Exposure to Environmental and Occupational Particulate Air Pollution as a Potential Contributor to Neurodegeneration and Diabetes: A Systematic Review of Epidemiological Research

Abstract

It has been hypothesised that environmental air pollution, especially airborne particles, is a risk factor for type 2 diabetes mellitus (T2DM) and neurodegenerative conditions. However, epidemiological evidence is inconsistent and has not been previously evaluated as part of a systematic review. Our objectives were to carry out a systematic review of the epidemiological evidence on the association between long-term exposure to ambient air pollution and T2DM and neurodegenerative diseases in adults and to identify if workplace exposures to particles are associated with an increased risk of T2DM and neurodegenerative diseases. Assessment of the quality of the evidence was carried out using the GRADE system, which considers the quality of the studies, consistency, directness, effect size, and publication bias. Available evidence indicates a consistent positive association between ambient air pollution and both T2DM and neurodegeneration risk, such as dementia and a general decline in cognition. However, corresponding evidence for workplace exposures are lacking. Further research is required to identify the link and mechanisms associated with particulate exposure and disease pathogenesis and to investigate the risks in occupational populations. Additional steps are needed to reduce air pollution levels and possibly also in the workplace environment to decrease the incidence of T2DM and cognitive decline.

Keywords: Alzheimer’s disease; Parkinson’s disease; air pollution; cognitive function; dementia; epidemiology; neurodegeneration; occupational; particulate matter; type 2 diabetes.

Figure 1

Flow chart of the literature search.

Figure 2

Following inhalation, particles may stimulate local or systemic effects. The hypothesised mechanism of toxicity of inhaled particles to the central nervous system (CNS) is summarized in (A). Impacts of inhaled particles on the CNS may emerge due to (i) particle translocation (via neurones or blood) to the CNS following inhalation or (ii) the release of systemically acting factors from the lung which impact on neurone function. Examples of the clinical impacts of inhaled particles at different target sites (lung, extrapulmonary organs, and CNS) are summarised in blue boxes; (B) The cellular and molecular events underlying particle toxicity to the lungs have been extensively investigated and hypothesised to involve the stimulation of inflammation and oxidative stress. More specifically, it is hypothesized that inhaled ultrafine particles interact with pulmonary cells (e.g., epithelial cells, alveolar macrophages) to stimulate an increase in intracellular ROS and Ca²⁺ concentration which leads to the expression of pro-inflammatory genes (e.g., cytokines) via the activation of transcription factors (such as NFκB). BBB = blood brain barrier. COPD = chronic obstructive pulmonary disease.