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儿童期肥胖与肥胖有关，成年后患慢性病的风险增加，这些不良反应可能持续一生。我们的研究发现，空气污染可以被视为儿童和青少年体重增加的可能危险因素。
- childhood
- air pollution
- obesity
- BMI
1. Introduction
Obesity has become a worldwide epidemic and urgent health issue [1]. The prevalence of overweight and obesity has increased considerably in the last few decades and nearly tripled since 1975. With regard to children and adolescents, 340 million of them were overweight or obese in 2016, and this number continues to grow at a rapid rate [2,3]. Childhood obesity has been associated with obesity and increased risks for chronic disease in adulthood [4,5], and these adverse effects may last the whole lifetime [6]. Research has identified multiple factors that can lead to childhood obesity and it has been shown that childhood obesity can be attributed to genetic, dietary, and behavioral factors [7]. Despite genetic and metabolic predispositions, the rising epidemic of obesity indicates environmental factors may play a role in accelerating the progression of childhood obesity [8].
The Global Burden of Disease study revealed that air pollution can be the most adverse environmental health hazard for disease and mortality worldwide [9,10]. Well over 80% of urban dwellers suffer from air pollution, and the most seriously affected individuals were low-income residents [11]. In recent years, mounting evidence suggests that air pollution can be an obesogenic factor [12]. It is mainly through the biochemical and behavioral pathways that air pollution affects body weight. Metabolic disorders [13], inflammatory reactions [14], reduced sleep duration and quality [15] that are caused by air pollution all contribute to the accumulation of adipose tissue and weight gain, as has been demonstrated in animal trials. Additionally, the decline in air quality reduces a person’s willingness to engage in outdoor activities [16], which in turn increases indoor time, in order to reduce the impact of pollution on the human body [17].
Although there are numerous original studies on air pollution and obesity, the effects remained inconsistent and differed among the populations, pollutant types, and pollutant concentrations [12]. We found that previous studies were more concentrated on exposure during pregnancy [18,19], whereas recent studies have increasingly examined the direct effects of children’s exposure to air pollution on obesity [20,21]. However, the findings seem to be inconsistent even in studies of children and adolescents only [22,23,24]. For instance, Fioravanti et al. suggested that the evidence that air pollution causes obesity was limited [23]. In contrast, some studies indicated that long-term exposure to air pollutants might be correlated with weight gain and the development of obesity [20,21,25,26]. Among the available review articles, the existing studies have been mostly concentrated on adults or whole populations, and quantitative synthesis of the contribution of air pollution to children and adolescents remains scarce [12,27,28]. A meta-analysis by Parasin et al. examined the relationship between air pollution and childhood obesity, but did not distinguish between exposure during pregnancy and individual exposure, and also did not standardize when combining the effects of pollutants across studies [29]. Therefore, we believe that the topic still has potential for further research. As such, that this study aimed to systematically review and quantitatively analyze the scientific evidence on the influence of exposure to air pollution on weight gain and obesity in childhood.
2. The Association between Childhood Exposure to Ambient Air Pollution and Obesity
It was showed that long-term exposure to particulate matter and NO2 was significantly correlated with the risk of childhood obesity, while BMI also showed similar elevated results. Although O3 and NOx also had a positive effect on the increase in weight status, none reached significant levels. Notably, as the aerodynamic diameter of particulate matter decreases, the fattening effect on children increases, and researchers have begun to concentrate on the smaller particle size pollutants (PM1).
Of the 15 studies that were included in the analysis, around 73% were published in the last three years, and most were conducted in developing countries. We compared a meta-analysis of the association between air pollutants and obesity in adults [28], where half of the included studies were published after 2019, with the difference that the study areas were predominantly developed countries. An identifiable trend is that concerns about air pollution and childhood obesity are rising rapidly in developing countries. One plausible explanation is that although developed countries still maintain high rates of childhood obesity [49,50], the effect of air pollutants on body weight has been limited because air pollution levels have declined significantly in these countries [28]. Developing countries, in contrast, appear confronted with a double crisis, with increasing prevalence and growth rates of childhood obesity on the one hand [51], and deteriorating air quality resulting from urbanization and industrialization on the other [52,53]. Thus, numerous original studies were conducted in developing countries in recent years, and the effects tend to be more significant, further providing foundations for the analysis of our research.
