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.

Di-(2-ethylhexyl) phthalate (DEHP) is a prevalent environmental contaminant that severely impacts the health of human and animals. Taxifolin (TAX), a plant flavonoid isolated from yew, exerts protective effects on cardiac diseases. Nevertheless, whether DEHP could induce cardiomyocyte hypertrophy and its mechanism remains unclear. This study aimed to highlight the specific molecular mechanisms of DEHP-induced cardiomyocyte hypertrophy and the protective potential of TAX against it. Chicken primary cardiomyocytes were treated with DEHP (500 μM) and/or TAX (0.5 μM) for 24 h. The levels of glucose and adenosine triphosphate (ATP) were detected, and cardiac hypertrophy-related genes were validated by real-time quantitative PCR (qRT-PCR) and Western blot (WB) in vitro. The results showed that DEHP-induced cardiac hypertrophy was ameliorated by TAX, as indicated by the increased cardiomyocyte area and expression of atrial natriuretic peptide (ANP), natriuretic peptides A-like (BNP) and β-myosin heavy cardiac muscle (β-MHC). Furthermore, DEHP induced cardiac hypertrophy via the interleukin 6 (IL-6)/Janus kinase (JAK)/signal transducer and activator of transcription 3 (STAT3) pathway in vitro. In addition, DEHP disrupted mitochondrial function and glycometabolism by activating the insulin-like growth factor 1 (IGF1)/phosphatidylinositol 3-kinase (PI3K) pathway and the peroxisome proliferator activated receptors (PPARs)/PPARG coactivator 1 alpha (PGC-1α) pathway to induce cardiac hypertrophy in vitro. Intriguingly, those DEHP-induced changes were obviously alleviated by TAX treatment. Taken together, cardiac hypertrophy was induced by DEHP via activating the IL-6/JAK/STAT3 signaling pathway, triggering glycometabolism disorder and mitochondrial dysfunction in vitro, can be ameliorated by TAX. Our findings may provide a feasible molecular mechanism for the treatment of cardiomyocyte hypertrophy induced by DEHP.

Congenital heart defects (CHDs) are a major cause of death in infancy and childhood. Major risk factors for most CHDs, particularly those resulting from the combination of environmental exposures with social determinants and behaviors, are still unknown. This study evaluated the main effect of maternal environmental tobacco smoke (ETS), and its interaction with social-demographics and environmental factors on CHDs in China. A population-based, matched case-control study of 9452 live-born infants and stillborn fetuses was conducted using the Guangdong Registry of Congenital Heart Disease data (2004–2014). The CHDs were evaluated by obstetrician, pediatrician, or cardiologist, and confirmed by cardia tomography/catheterization. Controls were randomly chosen from singleton newborns without any malformation, born in the same hospital as the cases and 1:1 matched by infant sex, time of conception, and parental residence (same city and town to ensure sufficient geographical distribution for analyses). Face-to-face interviews were conducted to collect information on demographics, behavior patterns, maternal disease/medication, and environmental exposures. Conditional logistic regression was used to estimate odds ratios and 95% confidence intervals of ETS exposure on CHDs while controlling for all risk factors. Interactive effects were evaluated using a multivariate delta method for maternal demographics, behavior, and environmental exposures on the ETS-CHD relationship. Mothers exposed to ETS during the first trimester of pregnancy were more likely to have infants with CHD than mothers who did not (aOR = 1.44, 95% CI 1.25–1.66). We also observed a significant dose-response relationship when mothers were exposed to ETS and an increasing number of risk factors and CHDs. There were greater than additive interactions for maternal ETS and migrant status, low household income and paternal alcohol consumption on CHDs. Maternal low education also modified the ETS-CHD association on the multiplicative scale. These findings may help to identify high-risk populations for CHD, providing an opportunity for targeted preventive interventions.

Gestational diabetes mellitus (GDM) is associated with adverse short- and long-term health outcomes among mothers and their offspring. GDM affects 0.6%–15% of pregnancies worldwide and its incidence is increasing. However, intervention strategies are lacking for GDM. Previous studies indicated a protective association between greenspace and type 2 diabetes mellitus (T2DM), while few studies have explored the association between greenness and GDM. This study aimed to investigate the association between residential greenness and GDM among women from 40 clinical centers in Guangdong province, south China. The study population comprised 5237 pregnant mothers of fetuses and infants without birth defects, from 2004 to 2016. There were n = 157 diagnosed with GDM according to World Health Organization criteria. We estimated residential greenness using the Normalized Difference Vegetation Index (NDVI), derived from satellite imagery using a spatial-statistical model. Associations between greenness during pregnancy and GDM were assessed by confounder-adjusted random effects log-binomial regression models, with participating centers as the random effect. One interquartile increments of NDVI₂₅₀ₘ, NDVI₅₀₀ₘ and NDVI₁₀₀₀ₘ were associated with 13% (RR = 0.87, 95%CI: 0.87–0.87), 8% (RR = 0.92, 95%CI: 0.91–0.92) and 3% (RR = 0.97, 95%CI: 0.97–0.97) lower risks for GDM, respectively. However, NDVI₃₀₀₀ₘ was not significantly associated with GDM (RR = 0.96, 95%CI: 0.78–1.19). The risk for GDM decreased monotonically with greater NDVI. The protective effect of greenness on GDM was stronger among women with lower socioeconomic status and in environments with a lower level air pollutants. Our results suggest that greenness might provide an effective intervention to decrease GDM. Greenness and residential proximity to greenspace should be considered in community planning to improve maternal health outcomes.

