Cai Yutong, Hansell Anna L, Blangiardo Marta, Burton Paul R, de Hoogh Kees, Doiron Dany, Fortier Isabel, Gulliver John, Hveem Kristian, Mbatchou Stéphane, Morley David W, Stolk Ronald P, Zijlema Wilma L, Elliott Paul, Hodgson Susan
Department of Epidemiology and Biostatistics, MRC-PHE Centre for Environment and Health, School of Public Health, Imperial College London, St Mary's Campus, Norfolk Place, W2 1PG, London, UK.
Directorate of Public Health and Primary Care, Imperial College Healthcare NHS Trust, London, UK.
Eur Heart J. 2017 Aug 1;38(29):2290-2296. doi: 10.1093/eurheartj/ehx263.
Blood biochemistry may provide information on associations between road traffic noise, air pollution, and cardiovascular disease risk. We evaluated this in two large European cohorts (HUNT3, Lifelines).
Road traffic noise exposure was modelled for 2009 using a simplified version of the Common Noise Assessment Methods in Europe (CNOSSOS-EU). Annual ambient air pollution (PM10, NO2) at residence was estimated for 2007 using a Land Use Regression model. The statistical platform DataSHIELD was used to pool data from 144 082 participants aged ≥20 years to enable individual-level analysis. Generalized linear models were fitted to assess cross-sectional associations between pollutants and high-sensitivity C-reactive protein (hsCRP), blood lipids and for (Lifelines only) fasting blood glucose, for samples taken during recruitment in 2006-2013. Pooling both cohorts, an inter-quartile range (IQR) higher day-time noise (5.1 dB(A)) was associated with 1.1% [95% confidence interval (95% CI: 0.02-2.2%)] higher hsCRP, 0.7% (95% CI: 0.3-1.1%) higher triglycerides, and 0.5% (95% CI: 0.3-0.7%) higher high-density lipoprotein (HDL); only the association with HDL was robust to adjustment for air pollution. An IQR higher PM10 (2.0 µg/m3) or NO2 (7.4 µg/m3) was associated with higher triglycerides (1.9%, 95% CI: 1.5-2.4% and 2.2%, 95% CI: 1.6-2.7%), independent of adjustment for noise. Additionally for NO2, a significant association with hsCRP (1.9%, 95% CI: 0.5-3.3%) was seen. In Lifelines, an IQR higher noise (4.2 dB(A)) and PM10 (2.4 µg/m3) was associated with 0.2% (95% CI: 0.1-0.3%) and 0.6% (95% CI: 0.4-0.7%) higher fasting glucose respectively, with both remaining robust to adjustment for air/noise pollution.
Long-term exposures to road traffic noise and ambient air pollution were associated with blood biochemistry, providing a possible link between road traffic noise/air pollution and cardio-metabolic disease risk.
血液生化指标可能有助于揭示道路交通噪音、空气污染与心血管疾病风险之间的关联。我们在欧洲的两个大型队列研究（HUNT3、生命线研究）中对此进行了评估。
采用简化版的欧洲通用噪声评估方法（CNOSSOS-EU）对2009年的道路交通噪音暴露情况进行建模。利用土地利用回归模型估算了2007年参与者居住地的年度环境空气污染水平（PM10、NO2）。使用统计平台DataSHIELD汇总了144082名年龄≥20岁参与者的数据，以便进行个体水平分析。采用广义线性模型评估2006 - 2013年招募期间采集的样本中，污染物与高敏C反应蛋白（hsCRP）、血脂以及（仅在生命线研究中）空腹血糖之间的横断面关联。汇总两个队列的数据后发现，日间噪音增加一个四分位数间距（IQR，5.1 dB(A)）与hsCRP升高1.1%[95%置信区间（95%CI：0.02 - 2.2%）]、甘油三酯升高0.7%（95%CI：0.3 - 1.1%）以及高密度脂蛋白（HDL）升高0.5%（95%CI：0.3 - 0.7%）相关；仅HDL与噪音的关联在调整空气污染后仍显著。PM10升高一个IQR（2.0 µg/m³）或NO2升高一个IQR（7.4 µg/m³）与甘油三酯升高相关（分别为1.9%，95%CI：1.5 - 2.4%和2.2%，95%CI：1.6 - 2.7%），且不受噪音调整的影响。此外，对于NO2，还观察到与hsCRP存在显著关联（1.9%，95%CI：0.5 - 3.3%）。在生命线研究中，噪音升高一个IQR（4.2 dB(A)）和PM10升高一个IQR（2.4 µg/m³）分别与空腹血糖升高0.2%（95%CI：0.1 - 0.3%）和0.6%（95%CI：0.4 - 0.7%）相关，且在调整空气/噪音污染后两者仍显著。
长期暴露于道路交通噪音和环境空气污染与血液生化指标相关，这为道路交通噪音/空气污染与心血管代谢疾病风险之间提供了可能的联系。
