The effects of ozone exposure and associated injury mechanisms on the central nervous system

Martínez-Lazcano, Juan Carlos; González-Guevara, Edith; Rubio, Carmen; Franco-Pérez, Javier; Custodio, Verónica; Hernández-Cerón, Miguel; Livera, Carlos; Paz, Carlos

doi:10.1515/revneuro-2012-0084

Cited by 65 publications

(29 citation statements)

References 57 publications

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“…Oxidative stress is involved in many neurodegenerative diseases, in which the over-production of O 3 leads to both pathological and functional brain injuries [33]. Moreover, the environmental O 3 exposure is associated with a series of adverse effects within the central nervous system, such as decreased cognitive response, decrease in motor activity and headaches, disturbances in the sleep-wake cycle, cell degeneration, and neurochemical alterations [34]. Taken together, the paradoxical effects of O 3 may depend on its concentration: while high concentration of O 3 may impair nervous system, low level of O 3 may act as a protector.…”

Section: Discussionmentioning

confidence: 99%

The Novel Relationship between Urban Air Pollution and Epilepsy: A Time Series Study

Fan

Kan

et al. 2016

PLoS ONE

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Background and purposeThe data concerning the association between environmental pollution and epilepsy attacks are limited. The aim of this study was to explore the association between acute air pollution exposure and epilepsy attack.MethodsA hospital record-based study was carried out in Xi’an, a heavily-polluted metropolis in China. Daily baseline data were obtained. Time-series Poisson regression models were applied to analyze the association between air pollution and epilepsy.ResultsA 10 μg/m3 increase of NO2, SO2, and O3 concentrations corresponded to 3.17% (95%Cl: 1.41%, 4.93%), 3.55% (95%Cl: 1.93%, 5.18%), and -0.84% (95%Cl: -1.58%, 0.09%) increase in outpatient-visits for epilepsy on the concurrent days, which were significantly influenced by sex and age. The effects of NO2 and SO2 would be stronger when adjusted for PM2.5. As for O3, a -1.14% (95%Cl: -1.90%, -0.39%) decrease was evidenced when adjusted for NO2. The lag models showed that the most significant effects were evidenced on concurrent days.ConclusionsWe discovered previously undocumented relationships between short-term air pollution exposure and epilepsy: while NO2 and SO2 were positively associated with outpatient-visits of epilepsy, O3 might be associated with reduced risk.

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Section: Discussionmentioning

confidence: 99%

The Novel Relationship between Urban Air Pollution and Epilepsy: A Time Series Study

Fan

Kan

et al. 2016

PLoS ONE

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“…The temporal pattern of metabolic changes seen in the present study suggests that neuronal response might be stimulated prior to inflammation. A number of animal studies have shown that O 3 can induce neuroinflammation and activate catecholeminergic neurons likely through lung vagus afferents (Gackiere et al, 2011; Martínez-Lazcano et al, 2013). Activation of these central nervous system locations can stimulate sympathetic and HPA-mediated release of adrenal stress hormones in the systemic circulation, which can perturb metabolic functions involving glucose, lipids, and amino acids (Seematter et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

Inhaled ozone (O3)-induces changes in serum metabolomic and liver transcriptomic profiles in rats

Miller

Karoly

Jones

et al. 2015

Toxicology and Applied Pharmacology

113

144

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Air pollution has been linked to increased incidence of diabetes. Recently, we showed that ozone (O3) induces glucose intolerance, and increases serum leptin and epinephrine in Brown Norway rats. In this study, we hypothesized that O3 exposure will cause systemic changes in metabolic homeostasis and that serum metabolomic and liver transcriptomic profiling will provide mechanistic insights. In the first experiment, male Wistar Kyoto (WKY) rats were exposed to filtered air (FA) or O3 at 0.25, 0.50, or 1.0 ppm, 6 h/day for two days to establish concentration-related effects on glucose tolerance and lung injury. In a second experiment, rats were exposed to FA or 1.0 ppm O3, 6 h/day for either one or two consecutive days, and systemic metabolic responses were determined immediately after or 18 h post-exposure. O3 increased serum glucose and leptin on day 1. Glucose intolerance persisted through two days of exposure but reversed 18 h-post second exposure. O3 increased circulating metabolites of glycolysis, long-chain free fatty acids, branched-chain amino acids and cholesterol, while 1,5-anhydroglucitol, bile acids and metabolites of TCA cycle were decreased, indicating impaired glycemic control, proteolysis and lipolysis. Liver gene expression increased for markers of glycolysis, TCA cycle and gluconeogenesis, and decreased for markers of steroid and fat biosynthesis. Genes involved in apoptosis and mitochondrial function were also impacted by O3. In conclusion, short-term O3 exposure induces global metabolic derangement involving glucose, lipid, and amino acid metabolism, typical of a stress–response. It remains to be examined if these alterations contribute to insulin resistance upon chronic exposure.

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“…In addition, pollutants may lead to an inflammatory reaction in the CNS or directly interfere with neuronal function that may affect sleep. 31…”

Section: Sleepmentioning

confidence: 99%

Air Pollution and Noncommunicable Diseases

Schraufnagel

Balmes

Cowl

et al. 2019

Chest

394

184

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Air pollution poses a great environmental risk to health. Outdoor fine particulate matter (particulate matter with an aerodynamic diameter < 2.5 mm) exposure is the fifth leading risk factor for death in the world, accounting for 4.2 million deaths and > 103 million disability-adjusted life years lost according to the Global Burden of Disease Report. The World Health Organization attributes 3.8 million additional deaths to indoor air pollution. Air pollution can harm acutely, usually manifested by respiratory or cardiac symptoms, as well as chronically, potentially affecting every organ in the body. It can cause, complicate, or exacerbate many adverse health conditions. Tissue damage may result directly from pollutant toxicity because fine and ultrafine particles can gain access to organs, or indirectly through systemic inflammatory processes. Susceptibility is partly under genetic and epigenetic regulation. Although air pollution affects people of all regions, ages, and social groups, it is likely to cause greater illness in those with heavy exposure and greater susceptibility. Persons are more vulnerable to air pollution if they have other illnesses or less social support. Harmful effects occur on a continuum of dosage and even at levels below air quality standards previously considered to be safe.

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The effects of ozone exposure and associated injury mechanisms on the central nervous system

Cited by 65 publications

References 57 publications

The Novel Relationship between Urban Air Pollution and Epilepsy: A Time Series Study

The Novel Relationship between Urban Air Pollution and Epilepsy: A Time Series Study

Inhaled ozone (O3)-induces changes in serum metabolomic and liver transcriptomic profiles in rats

Air Pollution and Noncommunicable Diseases

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