Particulate matter and atherosclerosis: a bibliometric analysis of original research articles published in 1973–2014

Exposure to air particulate matter (PM) may result in various diseases including cardiovascular diseases (CVD) such as atherosclerosis, myocardial infarction, stroke, myocardial ischemia, coronary diseases and cardiac arrhythmia. Its etiology and pathogenic mechanisms may be complex, which include pulmonary and systemic inflammation, accelerated atherosclerosis and altered cardiac autonomic functions [1, 2]. PM contributes to increased cardiac risk by initiating and promoting atherosclerotic progression, which is the underlying cause of most cardiovascular diseases [3]. There is ample epidemiological, clinical and experimental evidence supporting the association of PM with atherogenesis [4‐7]. Related research on PM exposure-enhanced atherosclerosis has attracted greater attention and is becoming an important, rapid-progressing field in the coming years. Therefore, it is necessary to survey bibliometric characteristics and portray the overall trend of these research fields.

Bibliometrics refers to a research methodology employed in library and information sciences, which utilizes quantitative analysis and statistics to describe the bibliographic information of articles (year publication, title, authors, publisher, affiliations, etc.) within a given topic, field, institution, and/or country [1, 8]. Recently, bibliometrics has been used to explore trends in biomedical, medical and environmental research fields; such as the mapping of global drinking water from 1992 to 2011 [8], air PM on the cardiovascular system [1], urban health for the period 1978–2012 [1], stem cell research in Iran [9], cardiovascular research from Latin America from 1999 to 2008 [10], and ophthalmology research from 1997 to 2009 [11]. Bibliometrics applies quantitative and statistical methods to analyze a variety of phenomena across scientific literatures. Literature data are mainly derived from international literature databases such as PubMed/MEDLINE [1], Springerlink [12], and Web of Science [13]. In the present study, we attempted to analyze the characteristics and trends within the research fields of PM and atherosclerosis using the bibliometric approach by conducting a search on the PubMed/MEDLINE database using Medical Subject Headings (MeSH) terms.

Topic 1 (Clusters 1, 3, and 9) included epidemiological studies on the associations between tobacco exposure and atherosclerosis. It is well-known that smoking is an important source of indoor air PM pollution [16] and levels of PM_2.5 is a marker for secondhand tobacco smoke (SHS) [17]. Both active smoking and exposure to environmental tobacco smoke (ETS) were associated with the progression of atherosclerosis [18, 19]. Cigarette smoking is a powerful risk factor for atherosclerotic diseases in middle-aged and aged populations [20‐22]. Moreover, smoking is associated with lipoprotein abnormalities, which promote arterial lipid accumulation and atherogenesis [23‐26]. SHS exposure or the inhalation of ETS is an independent risk factor for subclinical coronary atherosclerosis, coronary heart disease (CHD) and peripheral arterial disease (PAD). In addition, long-term exposure to SHS creates an imbalance in the lipid profile. This imbalance leads to lipid accumulation in the blood vessels of the heart and aorta in experimental models of human conditions in vivo, which in turn leads to atherosclerotic plaque formation [27]. In this topic, the association between familial and fetal tobacco smoke exposures and vascular damage also received close attention, because young adults/children/infants are at high risk of SHS exposure (Cluster 9). These studies show that thicker common carotid artery intima-media thickness (CIMT) in young adulthood is associated with fetal tobacco smoke exposure [28‐30]. Exposure to ETS is independently associated with decreased brachial artery flow-mediated dilation, decreased aortic elastic properties and increased ApoB levels among adolescents with increased cotinine level (a sensitive and specific biomarker of ETS exposure) [29, 31, 32]. Moreover, smoke-free legislation is associated with lower risk of smoking-related cardiac and cerebrovascular diseases [33‐35].

Topic 2 (Clusters 2 and 4) covered epidemiological studies on the associations between environmental PM exposures and atherosclerosis. Epidemiological findings show a clear association between long-term exposure to PM_2.5/PM₁₀ and atherosclerosis. The studies reviewed on this topic focused on the effects of PM air pollution on subclinical atherosclerosis by means of noninvasive imaging (a predictor of cardiovascular events). Long-term PM concentrations are associated with increased CIMT progression [36‐39], but does not appear to be associated with greater arterial stiffness [40]. CIMT, a marker of subclinical atherosclerosis, is associated with atherosclerosis development and progression in middle-aged populations [41]. The investigation of links between PM exposures and subclinical atherosclerosis mostly adopts the cohort and cross-sectional studies. The most studied cohort is the Multi-Ethnic Study of Atherosclerosis (MESA) conducted across six study sites in the USA [36, 38, 40, 42]. In addition, exposure to traffic is also associated with atherosclerosis [43].

Topic 3 (Clusters 6 and 10) included studies on the different roles of PM components/sources in health effects. On this topic, the source that has the most concern is vehicle emissions (Cluster 10), which is linked with heart rate variability (HRV) [44], cardiac repolarization [45] and endothelial gene regulation [46]. The sources of PM from fire/combustion emission are also issues of concern. Exposure to ultrafine particles during fire suppression is considered a potential contributing factor for CHD [47]. Combustion emissions cause pro-atherosclerotic responses in ApoE^−/− mice [48]. Moreover, these components (carbon black, metals, etc.) deserve closer attention. Nano-sized carbon black particles are associated with modest vasomotor impairment [49]. The zinc metal component of PM drives cardiovascular health effects, as well as the possible susceptibility induced by hyperlipidemia [50]. In addition, other air pollutants (nitrogen dioxide, sulfur dioxide, carbon monoxide, etc.) may also induce cardiovascular risk on their own, or combined with PM exposure. Elevated concentrations of PM and nitrogen dioxide increase the risk of supraventricular runs, as well as the number of ventricular runs [51].

Topic 4 (Clusters 5, 7, and 8) included toxicological studies on PM-induced arteriosclerosis. Mice, mice-knockout and disease model animals were chosen as study subjects for animal experiments (Cluster 8). ApoE^−/− mice, which is probably of more concern, lacks apolipoprotein E, a high-affinity ligand for lipoprotein receptors, and develops atherosclerotic plaques in a fashion similar to humans [52]. In ApoE^−/− mice, exposure to both ambient PM and tobacco smoke increased the plaque area in the pathological analysis of the aorta [6, 53‐56]. Vascular endothelial cells were chosen as study subjects to explore molecular biology mechanisms (Cluster 5). On this topic, the induction of oxidative stress [57, 58] and mitochondrial DNA (mtDNA) damage [53, 59, 60] play a key role in the progression of atherosclerosis (Cluster 7).

Increasing attention has been given to the research field of PM and atherosclerosis. The number of published articles has increased from five for the period 1973–1978 to 89 for the period 2009–2014. The characteristics of the research literature in the fields of PM and atherosclerosis can be obtained through the quantitative analysis of bibliographic information and MeSH terms. Bibliographic information includes annual publications, authors, journals, institutions and countries; which can support a deeper understanding of research directions in the future. Cluster analysis by MeSH terms can provide clues that suggest popular topics in these fields, and help determine research emphases and priorities. Based on the quantitative analysis of bibliographic information and MeSH terms, we found that “tobacco smoke pollution” and “smoke and air particulate matter” were the most studied targets in the research field of PM and atherosclerosis.

It should be pointed out that the overall characteristics of these studies might be affected to a certain extent by the interest and funding of the researchers. In conclusion, the bibliometric analysis method is an effective approach for providing the characterization of a given research field, and can be adopted by other research fields as well.