As the main air pollutants of concern in the present study, particulate matter significantly influenced childhood obesity and BMI growth. Our findings were consistent with the previous hypothesis that with smaller aerodynamic diameters of respirable particulate matter, the more toxic compounds would be adsorbed and also more easily inhaled deep into the lungs, therefore are more harmful to health [54,55]. In contrast to children, long-term exposure to PM10 and PM2.5 showed insignificant effects on adult obesity according to a meta-analysis that was conducted on adults [28]. Similar results were found for NO2 and O3, both pollutants were positively associated with the development of obesity. As can be seen, the effects of different pollutants on people can be diverse and complex, even for the same pollutant, the impact can vary depending on the characteristics of the population (i.e., age, gender, region). These specific mechanisms require further investigation and validation.
虽然暴露于空气污染和肥胖的机制尚未完全理解，但生化机制已被普遍提及并被接受为与空气污染物相关的主要肥胖致病机制[12，25，56]。首先，从人体新陈代谢的角度来看，从呼吸道进入体内的空气污染物可能会增加组织和系统中的氧化应激[57]。下午服用2.5例如，它可以影响棕色脂肪组织中线粒体中的基因表达，导致棕色脂肪储存中活性氧的产生增加，从而导致代谢功能障碍[13]，以及对脂质代谢和葡萄糖代谢的易感性[58]。其次，由空气污染物引发的炎症反应可导致血管损伤以及胰岛素抵抗，也会对体重产生影响[14]。研究还发现，睡眠呼吸障碍（SDB）的发生与暴露于空气污染物有关[59]。那些生活在高NO地区的人们2和下午2.5水平更容易患SDB，这反过来又导致身心健康差异[60]。睡眠剥夺与瘦素分泌水平降低、促甲状腺激素分泌降低和葡萄糖耐量降低相关，所有这些都可能增加BMI状态[15]。最后，行为机制可以在另一个方向上解释[12]。例如，空气污染会降低人们参加户外活动的意愿[16]。此外，它还可以改善反式脂肪和快餐的消耗[61]，这可能导致肥胖。然而，应该提请注意这样一个事实，即虽然空气污染的致肥胖机制已经在动物模型中得到验证，但人类或不同污染物仍然存在不确定性，应该进行更多的研究来阐明这些途径。
本研究的优势在于，它全面和定量地评估了长期接触空气污染物与儿童肥胖之间的关系。既往研究以全人群为重点[12]或成人[28]，但对儿童和青少年的研究有限[25，62]。同时，本研究纳入的大多数原始研究都是在过去三年中发表的，结果相对较新。第三，原始研究中的暴露剂量大多不同，因此很难比较效果，我们以标准化的方式转换数据以提高数据的可比性。最后，根据PRISMA清单要求的标准方法进行分析和整理。
然而，这种荟萃分析仍有许多局限性需要注意。首先，尽管我们系统地检索了目前可用的流行病学证据，但研究量仍然有限，异质性的潜在来源仍有待探索。当我们将结果整合到各个研究中时，文章的质量各不相同，没有以标准化的方式测量和估计暴露，分析方法不完善，文章中证据的确定性通常很差，因此在解释结果时也应该谨慎。其次，研究结果基于许多横断面研究;因此，因果关系很难准确确定。根据GRADE系统，观察性研究的证据水平仍然很低。第三，由于生长模式的复杂性，用于测量成人肥胖的BMI可能在一定程度上不适用于儿童和青少年。第四，对于年幼的儿童（2岁之前），早期肥胖可能与母亲暴露于空气污染导致的低出生体重随后的追赶增长有关[63]，需要进一步探索婴儿的机制。最后，肥胖是一种具有复杂原因的疾病，空气污染造成的直接作用的程度尚不清楚，残留的偏见（即社会经济条件，身体活动）仍可能影响结果。例如，高收入家庭（或受教育程度较高的父母）往往生活在更优越的住宅区，空气污染水平相对较低，绿色空间更好，饮食更有条理，而低收入家庭往往恰恰相反。同样，居住在污染较多地区的父母可能会限制孩子的户外活动，以减少接触空气污染物。这些潜在的混杂变量在研究中没有得到全面的捕捉和合理解释。
研究结果进一步揭示了空气污染对儿童肥胖症的风险。空气污染物的影响是直接和重大的，不仅对人类健康，而且对气候。因此，政策制定者也可以从这些调查结果中受益，即经济发展和城市化可能产生一些问题，特别是在发展中国家，并且需要思考如何制定适当的政策来平衡经济发展和环境污染。必须采取以全球合作为基础的空气污染和气候变化管理的协同办法。运输、能源和制造业等重要行业是PM、SO高排放的主要焦点2不x和温室气体。加快能源结构转型，利用技术推动低碳生产势在必行。同时，建立大气监测、排放监管、污染治理等一体化体系至关重要。
This entry is adapted from the peer-reviewed paper 10.3390/ijerph19084491
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