Student Research Committee, Department of Biostatistics, School of Allied Medical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran; Prevention of Metabolic Disorders Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Int J Hyg Environ Health. 2021 May;234:113719. doi: 10.1016/j.ijheh.2021.113719. Epub 2021 Mar 4.
Plenty of recent studies on the impact of air pollution on blood pressure (BP) exist; however, there is a lack of data for the highly polluted Eastern Mediterranean region. We evaluated the associations of short-term exposure to air pollutants with systolic BP (SBP) and diastolic BP (DBP) and the long-term impact of air pollutants on incident hypertension, among Tehranian adults. In the Tehran Lipid and Glucose Study, 4580 nonhypertensive participants aged 20-69 years (41.6% male) were followed from 2001 to 2018 through 3-year follow-ups and 4-5 examinations of them were recorded. The air pollutants included particulate matter with a diameter ≤10 μm (PM), carbon monoxide (CO), ozone (O), nitrogen dioxide (NO), and sulfur dioxide (SO). The mixed-effects transition model estimated the air pollution impact on BP. The proportional hazards Weibull model measured the long-term effects of air pollutants on the multivariate hazard of incident hypertension. The air pollutants were put in the models in the form of mean annual level, applying three versions of 1, 2, and 3 years before the follow-ups. During a median follow-up of 12.3 years, 1618 cases of hypertension were found. In the short-term, increase in CO did not affect SBP but decreased DBP with a delay effect lasting for 14 days; increase in NO raised SBP with a 14-day lag, however did not change DBP; increase in O reduced SBP with a 14-day lag but made slight non-significant increase in DBP; rise in PM concentrations led to increased SBP (lag 0-3 days) and DBP with lags of 0-3 days and 12-14 days and increase in SO made the largest increases in DBP with lags lasting for 14 days, but did not affect SBP. Regarding incident hypertension in the long-term, the increase in CO had no significant effect; increase in NO decreased the risk over the 2- and 3-year time spans; rise in O, PM, and SO levels increased the risk in all time spans; the largest hazard ratio [1.96 (95% CI: 1.48, 2.62)] for incident hypertension was attributable to PM in 3 years. Considering the major effects of air pollutants including O, SO, and especially PM on incident hypertension, urgent public health policies should be implemented to reduce the burden of air pollution in metropolitan city of Tehran.
大量研究探讨了空气污染对血压（BP）的影响；然而，在污染严重的东地中海地区，这方面的数据却很匮乏。我们评估了短期暴露于空气污染物与收缩压（SBP）和舒张压（DBP）之间的关联，以及空气中污染物对德黑兰成年人高血压发病的长期影响。在德黑兰血脂和血糖研究中，对 4580 名年龄在 20-69 岁的非高血压参与者（41.6%为男性）进行了为期 3 年的随访，并记录了他们 4-5 次的检查，随访时间从 2001 年到 2018 年。空气污染物包括直径≤10 μm 的颗粒物（PM）、一氧化碳（CO）、臭氧（O）、二氧化氮（NO）和二氧化硫（SO）。混合效应转移模型估计了空气污染对 BP 的影响。比例风险 Weibull 模型测量了空气中污染物对发病高血压的多变量风险的长期影响。将空气污染物以年平均水平的形式纳入模型，采用三种版本（前 1、2 和 3 年）。在中位数为 12.3 年的随访期间，发现了 1618 例高血压病例。在短期内，CO 的增加不会影响 SBP，但会使 DBP 延迟 14 天下降；NO 的增加会使 SBP 延迟 14 天升高，但不会改变 DBP；O 的增加会使 SBP 延迟 14 天下降，但使 DBP 略有非显著升高；PM 浓度的升高会导致 SBP（滞后 0-3 天）和 DBP（滞后 0-3 天和 12-14 天）升高，SO 的升高会使 DBP 最大幅度升高，滞后时间为 14 天，但对 SBP 没有影响。关于长期的高血压发病，CO 的增加没有显著影响；NO 的增加会降低 2 年和 3 年的发病风险；O、PM 和 SO 水平的升高会增加所有时间段的发病风险；最大的发病风险比（1.96（95%CI：1.48，2.62））归因于 3 年内的 PM。考虑到空气污染物（包括 O、SO 和特别是 PM）对高血压发病的主要影响，应实施紧急公共卫生政策，以减轻德黑兰大都市的空气污染负担。
