Although these issues complicate interpretation of human stu

Although these issues complicate interpretation of human studies, they exemplify the problem of so-called regrettable substitution. The economic benefits of substituting BPA in the linings of aluminium cans with an alternative free of health effects (US$1·74 billion per year) were found to nearly outweigh the costs of a natural alternative oleoresin ($2·2 billion per year), and this analysis was limited to benefits associated with reductions in BPA-attributable childhood obesity and coronary artery disease. Oleoresin is not necessarily a feasible alternative for all canned foods, but substitution of BPA with BPF, BPS, or another bisphenol might result in the same associations with adverse health outcomes as BPA, after years of studies in the laboratory and human beings. The European Commission has the opportunity to set the platform for a stronger regulatory framework for bisphenols and other endocrine disrupting chemicals (EDCs) that necessitate the use of safer alternatives when laboratory and other studies suggest that they cause adverse effects. The stakes are high; EDC-associated diseases and disabilities extend well beyond bisphenols to a broader array of synthetic chemicals, with effects including adverse neurodevelopmental outcomes, diabetes, cardiovascular disease, and male and female reproductive disorders. The costs of EDC exposures are estimated to be €163 billion in the European Union and $340 billion in the USA. Although these estimates are based on known exposures, they suggest the large, potential societal benefits of proactive and thorough screening of new chemicals before they can be introduced into the market, and reconsidering the use of non-A bisphenols and other potentially regrettable substitutes.
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 AZD1152 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 matter (≤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.