###### Abstract  
Both psychosocial and physical environmental stressors have been linked to chronic mental health and chronic medical conditions. The psycho-immune-neuroendocrine (PINE) network details metabolomic pathways which are responsive to varied stressors and link chronic medical conditions with mental disorders, such as major depressive disorder via a network of pathophysiological pathways. The primary objective of this review is to explore evidence of relationships between airborne particulate matter (PM, as a concrete example of a physical environmental stressor), the PINE network and chronic non-communicable diseases (NCDs), including mental health sequelae, with a view to supporting the assertion that physical environmental stressors (not only psychosocial stressors) disrupt the PINE network, leading to NCDs. Biological links have been established between PM exposure, key sub-networks of the PINE model and mental health sequelae, suggesting that in theory, long-term mental health impacts of PM exposure may exist, driven by the disruption of these biological networks. This disruption could trans-generationally influence health; however, long-term studies and information on chronic outcomes following acute exposure event are still lacking, limiting what is currently known beyond the acute exposure and all-cause mortality. More empirical evidence is needed, especially to link long-term mental health sequelae to PM exposure, arising from PINE pathophysiology. Relationships between physical and psychosocial stressors, and especially the concept of such stressors acting together to impact on PINE network function, leading to linked NCDs, evokes the concept of syndemics, and these are discussed in the context of the PINE network. psycho-immune-neuroendocrine network; chronic illness risk network; biological networks; metabolomic pathways; mental health; non-communicable disease; biopsyosocial model; syndemic; particulate matter +
Footnote †: journal: Journal of and Public Health  
conditions [4, 5]. These multiple (and sometimes multimorbid) conditions were described in terms of a chronic illness risk network (CIRN) [5], with non-communicable diseases (NCDs) including atherosclerosis and coronary heart disease (CHD), type 2 diabetes mellitus (T2 DM), cerebrovascular accident (CVA) and vascular cognitive impairment (VCI), together with mental disorders such as major depressive disorder (MDD). While psychosocial stressors have long been implicated in the onset of CIRN conditions, we assert that physical environmental stressors are similarly responsible for PINE pathophysiological change. We propose that environmental factors act both as risk factors and modifiers for PINE network dysfunction and progression to NCDs, following a stress diathesis model originally described by [6] ([PERSON], 1963), and explored briefly in relation to the PINE model [7]. The syndemic framework was developed to understand interacting diseases promoted by social, economic, environmental and political features of a population. The hallmark of a syndemic is the presence of two or more disease states that adversely influence each other and enhance vulnerability, and which are exaggerated by socioeconomic factors. One potent example of a physical environmental stressor is airborne particulate matter (PM), which can impact the PINE network, potentially leading to NCDs. PM is classified based on particle size, and there are three main classifications [8]. PM10 particles, also known as course particles, are particles \(\leq\)10 um in diameter commonly released via direct, rather than secondary, environmental stimulation such as dust storms or construction work [9]. PM2.5 particles are known as fine particles with a diameter \(\leq\)2.5 um, and due to their small size, travel further and accumulate greater than PM10, and penetrate deeper into human tissues [10]. PM2.5 originate primarily from fossil fuel combustion. Finally, PM0.1, known as ultra-fine particles, are particles \(\leq\)0.1 um in diameter [11].