ng/L, p < 0.01) and 2-hydroxynaphthalene (6039 vs. 5468 ng/L, p < 0.01) than those without albuminuria. Children with albuminuria had lower adjusted levels of 9-hydroxyfluorene (162 vs. 187 ng/L, p = 0.04), 1-hydroxyphenanthrene (92 vs. 108 ng/L, p < 0.01), and 1-hydroxypyrene (118 vs. 138 ng/L, p < 0.01) than those without albuminuria. The ratios of smoker to nonsmoker adjusted levels for adults varied from a low of 1.4 for 2-hydroxyphenanthrene to a high of 5.6 for 3-hydroxyfluorene. Exposure to environmental tobacco smoke at home was associated with higher levels of most OH-PAHs among children, adolescents, and adults. Consumption of red meat not processed at high temperatures was associated with increased levels of 1-hydroxypyrene (β = 0.00040, p = 0.01), 1-, 2-, and 3-hydroxyphenanthrene, 3-, and 9-hydroxyfluorene. Consumption of red meat processed at high temperatures was associated with increased levels of 2-hydroxynaphthalene (β = 0.00046, p = 0.02) among adults. Consumption of fish processed at high temperatures was associated with decreased levels of 1-hydroxynaphtahlene (β = − 0.00088, p < 0.01), 2-, 3-, and 9-hydroxyfluorene, 1-, 2-, and 3-hydroxyphenanthrene. Among adults, alcohol consumption and caffeine may be associated with increased levels of certain OH-PAHs. Oxidative stress and inflammation associated with exposure to PAHs are associated with albuminuria and have the potential to lead to the development of diabetes.

The knowledge about the effects of environmental temperature on human epigenome is a potential key to understand the health impacts of temperature and to guide acclimation under climate change. We performed a systematic review on the epidemiological studies that have evaluated the association between environmental temperature and human epigenetic modifications. We identified seven original articles on this topic published between 2009 and 2019, including six cohort studies and one cross-sectional study. They focused on DNA methylation in elderly people (blood sample) or infants (placenta sample), with sample size ranging from 306 to 1798. These studies were conducted in relatively low temperature setting (median/mean temperature: 0.8–13 °C), and linear models were used to evaluate temperature-DNA methylation association over short period (≤28 days). It has been reported that short-term ambient temperature could affect global human DNA methylation. A total of 15 candidate genes (ICAM-1, CRAT, F3, TLR-2, iNOS, ZKSCAN4, ZNF227, ZNF595, ZNF597, ZNF668, CACNA1H, AIRE, MYEOV2, NKX1-2 and CCDC15) with methylation status associated with ambient temperature have been identified. DNA methylation on ZKSCAN4, ICAM-1 partly mediated the effect of short-term cold temperature on high blood pressure and ICAM-1 protein (related to cardiovascular events), respectively. In summary, epidemiological evidence about the impacts of environment temperature on human epigenetics remains scarce and limited to short-term linear effect of cold temperature on DNA methylation in elderly people and infants. More studies are needed to broaden our understanding of temperature related epigenetic changes, especially under a changing climate.

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.

Cardiovascular diseases (CVD) are leading global health issue. More studies have linked indoor air pollution from solid fuel usage to hypertension risk, a leading risk factor for CVD. We conducted a systematic review and meta-analysis of observational studies assessing the relationship of indoor air pollution from solid fuel with hypertension risk. Using a protocol standardized a priori, two independent reviewers searched PubMed, the Cochrane Library, Ovid MEDLINE, Web of Science and EMBASE for available studies published before Dec.1, 2019. A random effects model was used to analyse the pooled results. Out of 3740 articles, 47 were reviewed in depth and 11 contributing to this meta-analysis. The use of household solid fuel was significantly associated with an increased risk of hypertension (OR = 1.52, 95% CI = 1.26 to 1.85). The smoking-controlled group (OR = 2.38, 95% CI = 1.58 to 3.60) had greater effect size of hypertension than the uncontrolled group (OR = 1.11, 95% CI = 1.10 to 1.11). These findings implicate that indoor air pollution from solid fuel may be an important risk factor for hypertension.

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.

Epidemiological studies have demonstrated association between the total mass of fine particulate matter (PM2.5) exposures and inflammation. There are few studies exploring the associations between PM2.5 constituents and the biomarkers of inflammation in older adults and the underlying biological mechanisms are not exact. In this study, we examined the associations between PM2.5 and its constituents (organic carbon (OC), elemental carbon (EC), total carbon (TC), polycyclic aromatic hydrocarbons (PAHs) and complement three factor (C3), an important biomarker of inflammation in a repeated panel of 175 older adults in Beijing, China. We have constructed three different linear mixed effect models (single-pollutant model, constituent-PM2.5 joint model, and constituent-residual model) to evaluate the association of PM2.5 and its constituents and complement C3, controlling for concentration of high sensitive C-reactive protein (hs-CRP), day of week, mean temperature, relative humidity, location and potential individual confounders. We found robust positive associations of OC, EC, TC, PAHs and PM2.5 mass concentration with complement C3 at different lag patterns. The cumulative effects of pollutants increased across average of 2–5 days. Individuals aged 65 and above, or with diabetes, or BMI ≥30, or with no-cardiopathy, or with hypertension also exhibited positive associations between PM2.5 and complement C3. The results revealed that short-term exposure to PM2.5 and its constituents could result in a significant increase in serum level of complement C3. These findings suggested a possible involvement of complement C3 in the effect of PM2.5 on inflammatory reaction.