Background: Triglyceride–glucose (TyG) index, a simple surrogate marker of insulin resistance, has been reported to be associated with arterial stiffness. However, previous studies were limited by the cross-sectional design. The purpose of this study was to explore the longitudinal association between TyG index and progression of arterial stiffness. Methods: A total of 6028 participants were derived from the Kailuan study. TyG index was calculated as ln [fasting triglyceride (mg/dL) × fasting glucose (mg/dL)/2]. Arterial stiffness was measured using brachial-ankle pulse wave velocity (baPWV). Arterial stiffness progression was assessed by the annual growth rate of repeatedly measured baPWV. Multivariate linear regression models were used to estimate the cross-sectional association of TyG index with baPWV, and Cox proportional hazard models were used to investigate the longitudinal association between TyG index and the risk of arterial stiffness. Results: Multivariate linear regression analyses showed that each one unit increase in the TyG index was associated with a 39 cm/s increment (95%CI, 29–48 cm/s, P < 0.001) in baseline baPWV and a 0.29 percent/year increment (95%CI, 0.17–0.42 percent/year, P < 0.001) in the annual growth rate of baPWV. During 26,839 person-years of follow-up, there were 883 incident cases with arterial stiffness. Participants in the highest quartile of TyG index had a 58% higher risk of arterial stiffness (HR, 1.58; 95%CI, 1.25–2.01, P < 0.001), as compared with those in the lowest quartile of TyG index. Additionally, restricted cubic spline analysis showed a significant dose–response relationship between TyG index and the risk of arterial stiffness (P non-linearity = 0.005). Conclusion: Participants with a higher TyG index were more likely to have a higher risk of arterial stiffness. Subjects with a higher TyG index should be aware of the following risk of arterial stiffness progression, so as to establish lifestyle changes at an early stage.

Objective: To estimate the risks of daily hospital admissions for cause specific major cardiovascular diseases associated with short term exposure to ambient fine particulate matter (aerodynamic diameter ≤2.5 μm; PM_2.5) pollution in China.Design: National time series study.Setting: 184 major cities in China.Population: 8 834 533 hospital admissions for cardiovascular causes in 184 Chinese cities recorded by the national database of Urban Employee Basic Medical Insurance from 1 January 2014 to 31 December 2017.Main outcome measures: Daily counts of city specific hospital admissions for primary diagnoses of ischaemic heart disease, heart failure, heart rhythm disturbances, ischaemic stroke, and haemorrhagic stroke among different demographic groups were used to estimate the associations between PM_2.5 and morbidity. An overdispersed generalised additive model was used to estimate city specific associations between PM_2.5 and cardiovascular admissions, and random effects meta-analysis used to combine the city specific estimates.Results: Over the study period, a mean of 47 hospital admissions per day (standard deviation 74) occurred for cardiovascular disease, 26 (53) for ischaemic heart disease, one (five) for heart failure, two (four) for heart rhythm disturbances, 14 (28) for ischaemic stroke, and two (four) for haemorrhagic stroke. At the national average level, an increase of 10 μg/m³ in PM_2.5 was associated with a 0.26% (95% confidence interval 0.17% to 0.35%) increase in hospital admissions on the same day for cardiovascular disease, 0.31% (0.22% to 0.40%) for ischaemic heart disease, 0.27% (0.04% to 0.51%) for heart failure, 0.29% (0.12% to 0.46%) for heart rhythm disturbances, and 0.29% (0.18% to 0.40%) for ischaemic stroke, but not with haemorrhagic stroke (−0.02% (−0.23% to 0.19%)). The national average association of PM_2.5 with cardiovascular disease was slightly non-linear, with a sharp slope at PM_2.5 levels below 50 μg/m³, a moderate slope at 50-250 μg/m³, and a plateau at concentrations higher than 250 μg/m³. Compared with days with PM_2.5 up to 15 μg/m³, days with PM_2.5 of 15-25, 25-35, 35-75, and 75 μg/m³ or more were significantly associated with increases in cardiovascular admissions of 1.1% (0 to 2.2%), 1.9% (0.6% to 3.2%), 2.6% (1.3% to 3.9%), and 3.8% (2.1% to 5.5%), respectively.According to projections, achieving the Chinese grade 2 (35 μg/m³), Chinese grade 1 (15 μg/m³), and World Health Organization (10 μg/m³) regulatory limits for annual mean PM_2.5 concentrations would reduce the annual number of admissions for cardiovascular disease in China. Assuming causality, which should be done with caution, this reduction would translate into an estimated 36 448 (95% confidence interval 24 441 to 48 471), 85 270 (57 129 to 113 494), and 97 516 (65 320 to 129 820), respectively.Conclusions: These data suggest that in China, short term exposure to PM_2.5 is associated with increased hospital admissions for all major cardiovascular diseases except for haemorrhagic stroke, even for exposure levels not exceeding the current regulatory limits.

