RESUMO
Objective@#To investigate the effect of long-term exposure of nitrogen dioxide on the incidence of hypertension.@*Methods@#From March to December 2009, 37 386 eligible residents from four cities in northern China (Tianjin, Shenyang, Taiyuan, and Rizhao) were enrolled in a follow-up study by using the random cluster sampling method. Demographic characteristics, lifestyle, history of diseases, and self-report situation of hypertension were collected by using questionnaire. Based on the average annual concentration of NO2 during the period from the cohort to the onset of hypertension as an estimate of exposure, the effect of NO2 exposure on hypertension was analyzed by employing Cox proportional hazards model. The interactions between NO2 exposure and different characteristics (age, sex, body mass index, smoking, alcohol consumption, education, economy, exercise, and fruit intake) were also examined.@*Results@#The baseline age of residents was (43.74±13.78) years, and the body mass index (BMI) was (22.56±2.92) kg/m2. During an average follow-up time of 11.40 years, 2 619 (7.0%) new cases of hypertension were reported. The overall mean environmental pollution levels during the study period for the entire cohort was (40.74±17.07) μg/m3. After adjusting for age, sex, BMI, family history of hypertension, socio-economic information, and lifestyle, the hazard ratio (HR) of incident hypertension with a 10 μg/m3 increase of NO2 was 1.21 (95%CI: 1.18-1.25). Compared with residents aged 60 years and over (HR=1.19, 95%CI: 1.14-1.26), former and current smoking (HR=1.20, 95%CI: 1.14-1.25), and high-frequency fruit consumption (HR=1.17, 95%CI: 1.13-1.21), residents younger than 60 years (HR=1.28, 95%CI: 1.25-1.32), non-smoker (HR=1.23, 95%CI: 1.19-1.27), and low-frequency fruit consumption (HR=1.27, 95%CI: 1.20-1.35) had stronger interaction effect with NO2 (all P values for interaction<0.05).@*Conclusion@#NO2 exposure may lead to the onset of hypertension, which has a stronger effect on people younger than 60 years old, without smoking history and with low-frequency fruit consumption.
RESUMO
BACKGROUND: Particulate matter 2.5 (PM2.5) has proven to be associated with morbidity and mortality from cardiovascular diseases. However, whether PM2.5 could promote the formation of abdominal aortic aneurysm (AAA) is unclear. Present study aimed to explore the relationship between PM2.5 exposure and AAA development. METHODS: Ang â ¡-infused apoe-/- mice were treated with PM2.5 or saline by intranasal instillation. Four weeks later, histological and immunohistological analyses were used to evaluate the effect of PM2.5 on AAA formation. Human aortic smooth muscle cells (HASMCs) were also employed to further analyze the adverse effect of PM2.5 in vitro. RESULTS: We found that PM2.5 could significantly increase the AAA incidence, the maximal abdominal aortic diameter and could promote the degradation of elastin. Additionally, the expression of senescence markers, P21 and P16 were also enhanced after PM2.5 exposure. We also found that PM2.5 significantly increased the AAA related pathological changes, MMP2 and MCP-1 expression in HASMCs. Meanwhile, PM2.5 could increase the expression of senescence markers P21, P16 and SA-ß-gal activity, also the reactive oxygen species levels in vitro. CONCLUSIONS: PM2.5 promoted the formation of AAA in an Ang â ¡-induced AAA model. The underlying mechanism might be cellular senescence after PM2.5 exposure.