Exposure to the emerging contaminant bisphenol A (BPA) is ubiquitous and associated with cardiovascular disorders. BPA effect as endocrine disruptor is widely known but other mechanisms underlying heart disease, such as epigenetic modifications, remain still unclear. A compound of green tea, epigallocatechin gallate (EGCG), may act both as anti-estrogen and as inhibitor of some epigenetic enzymes. The aims of this study were to analyze the molecular processes related to BPA impairment of heart development and to prove the potential ability of EGCG to neutralize the toxic effects caused by BPA on cardiac health. Zebrafish embryos were exposed to 2000 and 4000 μg/L BPA and treated with 50 and 100 μM EGCG. Heart malformations were assessed at histological level and by confocal imaging. Expression of genes involved in cardiac development, estrogen receptors and epigenetic enzymes was analyzed by qPCR whereas epigenetic modifications were evaluated by whole mount immunostaining. BPA embryonic exposure led to changes in cardiac phenotype, induced an overexpression of hand2, a crucial factor for cardiomyocyte differentiation, increased the expression of estrogen receptor (esr2b), promoted an overexpression of a histone acetyltransferase (kat6a) and also caused an increase in histone acetylation, both mechanisms being able to act in sinergy. EGCG treatment neutralized all the molecular alterations caused by BPA, allowing the embryos to go on with a proper heart development. Both molecular mechanisms of BPA action (estrogenic and epigenetic) likely lying behind cardiogenesis impairment were successfully counteracted by EGCG treatment.

Epidemiological evidence has shown a significant association between short-term exposure to air pollution and mortality risk for circulatory system diseases (CSD). However, informative insights on the significance and magnitude of its relationship in the process of government interventions on abating air pollution are still lacking, particularly in a burgeoning Chinese city. In this study, we conducted a time series study in Lishui District, Nanjing, to examine the effect of ambient particulate matter (PM), e.g., PM₂.₅ and PM₁₀, on daily death counts of CSD which included cardiovascular disease (CVD), cerebrovascular disease (CEVD), and arteriosclerotic heart disease (ASHD) mortality from January 1, 2015, to December 31, 2019. The results revealed that each 10 μg/m³ increase in PM₂.₅ and PM₁₀ concentration at lag0 day was associated with an increase of 1.33% (95% confidence interval, 0.08%, 2.60%) and 1.12% (0.43%, 1.82%) in CSD mortality; 2.42% (0.44%, 4.43%) and 1.43% (0.32%, 2.55%) in CVD mortality; 1.20% (− 0.31%, 2.73%) and 1.21% (0.38%, 2.05%) in CEVD mortality; and 2.78% (0.00%, 5.62%) and 1.66% (0.14%, 3.21%) in ASHD mortality, respectively. For cumulative risk, the corresponding increase in daily mortality for the same change in PM₂.₅ concentration at lag03 day was significantly associated with 1.94% (0.23%, 3.68%), 3.17% (0.58%, 5.84%), 2.38% (0.17%, 4.63%), and 4.92% (1.18%, 8.81%) for CSD, CVD, CEVD, and ASHD, respectively. The exposure–response curves were approximately nonlinear over the entire exposure range of the PM concentrations. We also analyzed the effect modifications by season (warm or cold), age group (0–64 years, 65–74 years, or ≥ 75 years), and sex (male or female). Although not statistically significant, stratified analysis showed greater vulnerability to PM exposure for cold season, population over 65 years of age, and female group.

We expected to explore the associations of hearing loss and hearing thresholds at different frequencies with total and cause-specific mortality. In this study, 11,732 individuals derived from the National Health and Nutrition Examination Survey (NHANES) 1999–2012 were included. Data of death was extracted from the NHANES Public-Use Linked Mortality File through December 31, 2015. Cox proportional hazards models were used to explore the associations between hearing loss, hearing thresholds at different frequencies, and total or cause-specific mortality. A total of 1,253 deaths occurred with a median follow-up of 12.15 years. A significant positive dose-response relationship between hearing loss in speech frequency and total mortality was observed, and the HRs and 95% CIs were 1.16 (0.91, 1.47), 1.54 (1.19, 2.00), and 1.85 (1.36, 2.50), respectively, for mild, moderate, and severe speech-frequency hearing loss (SFHL) with a P ₜᵣₑₙd of 0.0003. In addition, moderate (HR: 1.90, 95% CI: 1.20–3.00) and greater (3.50, 1.38–8.86) SFHL significantly elevated risk of heart disease mortality. Moreover, hearing thresholds of >25 dB at 500, 1000, or 2000 Hz were significantly associated with elevated mortality from all causes (1.40, 1.17–1.68; 1.44, 1.20–1.73; and 1.33, 1.10–1.62, respectively) and heart disease (1.89, 1.08–3.34; 1.95, 1.21–3.16; and 1.89, 1.16–3.09, respectively). Hearing loss is associated with increased risks of total mortality and heart disease mortality, especially for hearing loss at speech frequency. Preventing or inhibiting the pathogenic factors of hearing loss is important for reducing the risk of death.

