Abstract

View the most recent version.

Background

A growing number of epidemiological studies have linked air pollution exposure to psychological conditions. Laboratory studies indicate that air pollutants can activate the neuroendocrine stress axis and modulate stress hormone levels, which could contribute to the development or exacerbation of psychological distress. The present study examined the spatial associations between air pollutants (fine particulate matter [PM_2.5], nitrogen dioxide [NO₂] and ground-level ozone [O₃]) and psychological distress among subjects in the most populous provinces in Canada.

Data and methods

Subjects were sampled from the Canadian Community Health Survey in three regions (Quebec in 2005 [n=25,800], British Columbia and Alberta in 2005 [n=23,000], and Ontario in 2011 [n=36,000]), and were assigned estimates of annual exposure to three ambient air pollutants (PM_2.5, NO₂ and O₃) for the same years. Individual psychological distress was assessed using the Kessler Psychological Distress Scale (K10), based on anxiety and depressive symptoms in the past month. Regression models (both ordinary least squares and simultaneous autoregressive models) were applied to estimate associations between K10 distress scores and each air pollutant, after adjusting for individual (demographic, socioeconomic and behavioural) and neighbourhood covariates.

Results

Psychological distress was positively associated with PM_2.5 and NO₂ in all three regions, and with O₃ in Quebec. However, after further adjusting for individual and neighbourhood covariates, the associations between distress and air pollution remained statistically significant only in Quebec.

Conclusion

Some evidence for positive associations between psychological distress and ambient air pollution after adjusting for spatial autocorrelation was found.

Keywords

distress, Kessler Psychological Distress Scale (K10), ambient air pollution, fine particulate matter, PM_2.5, nitrogen dioxide, ground-level ozone

DOI: https://www.doi.org/10.25318/82-003-x202000700001-eng

Findings

In addition to having well-established associations with respiratory and cardiovascular morbidity and mortality, air pollution has been linked to a range of neurological and psychiatric disorders, including dementia, cognitive decline or impairment, anxiety and depression, and suicide. A growing body of controlled experimental research supports these epidemiological associations. This research includes evidence that air pollution can impair spatial learning and memory, and provoke depressive-like behaviour in mice. A number of biological mechanisms have been proposed to explain these associations. For example, exposure to inhaled pollutants has been shown to activate the hypothalamic-pituitary-adrenal (HPA) stress axis in rats, resulting in increased blood levels of the glucocorticoid corticosterone, and systemic regulation of stress, metabolic, and inflammatory pathways across multiple tissues. Acute activation of the HPA axis is a critical adaptive response to stressors. However, chronic stress and glucocorticoid dysregulation are associated with many disease processes, including anxiety, depression, impaired cognition, chronic pain and fatigue syndrome, obesity, diabetes, and cardiovascular disease. Chronic exposure to air pollution—in conjunction with exposure to other stressors and interaction with host susceptibility traits—could lead to HPA axis dysfunction and observable stress-related or distress-related outcomes, including neurological, metabolic, cardiovascular and reproductive disorders. Accordingly, stress-related outcomes in the causal pathway between air pollutant exposure and disease should be investigated to substantiate the link between pollutant-dependent neuroendocrine stress responses and impacts on the brain. [Full article]

Authors

Lauren Pinault (lauren.pinault@canada.ca), Tanya Christidis, and Michael Tjepkema are with the Health Analysis Division at Statistics Canada, Ottawa, Ontario. Errol M. Thomson (errol.thomson@canada.ca) is with the Hazard Identification Division in the Environmental Health Science and Research Bureau at Health Canada, Ottawa, Ontario. Ian Colman is with the Faculty of Medicine at the University of Ottawa. Aaron van Donkelaar is with the Department of Physics and Atmospheric Science at Dalhousie University, Halifax, Nova Scotia, and also at the Department of Energy, Environmental & Chemical Engineering, Washington University, St. Louis, Missouri, USA. Randall V. Martin is with the Department of Energy, Environmental & Chemical Engineering, Washington University, St. Louis, Missouri, USA, and also the Department of Physics and Atmospheric Science at Dalhousie University, Halifax, Nova Scotia and the Harvard-Smithsonian Center for Astrophysics. Perry Hystad is with the College of Public Health and Human Sciences at Oregon State University. Hwashin Shin and Richard T. Burnett are with the Population Studies Division in the Environmental Health Science and Research Bureau at Health Canada, Ottawa, Ontario. Daniel L. Crouse is with the Health Effects Institute, Boston, MA.

End of text box