Background: Air pollutants are considered as non-negligible risk factors of idiopathic pulmonary fibrosis (IPF). However, the relationship between long-term air pollution and the incidence of IPF is unknown. Our objective was to explore the associations of air pollutants with IPF risk and further assess the modification effect of genetic susceptibility.Methods: We used land-use regression model estimated concentrations of nitrogen dioxide (NO₂), nitrogen oxides (NO_x) and particulate matter (fine particulate matter with diameter <2.5 μm (PM_2.5) and particulate matter with diameter <10 μm (PM₁₀)). The polygenic risk score (PRS) was constructed using 13 independent single nucleotide polymorphisms. Cox proportional hazard models were used to evaluate the associations of air pollutants with IPF risk and further investigate the modification effect of genetic susceptibility. Additionally, absolute risk was calculated.Results: Among 433 738 participants from the UK Biobank, the incidence of IPF was 27.45 per 100 000 person-years during a median follow-up of 11.78 years. The adjusted hazard ratios of IPF for each interquartile range increase in NO₂, NO_xand PM_2.5were 1.11 (95% CI 1.03–1.19), 1.07 (95% CI 1.01–1.13) and 1.09 (95% CI 1.02–1.17), respectively. PM_2.5had the highest population attribution risk, followed by NO_xand NO₂. There were additive interactions between NO₂, NO_xand PM_2.5and genetic susceptibility. Participants with a high PRS and high air pollution had the highest risk of incident IPF compared with those with a low PRS and low air pollution (adjusted hazard ratio: NO₂3.94 (95% CI 2.77–5.60), NO_x3.08 (95% CI 2.21–4.27), PM_2.53.65 (95% CI 2.60–5.13) and PM₁₀3.23 (95% CI 2.32–4.50)).Conclusion: Long-term exposures to air pollutants may elevate the risk of incident IPF. There are additive effects of air pollutants and genetic susceptibility on IPF risk.

The effect of long-term exposure to air pollution on the development of chronic obstructive pulmonary disease (COPD) is still controversial, and the role of the interactions of air pollution with genetic risk and lifestyle in COPD risk is unclear. We included 452762 participants derived from the UK Biobank. Annual concentrations of air pollutions, including particle matter (PM_2.5, PM₁₀), nitrogen oxides (NO_x), and nitrogen dioxide (NO₂), were assessed using land-use regression model. We applied Cox proportional hazard model to evaluate the associations between air pollution and COPD risk. In addition, we constructed a polygenic risk score and a lifestyle score, and assessed whether genetic susceptibility and lifestyle modified the effect of air pollution on the COPD risk. Each interquartile range (IQR) increase in annual concentrations of PM_2.5, PM₁₀, NO_x, and NO₂ was associated with 1.17 (95% CI: 1.15,1.19), 1.05 (95% CI: 1.03,1.06), 1.13 (95% CI: 1.11,1.14), and 1.19 (95% CI: 1.16,1.21) times the risk of COPD, respectively. We observed an additive interaction between PM_2.5 and genetic risk (P-_interact=0.095), and a negative interaction between PM_2.5 and lifestyle (P-_interact=0.062). The HRs for each IQR increase in PM_2.5 were 1.21, (95% CI: 1.16-1.25) and 1.24, (95% CI: 1.21-1.26) in individuals with healthy and unfavourable lifestyle, respectively; and 1.16, (95% CI: 1.13-1.19) and 1.19, (95% CI: 1.16-1.22) in those with low genetic risk and high genetic risk, respectively. Participants with high air pollution exposure, high genetic risk and unfavourable lifestyle showed the highest risk of COPD. Long-term exposure to air pollution was associated with increased risk of COPD, especially in those with high genetic risk and unfavourable lifestyle. None.

Air pollutants are important contributors to cardiovascular diseases, but associations between long-term exposure to air pollutants and the risk of abdominal aortic aneurysm (AAA) are still unknown. This study was conducted using a sample of 449 463 participants from the UK Biobank. Hazard ratios and 95% confidence intervals for the risk of AAA incidence associated with long-term exposure to air pollutants were estimated using the Cox proportional hazards model with time-varying exposure measurements. Additionally, the cumulative incidence of AAA was calculated by using the Fine and Grey sub-distribution hazards regression model. Furthermore, this study investigated the combined effects and interactions between air pollutants exposure and genetic predisposition in relation to the risk of AAA onset. Long-term exposure to particulate matter with an aerodynamic diameter <2.5 µm [PM_2.5, 1.21 (1.16, 1.27)], particulate matter with an aerodynamic diameter <10 µm [PM₁₀, 1.21 (1.16, 1.27)], nitrogen dioxide [NO₂, 1.16 (1.11, 1.22)], and nitrogen oxides [NO_x, 1.10 (1.05, 1.15)] was found to be associated with an elevated risk of AAA onset. The detrimental effects of air pollutants persisted even in participants with low-level exposure. For the joint associations, participants with both high levels of air pollutants exposure and high genetic risk had a higher risk of developing AAA compared with those with low concentrations of pollutants exposure and low genetic risk. The respective risk estimates for AAA incidence were 3.18 (2.46, 4.12) for PM_2.5, 3.09 (2.39, 4.00) for PM₁₀, 2.41 (1.86, 3.13) for NO₂, and 2.01 (1.55, 2.61) for NO_x. In this study, long-term air pollutants exposure was associated with an increased risk of AAA incidence. Besides the separate associations of air pollution or genetic susceptibility with the risk of developing abdominal aortic aneurysm, there was a potential interplay between genetic susceptibility and air pollution.