Congenital anomalies are the main causes of infant death and disability. Previous studies have suggested that maternal exposure to particulate matter is related to congenital malformation. However, the conclusions of this study remain controversial. Hence, meta-analyses were performed to assess the relationship between maternal exposure to particulate matter and the risk of congenital anomalies. The Medline, Embase, and Web of Science databases were systemically searched from inception until August 2020 to find articles related to birth defects and particulate matter. The pooled risk estimated for the combination of pollution outcomes was calculated for each study by performing fixed effects or random effects models. The existence of heterogeneity and publication bias in relevant studies was also examined. Thirty studies were included in the analysis. A statistically increased summary risk valuation was found. PM₁₀ exposure was associated with an increased risk of congenital heart disease, neural tube defects, and cleft lip with or without cleft palate (OR per 10 μg/m³ = 1.05, 95% CI, 1.03–1.07; OR per 10 μg/m³ = 1.04, 95% CI, 1.01–1.06; OR per 10 μg/m³ = 1.03, 95% CI, 1.01–1.06). Maternal exposure to particulate matter might be associated with an increased risk of congenital anomalies. Our results indicate the dangers of particulate matter exposure on fetal development and the importance of protection against exposure to such particles during pregnancy. The schematic representation of the association between maternal exposure to PM₂.₅/PM₁₀ and congenital anomalies in offspring, and geographic distribution of the included reports in the meta-analyses.

High-altitude hypoxic environment exposure is considered one of the risk factors for congenital heart disease (CHD), but the genetic factors involved are still unclear. CCN1, one of the synergistic molecules in the hypoxic response, is also an indispensable molecule in cardiac development. Considering that CCN1 may play an important role in the occurrence of CHD in high-altitude areas, we investigated the association between CCN1 polymorphisms and CHD susceptibility in Northwest Chinese population from different high-altitude areas. We conducted a case-control study with a total of 395 CHD cases and 486 controls to evaluate the associations of CCN1 polymorphisms with CHD risk. Our results showed that the protective alleles rs3753793-C (OR = 0.59, 95% CI = 0.42–0.81, P = 0.001), rs2297141-A (OR = 0.66, 95% CI = 0.49–0.90, P = 0.001), and C-A haplotype of rs3753793-rs2297141 (OR = 0.58, 95% CI = 0.42–0.82, P = 0.002) were significantly associated with a decreased atrial septal defect (ASD) risk. Further subgroup analysis in different geography populations revealed robust association of SNP rs2297141 with ASD risk in a Han population residing in high altitude of 2500–4287 m. We also found that the frequency of protective alleles was higher in high-altitude population, and the alleles were responsible for the difference of oxygen physiology–related erythrocyte parameters in different high-altitude populations. rs3753793-C and rs2297141-A are likely related to high altitude and hypoxia adaptation, which may also be the reason for the association between CCN1 polymorphism and ASD risk.

Increasing globalization, industrialization, population, and burning of fossil fuels have been adversely affecting the environment for a long time. The consequences of the effects can be seen even within a short period of time in the current scenario. The air pollutants such as SO2, NO2, CO, and PM are the main contributors to the adverse health effects. Long-term and short-term exposure to pollutants may cause acute and chronic effects on the human body as they can enter deep into the organ and circulate in the bloodstream. The ultimate purpose of this review is to develop a quantitative perceptive of the existing state of facts about potential health effects concerning the dose-response relationship between exposure level of air pollutants and induced diseases. We have drawn around 376 scientific research papers on high-impact factors related to air pollution and health. These publications were analyzed with consideration of experimental methods, design, observations, and reports on the exposure through inhalation which may emulate the normal direction of exposure inside the human organs. The present study suggests the effects of epidemiological studies on associations between pollutant concentrations and human health. Most of the inferences evidenced the severe adverse effects of particulate matter (PM2.5 & PM10) on the respiratory and cardiovascular systems. Our present investigation reveals the health risk due to pollutants’ exposure to the vulnerable population anguishing with asthma, COPD, cardiovascular disease, diabetes, cancer (physiological diseases); dementia, depression, and stress (psychological diseases).