LIU Yifei, GUAN Suzhen, XU Haiming, ZHANG Na, HUANG Min, LIU Zhihong. Meta-analysis of effects of long-term exposure to PM2.5 on C-reactive protein levels[J]. Journal of Environmental and Occupational Medicine, 2022, 39(12): 1398-1403. DOI: 10.11836/JEOM22091
Citation: LIU Yifei, GUAN Suzhen, XU Haiming, ZHANG Na, HUANG Min, LIU Zhihong. Meta-analysis of effects of long-term exposure to PM2.5 on C-reactive protein levels[J]. Journal of Environmental and Occupational Medicine, 2022, 39(12): 1398-1403. DOI: 10.11836/JEOM22091

Meta-analysis of effects of long-term exposure to PM2.5 on C-reactive protein levels

Funds: This study was funded.
More Information
  • Corresponding author:

    LIU Zhihong, E-mail: zhihongliu2021@163.com

  • Received Date: March 12, 2022
  • Accepted Date: November 03, 2022
  • Available Online: February 14, 2023
  • Background 

    Fine particulate matter (PM2.5) is a serious air pollutant associated with elevated levels of C-reactive protein (CRP), an inflammatory indicator.

    Objective 

    To assess the potential impacts of long-term exposure to PM2.5 on CRP levels based on previous epidemiological studies.

    Methods 

    PubMed, Embase, Web of Science, CNKI, and Wanfang databases were searched to screen the cohort studies published from January 1, 2000 to January 1, 2022 on the effects of long-term exposure to PM2.5 on CRP levels. "Fine Particulate Matter", "PM2.5", "Particulate Air Pollutants", "Ambient Particulate Matter", "CRP", "C-reactive Protein", and "High Sensitivity C-reactive Protein" in English or Chinese were the key words used in the search. The percentage change in CRP level per 10 μg·m−3 increase in PM2.5 concentration in each study was extracted, followed by meta-analysis, subgroup analysis, and sensitivity analysis.

    Results 

    A total of 1241 articles were retrieved, and 7 articles were included. Random-effects models were used to merge the included data, and it was found that the percentage of CRP level increased by 10.41% (95%CI: 2.24%-18.57%, P<0.05), when PM2.5 concentration increased by 10 μg·m−3, І2=84.2%. The subgroup analysis conducted with grouping based on the annual mean concentration of PM2.5 long-term exposure showed that the intra-group heterogeneity was significantly reduced in the <15 μg·m−3 and the 15- μg·m−3 groups, and the subgroup forest analysis showed differences between the two groups. The results of sensitivity analysis showed that there was a high degree of heterogeneity among the 7 studies, and the 2 papers with the highest annual average PM2.5 concentration were the sources of heterogeneity. The Egger test and the funnel plot indicated that no obvious publication bias was found.

    Conclusion 

    Long-term exposure to PM2.5 can raise levels of CRP in human body.

  • [1]
    薛涛, 刘俊, 张强, 等. 2013~2017年中国PM2.5污染的快速改善及其健康效益[J]. 中国科学:地球科学, 2019, 62(12): 1847-1856. doi: 10.1007/s11430-018-9348-2

