Relationship between life-time exposure to ambient fine particulate matter and carotid artery intima-media thickness in Australian children aged 11–12 years☆
Graphical abstract
Introduction
Air pollutants are known to contribute to cardiovascular health outcomes (Franklin et al., 2015; Ruckerl et al., 2011). Among air pollutants, outdoor particulate matter with an aerodynamic diameter less than or equal to 2.5 μm (PM2.5) is associated with increased ischemic heart disease and incident myocardial infarction, cerebrovascular mortality and incident stroke in a recent review and meta-analysis (Alexeeff et al., 2021). For each 10-μg/m3 increase in long-term PM2.5 exposure, the hazard ratios for ischemic heart disease mortality, incident acute myocardial infarction, incident stroke are 1.23 (95% confidence interval, CI 1.15–1.31), 1.08 (CI 0.99–1.18), 1.13 (CI 1.11, 1.15), respectively (Alexeeff et al., 2021). Accelerated atherosclerosis has been proposed as a mechanism for the observed effects of PM2.5 on cardiovascular system based on animal (Araujo et al., 2008; Soares et al., 2009) and human studies (Hennig et al., 2020; Kunzli et al., 2011).
Carotid intima-media thickness (CIMT) is a marker for atherosclerosis, and is known to predict clinical cardiovascular events (including myocardial infarction, angina pectoris) and cerebrovascular events (including stroke or transient ischemic attack) (Bots et al., 1997; Chambless et al., 2000; Chambless et al., 1997; Geisel et al., 2017; Iglesias del Sol et al., 2002; O'Leary et al., 1999; Rosvall et al., 2005). CIMT predicts cardiovascular risk (Den Ruijter et al., 2012; Lorenz et al., 2007), and has even been considered as a screening tool and a surrogate marker of vascular event risk (Beller, 2009; Bots, 2006; Falk and Shah, 2011).
Investigations on air pollutants effects on CIMT have been reported. Relationship between CIMT and air pollutants, especially particulates is considered as evidence for particulates-induced atherosclerosis. Despite several studies reported relationship between CIMT and exposure to air pollutants, most studies have been done on adults (Diez Roux et al., 2008; Kim et al., 2014; Kunzli et al., 2005; Lenters et al., 2010; Su et al., 2015; Tonne et al., 2012). Whether air pollutants affect CIMT in children remains unknown. This investigation examines the relationship between CIMT and childhood exposure to air pollutants in a long-term follow-up study in Australian children.
Section snippets
Participants
The authors applied for and were granted the permission (ref#781764) to access the Growing Up in Australia- Longitudinal Study of Children in Australia (LSAC) - Restricted Release 7.2 and Child Health CheckPoint BioMarkers data file- General. An ethics application (Project Title: Air quality effects on children health using Longitudinal Study of Australian Children) was filed, and approved by the Human Ethics Office of the University of Sydney. The recruitment and participation of the
Characteristics of the participants
Fig. 1 shows the enrolment of children to LSAC, the CheckPoint and carotid artery ultrasound results. From the initial 5107 participants of LSAC in 2004, 3764 (73.7%) remained in wave 6 in 2014. Among them, 1874 consented to the Checkpoint assessment, and 1489 underwent carotid artery ultrasound study, and only 1063 children (20.8% of 5107) with acceptable quality in carotid IMT measurements, serum cholesterol (including LDL-C and HDL-C), and modeled estimates of NO2 and PM2.5 exposure were
Discussion
Despite many studies addressing the relationship between air pollutants and increased carotid IMT, most have been conducted in adults (Diez Roux et al., 2008; Kim et al., 2014; Kunzli et al., 2005; Lenters et al., 2010; Su et al., 2015; Tonne et al., 2012). This is the first investigation, of which we are aware, demonstrating a relationship in children between CIMT at age of twelve, and lifetime exposure to PM2.5 from birth. The relationship is similar in girls and boys, significant for both
Conclusion
There is evidence that life-time average exposure to PM2.5 among children has measurable adverse impacts on vascular structure by age 11–12 years. Although the longer-term impacts are yet unknown, findings of increased CIMT should not be ignored and may have important clinical and public health implications.
Credit author statement
Yue Leon Guo: Conceptualization, Formal analysis, Writing – original draft, Rosario D. Ampon: Programming, Software, Ivan Hanigan: Data curation, Luke D. Knibbs: Data curation, Validation, Writing – original draft, Christy Geromboux: Data curation, Ta-Chen Su: Methodology, Writing – review & editing, Kazuaki Negishi: Methodology, Writing – review & editing, Leanne Poulos: Project administration, Software, Geoff Morgan: Methodology, Writing – review & editing, Bin Jalaludin: Conceptualization,
Declaration of competing interest
The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Dr. Negishi is supported by a Fellowship (Award Reference No.101868) from the National Heart Foundation of Australia, which had no role in the preparation of this manuscript.
Acknowledgment
This paper uses unit record data from Growing Up in Australia, the Longitudinal Study of Australian Children (LSAC). The study is conducted in partnership between the Department of Social Services (DSS), the Australian Institute of Family Studies (AIFS) and the Australian Bureau of Statistics (ABS). The authors thank the participants of the LSAC and CheckPoint study, the LSAC staff and students for their contributions. Professor Yue Leon Guo is a visiting academic in University of Sydney
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This paper has been recommended for acceptance by Payam Dadvand.