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  • br Environmental pollution is a

    2019-04-22


    Environmental pollution is a global problem and the subject of increasing worldwide public health concern. In particular, air pollution is regarded as the largest single environmental risk to health. More than 80% of people living in urban areas that monitor air pollution are exposed to air quality levels that exceed the WHO limits, and all regions of the world are affected. Declines in urban air quality increase the risk of cerebrovascular accidents, coronary artery disease, lung carcinoma, and chronic and acute respiratory diseases (eg, asthma, obstructive lung disease, and acute lower respiratory infections). Associations between air pollution and central nervous system diseases have also been shown, but we believe that relatively little attention has been given to the possible role of pollution as a risk factor for neurodevelopmental (eg, schizophrenia) and neurodegenerative (eg, dementia) diseases. Therefore, we read with great interest the articles by Chen and colleagues in and by Gao and colleagues in . The former was a large population-based cohort study conducted in Ontario, Canada, whose findings showed that urban residents, especially individuals living close to heavy traffic roads had an increased incidence of dementia. Notably, long-term exposure to fine particulate order AZD4547 (≤2·5 μm in diameter; PM) and nitrogen dioxide was positively associated with dementia. The latter study was a time-series analysis done in Beijing, China, investigating the acute effects of particulate matter on hospital admissions for mental disorders. The authors reported that elevated levels of PM (particulate matter ≤10 μm in diameter), PM, and PM (2·5–10 μm in diameter), were significantly associated with a small increase in hospital admissions for schizophrenia. Schizophrenia evidently has a multifactorial (genetic and environmental) aetiology, and is a complex, and clinically heterogeneous neurodevelopmental syndrome, associated with variable functional impairments in social, emotional, perceptual, and cognitive domains. A biological association between schizophrenia and dementia has been debated for a long time, since Emil Kraepelin named schizophrenia as dementia praecox (premature dementia). The question of whether cognitive impairment is a core feature of schizophrenia is still a matter of debate. Evidence of deficits in multiple cognitive domains such as memory, attention, and visuospatial orientation, is noted in individuals with schizophrenia. Patients with schizophrenia show different degrees of cognitive impairment, and have poorer performance than healthy counterparts. Not infrequently, impairments in cognition can manifest years before the first psychotic episode, and usually cognitive dysfunctions are chronic. More recently, it has been proposed that schizophrenia could be a syndrome of accelerated ageing, suggesting that physiological abnormalities associated with schizophrenia could contribute to the increased mortality of individuals affected by this disorder. It has been furthermore shown that patients with schizophrenia have a substantially increased relative risk of dementia that could not be explained by established dementia risk factors, such as cardiovascular disease and diabetes. A comprehensive hypothetical model may be explained by the presence of a progressive, neurodegenerative component in addition to a neurodevelopmental component in subjects with schizophrenia. The pathophysiological factors of the link between schizophrenia and dementia remain unclear. Urbanicity (being born or raised in cities) has been commonly described as one of the risk factors for schizophrenia and other non-affective psychosis, and pollution exposure (eg, exposure to xenobiotic heavy metals such as lead and cadmium, constituents of air pollution such as particulate matter, and nitrogen and sulphur oxides, organic solvents, and other constituents of environmental pollution) could potentially mediate the association between urbanicity and elevated risk, at least in part.