    XUE T, LIU J, ZHANG Q, et al. Rapid improvement of PM2.5 pollution and associated health benefits in China during 2013–2017[J]. Sci China Earth Sci, 2019, 62(12): 1847-1856. doi: 10.1007/s11430-018-9348-2
    [2]
    BROOK R D, RAJAGOPALAN S, POPE III C A, et al. Particulate matter air pollution and cardiovascular disease: an update to the scientific statement from the American heart association[J]. Circulation, 2010, 121(21): 2331-2378. doi: 10.1161/CIR.0b013e3181dbece1
    [3]
    LIU Q, GU X, DENG F, et al. Ambient particulate air pollution and circulating C-reactive protein level: a systematic review and meta-analysis[J]. Int J Hyg Environ Health, 2019, 222(5): 756-764. doi: 10.1016/j.ijheh.2019.05.005
    [4]
    PATEL V, KANTIPUDI N, JONES G, et al. Air pollution and cardiovascular disease: a review[J]. Crit Rev Biomed Eng, 2016, 44(5): 327-346. doi: 10.1615/CritRevBiomedEng.2017019768
    [5]
    COZLEA D L, FARCAS D M, NAGY A, et al. The impact of C reactive protein on global cardiovascular risk on patients with coronary artery disease[J]. Curr Health Sci J, 2013, 39(4): 225-231.
    [6]
    CHEN S Y, CHAN C C, SU T C. Particulate and gaseous pollutants on inflammation, thrombosis, and autonomic imbalance in subjects at risk for cardiovascular disease[J]. Environ Pollut, 2017, 223: 403-408. doi: 10.1016/j.envpol.2017.01.037
    [7]
    KAPTOGE S, WHITE I R, THOMPSON S G, et al. Associations of plasma fibrinogen levels with established cardiovascular disease risk factors, inflammatory markers, and other characteristics: individual participant meta-analysis of 154, 211 adults in 31 prospective studies: the fibrinogen studies collaboration[J]. Am J Epidemiol, 2007, 166(8): 867-879. doi: 10.1093/aje/kwm191
    [8]
    RIDKER P M, GLYNN R J, HENNEKENS C H. C-reactive protein adds to the predictive value of total and HDL cholesterol in determining risk of first myocardial infarction[J]. Circulation, 1998, 97(20): 2007-2011. doi: 10.1161/01.CIR.97.20.2007
    [9]
    SPROSTON N R, ASHWORTH J J. Role of C-reactive protein at sites of inflammation and infection[J]. Front Immunol, 2018, 9: 754. doi: 10.3389/fimmu.2018.00754
    [10]
    STANG A. Critical evaluation of the Newcastle-Ottawa scale for the assessment of the quality of nonrandomized studies in meta-analyses[J]. Eur J Epidemiol, 2010, 25(9): 603-605. doi: 10.1007/s10654-010-9491-z
    [11]
    HOFFMANN B, MOEBUS S, DRAGANO N, et al. Chronic residential exposure to particulate matter air pollution and systemic inflammatory markers[J]. Environ Health Perspect, 2009, 117(8): 1302-1308. doi: 10.1289/ehp.0800362
    [12]
    DABASS A, TALBOTT E O, RAGER J R, et al. Systemic inflammatory markers associated with cardiovascular disease and acute and chronic exposure to fine particulate matter air pollution (PM2.5) among US NHANES adults with metabolic syndrome[J]. Environ Res, 2018, 161: 485-491. doi: 10.1016/j.envres.2017.11.042
    [13]
    VIEHMANN A, HERTEL S, FUKS K, et al. Long-term residential exposure to urban air pollution, and repeated measures of systemic blood markers of inflammation and coagulation[J]. Occup Environ Med, 2015, 72(9): 656-663. doi: 10.1136/oemed-2014-102800
    [14]
    TRIPATHY S, MARSLAND A L, KINNEE E J, et al. Long-term ambient air pollution exposures and circulating and stimulated inflammatory mediators in a cohort of midlife adults[J]. Environ Health Perspect, 2021, 129(5): 057007. doi: 10.1289/EHP7089
    [15]
    ZHANG Z, CHANG L, LAU A K H, et al. Satellite-based estimates of long-term exposure to fine particulate matter are associated with C-reactive protein in 30 034 Taiwanese adults[J]. Int J Epidemiol, 2017, 46(4): 1126-1136. doi: 10.1093/ije/dyx069
    [16]
    ELBARBARY M, OGANESYAN A, HONDA T, et al. Systemic inflammation (C-reactive protein) in older Chinese adults is associated with long-term exposure to ambient air pollution[J]. Int J Environ Res Public Health, 2021, 18(6): 3258. doi: 10.3390/ijerph18063258
    [17]
    OSTRO B, MALIG B, BROADWIN R, et al. Chronic PM2.5 exposure and inflammation: determining sensitive subgroups in mid-life women[J]. Environ Res, 2014, 132: 168-175. doi: 10.1016/j.envres.2014.03.042
    [18]
    周骥, 孙庆华, 许建明, 等. 上海地区不同PM2.5污染过程对炎症应激影响的差异性[J]. 气象, 2018, 44(12): 1612-1617.

    ZHOU J, SUN Q H, XU J M, et al. Effects of different PM2.5 pollution processes on inflammatory stress in shanghai area[J]. Meteor Mon, 2018, 44(12): 1612-1617.
    [19]
    ATKINSON R W, COHEN A, MEHTA S, et al. Systematic review and meta-analysis of epidemiological time-series studies on outdoor air pollution and health in Asia[J]. Air Qual Atmos Health, 2012, 5(4): 383-391. doi: 10.1007/s11869-010-0123-2
    [20]
    BONZINI M, TRIPODI A, ARTONI A, et al. Effects of inhalable particulate matter on blood coagulation[J]. J Thromb Haemost, 2010, 8(4): 662-668. doi: 10.1111/j.1538-7836.2009.03694.x
    [21]
    OHLSON C G, BERG P, BRYNGELSSON I L, et al. Inflammatory markers and exposure to occupational air pollutants[J]. Inhal Toxicol, 2010, 22(13): 1083-1090. doi: 10.3109/08958378.2010.520356
    [22]
    WATTERSON T L, HAMILTON B, MARTIN R, et al. Urban particulate matter causes ER stress and the unfolded protein response in human lung cells[J]. Toxicol Sci, 2009, 112(1): 111-122. doi: 10.1093/toxsci/kfp186
    [23]
    RAMAGE L, PROUDFOOT L, GUY K. Expression of C-reactive protein in human lung epithelial cells and upregulation by cytokines and carbon particles[J]. Inhal Toxicol, 2004, 16(9): 607-613. doi: 10.1080/08958370490464599
    [24]
    UPADHYAY S, GANGULY K, STOEGER T, et al. Cardiovascular and inflammatory effects of intratracheally instilled ambient dust from Augsburg, Germany, in spontaneously hypertensive rats (SHRs)[J]. Part Fibre Toxicol, 2010, 7: 27. doi: 10.1186/1743-8977-7-27
    [25]
    ROHR A C, WAGNER J G, MORISHITA M, et al. Cardiopulmonary responses in spontaneously hypertensive and Wistar-Kyoto rats exposed to concentrated ambient particles from Detroit, Michigan[J]. Inhal Toxicol, 2010, 22(6): 522-533. doi: 10.3109/08958370903524509
    [26]
    郭春梅, 赵珊珊, 赵一铭, 等. 我国居住建筑室内PM2.5研究现状及进展[J]. 环境监测管理与技术, 2018, 30(4): 12-17.

    GUO C M, ZHAO S S, ZHAO Y M, et al. Research progress and status on indoor PM2.5 from residential building in China[J]. Admin Tech Environ Monit, 2018, 30(4): 12-17.
    [27]
    SACKS J D, STANEK L W, LUBEN T J, et al. Particulate matter–induced health effects: who is susceptible?[J]. Environ Health Perspect, 2011, 119(4): 446-454. doi: 10.1289/ehp.1002255

Catalog

    Article views (391) PDF downloads (84) Cited by()

    /

    DownLoad:  Full-Size Img  PowerPoint
    Return
    Return