While the health impacts of larger particulate matter, such as PM₁₀ and PM₂.₅, have been studied extensively, research regarding ultrafine particles (UFPs or PM₀.₁) and particle surface area concentration (PSC) is lacking. This case-crossover study assessed the associations between exposure to PSC and UFP number concentration (UFPnc) and hospital admissions for cardiovascular diseases (CVDs) in New York State (NYS), 2013–2018. We used a time-stratified case-crossover design to compare the PSC and UFPnc levels between hospitalization days and control days (similar days without admissions) for each CVD case. We utilized NYS hospital discharge data to identify all CVD cases who resided in NYS. UFP simulation data from GEOS-Chem-APM, a state-of-the-art chemical transport model, was used to define PSC and UFPnc. Using a multi-pollutant model and conditional logistic regression, we assessed excess risk (ER)% per inter-quartile change of PSC and UFPnc after controlling for meteorological factors, co-pollutants, and time-varying variables. We found immediate and lasting associations between PSC and overall CVDs (lag0–lag0-6: ERs% (95% CI%) ranges: 0.4 (0.1,0.7) - 0.9 (0.7–1.2), and delayed and prolonged ERs%: 0.1–0.3 (95% CIs: 0.1–0.5) between UFPnc and CVDs (lag0-3–lag0-6). Exposure to larger PSC was associated with immediate ER increases in stroke, hypertension, and ischemic heart diseases (1.1%, 0.7%, 0.8%, respectively, all p < 0.05). The adverse effects of PSC on CVDs were highest among children (5–17 years old), in the fall and winter, and during cold temperatures. In conclusion, we found an immediate, lasting effects of PSC on overall CVDs and a delayed, prolonged impact of UFPnc. PSC was a more sensitive indicator than UFPnc. The PSC effects were higher among certain CVD subtypes, in children, in certain seasons, and during cold days. Further studies are needed to validate our findings and evaluate the long-term effects.

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.

Organophosphate esters (OPEs) are widely added to various industrial and consumer products, and are mainly used as flame retardants and plasticizers. Existing epidemiological studies suggest that OPE exposure may be linked to increased blood pressure (BP) and hypertension risk in adults. However, it remains unclear whether OPE exposure is associated with increased BP in children and adolescents. Here, we investigated the associations between OPE exposure and BP levels in 6–18-year-old children and adolescents from a cross-sectional study in Liuzhou, China. OPE metabolites were determined in spot urine samples (n = 1194) collected between April and May 2018. Three measurements of systolic and diastolic BP for each participant were averaged as study outcomes. Associations of OPE exposure with age-, sex- and height-standardized BP were assessed using linear regression models. We found that each natural log unit increment of bis(1,3-dichloro-2-propyl) phosphate (BDCIPP) was associated with a 0.06 standard deviation unit (95% confidant interval (CI): 0.01, 0.11) increase in systolic BP z-score. When conducting stratified analysis based on sex, age, and BMI category, BDCIPP was shown to be positively associated with systolic/diastolic BP z-score in females, but not in males. The associations between bis(2-butoxyethyl) phosphate (BBOEP) and systolic/diastolic BP z-score were pronounced in adolescents, but not in children. Moreover, a significant positive association between 1-hydroxy-2-propyl bis(1-chloro-2-propyl) phosphate (BCIPHIPP) and diastolic BP z-score was observed in obese subjects. The present study provides the first evidence that OPE exposure was related to increased BP in children and adolescents. Given the scarcity of high-quality evidence supporting these results, the health effects of OPEs are warrant investigation in well-designed prospective studies.

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.

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.

β-blockers are a class of medications widely used to treat cardiovascular disorders, including abnormal heart rhythms, high blood pressure, and angina pectoris. The prevalence of β-blockers has generated a widespread concern on their potential chronic toxicity on aquatic organisms, highlighting the necessity of comprehensive studies on their environmental distribution, fate, and toxicity. This review summarizes the up-to-date knowledge on the source, global distribution, analytical methods, transformation, and toxicity of β-blockers. Twelve β-blockers have been detected in various environmental matrices, displaying significant temporal and spatial variations. β-blockers can be reduced by 0–99% at wastewater treatment plants, where secondary processes contribute to the majority of removal. Advanced oxidation processes, e.g., photocatalysis and combined UV/persulfate can transform β-blockers more rapidly and completely than conventional wastewater treatment processes, but the transformation products could be more toxic than the parent compounds. Propranolol, especially its (S)-enantiomer, exhibits the highest toxicity among all β-blockers. Future research towards improved detection methods, more efficient and cost-effective removal techniques, and more accurate toxicity assessment is needed to prioritize β-blockers for environmental monitoring and control worldwide.

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.

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.

Concerning PM2.5 concentrations, rapid industrialization, along with increase in cardiovascular disease (CVD) were recorded in Pakistan, especially in urban areas. The degree to which air pollution contributes to the increase in the burden of CVD in Pakistan has not been assessed due to lack of data. This study aims to describe the characteristics of PM2.5 constituents and investigate the impact of individual PM2.5 constituent on cardiovascular morbidity in Karachi, a mega city in Pakistan. Daily levels of twenty-one constituents of PM2.5 were analyzed using samples collected at two sites from fall 2008 to summer 2009 in Karachi. Hospital admission and emergency room visits due to CVD were collected from two large hospitals. Negative Binominal Regression was used to estimate associations between pollutants and the risk of CVD. All PM2.5 constituents were assessed in single-pollutant models and selected constituents were assessed in multi-pollutant models adjusting for PM2.5 mass and gaseous pollutants. The most common CVD subtypes among our participants were ischemic heart disease, hypertension, heart failure, and cardiomyopathy. Extremely high levels of PM2.5 constituents from fossil-fuels combustion and industrial emissions were observed, with notable peaks in winter. The most consistent associations were found between exposure to nickel (5–14% increase per interquartile range) and cardiovascular hospital admissions. Suggestive evidence was also observed for associations between cardiovascular hospital admissions and Al, Fe, Ti, and nitrate. Our findings suggested that PM2.5 generated from fossil-fuels combustion and road dust resuspension were associated with the increased risk of CVD in Pakistan.

Knowledge of environmental risk factors for stroke and their role are limited. We performed a case-cohort study to evaluate the association between serum persistent organic pollutants (POPs) level and stroke risk.526 subcohort members and 111 stroke incidence cases were identified from the Korean Cancer Prevention Study-II. Serum levels of POPs were measured using gas chromatography/high-resolution mass spectrometry. The hazard ratios (HRs) for stroke (ischemic, hemorrhagic, and all stroke types) were estimated using the weighted Cox regression model. Age, sex, body mass index, smoking status, physical activity, family history of cardiovascular disease, and hypertension were adjusted in the weighted Cox regression model.After adjusting for potential confounding factors, increased risk for stroke was observed among participants with serum concentration of p,p'-DDE in the highest tertile compared to those in the lowest tertile (HR = 4.10, 95% CI: 1.58, 10.59). A similar association was estimated for PCB118 (HR = 2.33, 95% CI: 1.04, 5.22), PCB156 (HR = 3.42, 95% CI: 1.42, 8.23), and PCB138 (HR = 3.80, 95% CI: 1.48, 9.76). For TEQ, stroke was three times as likely to occur among subjects with TEQ in the highest tertile compared to those in the lowest tertile (HR = 3.12, 95% CI: 1.27, 7.65). PCBs were positively associated with ischemic stroke, but not with hemorrhagic stroke.Elevated serum POPs levels were associated with an increased risk of stroke, especially ischemic stroke.