Ozone-induced paradoxical sleep decrease is related to diminished acetylcholine levels in the medial preoptic area in rats

Alfaro-Rodríguez, Alfonso; González-Piña, Rigoberto

doi:10.1016/j.cbi.2004.10.001

Cited by 12 publications

(5 citation statements)

References 25 publications

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“…Exposure to 0.5 ppm O 3 led to significant reductions in paradoxical sleep pattern, an effect manifested primarily in the daytime when rats were sleeping. More recent studies suggest that these patterns are related to O 3 -induced alterations in neurotransmitter levels in the medial preoptic area of the CNS (Alfaro-Rodriguez & Gonzalez-Pina, 2005;Gonzalez-Pina & Alfaro-Rodriguez, 2003). These effects occurred during O 3 exposure or shortly after recovery, whereas the fever-like effects shown in this study persisted for at least 24 h after exposure.…”

Section: Discussioncontrasting

confidence: 51%

Episodic ozone exposure in adult and senescent Brown Norway rats: acute and delayed effect on heart rate, core temperature and motor activity

Gordon

Johnstone

Aydin

et al. 2014

Inhalation Toxicology

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Setting exposure standards for environmental pollutants may consider the aged as a susceptible population but the few published studies assessing susceptibility of the aged to air pollutants are inconsistent. Episodic ozone (O₃) is more reflective of potential exposures occurring in human populations and could be more harmful to the aged. This study used radiotelemetry to monitor heart rate (HR), core temperature (T(c)) and motor activity (MA) in adult (9-12 months) and senescent (20-24 months) male, Brown Norway rats exposed to episodic O₃ (6 h/day of 1 ppm O₃ for 2 consecutive days/week for 13 weeks). Acute O₃ initially led to marked drops in HR and T(c). As exposures progressed each week, there was diminution in the hypothermic and bradycardic effects of O₃. Senescent rats were less affected than adults. Acute responses were exacerbated on the second day of O₃ exposure with adults exhibiting greater sensitivity. During recovery following 2 d of O₃, adult and senescent rats exhibited an elevated T(c) and HR during the day but not at night, an effect that persisted for at least 48 h after O₃ exposure. MA was elevated in adults but not senescent rats during recovery from O₃. Overall, acute effects of O₃, including reductions in HR and T(c), were attenuated in senescent rats. Autonomic responses during recovery, included an elevation in T(c) with a pattern akin to that of a fever and rise in HR that were independent of age. An attenuated inflammatory response to O₃ in senescent rats may explain the relatively heightened physiological response to O₃ in younger rats.

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Section: Discussioncontrasting

confidence: 51%

Episodic ozone exposure in adult and senescent Brown Norway rats: acute and delayed effect on heart rate, core temperature and motor activity

Gordon

Johnstone

Aydin

et al. 2014

Inhalation Toxicology

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“…Comparisons were performed between prenatal clean-air exposed rats (clear bars) and prenatal O3-exposed rats (dark bars). Non-paired t-test (*P B 0.05) extracellular 5-HIAA and acetylcholine activity while rats were breathing concentrations ranging from 0.1 to 0.5 ppm [6,7]. Maximum levels of O3 measured in Mexico City have been 0.49 ppm [46].…”

Section: Discussionmentioning

confidence: 99%

“…For example, it has been demonstrated that paradoxical sleep disruptions caused by O3 exposure are mediated by changes in serotonin (5-HT) activity in the dorsal raphe [6] and also by extracellular acetylcholine in the hypothalamic medial preoptic area [7]. These disruptions could be mediated by secondary products, such as hydrogen peroxide, aldehydes, and free radicals, which are produced by initial reactions between O3 and the respiratory system.…”

Section: Introductionmentioning

confidence: 98%

Prenatal Exposure to Ozone Disrupts Cerebellar Monoamine Contents in Newborn Rats

et al. 2007

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Ozone (O3) is widely distributed in environments with high levels of air pollution. Since cerebellar morphologic disruptions have been reported with prenatal O3 exposure, O3 may have an effect on some neurotransmitter systems, such as monoamines. In order to test this hypothesis, we used 60 male rats taken from either, mothers exposed to 1 ppm of O3 during the entire pregnancy, or from mothers breathing filtered and clean air during pregnancy. The cerebellum was extracted at 0, 5, and 10 postnatal days. Tissues were processed in order to analyze by HPLC, dopamine (DA) levels, 3,4 dihydroxyphenilacetic acid (DOPAC) and homovanillic acid (HVA), norepinephrine (NA), serotonin, and 5-hydroxy-indole-acetic acid (5-HIAA) contents. Results showed a decrease of DA, NA, DOPAC and HVA mainly in 0 and 5 postnatal days. There were no changes in 5-HT levels, and 5-HIAA showed an increase after 10 postnatal days. DOPAC + HVA/DA ratio showed changes in 0 and 10 postnatal days, while 5-HIAA/5-HT ratio showed a slight decrease in 0 days. The data suggest that prenatal O3 exposure disrupts the cerebellar catecholamine system rather than the indole-amine system. Disruptions in cerebellar NA could lead to ataxic symptoms and also could limit recovery after cortical brain damage in adults. These finding are important given that recovery mechanisms observed in animals are also observed in humans.

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“…One high-quality study measured actigraphy over a 6-week period and evaluated within-person associations between air pollutants (O 3 , PM 2.5 , SO 2 , NO 2 , CO) and wake after sleep onset, sleep efficiency, sleep duration, and self-reported sleep quality, and reported an association between daily maximum ozone levels and longer sleep duration [87]. Experimental evidence suggests that O 3 exposure increases slow wave sleep (SWS) [291][292][293] and alters serotonin levels [294,295], possibly due to altered acetylcholine signaling [292]. While the other 3 included studies with O 3 measures did not report associations, sleep outcomes were ascertained using questionnaires, ICD-10 codes, or text-mining rather than actigraphy or PSG.…”

Section: Air Pollutionmentioning

confidence: 99%

Is exposure to chemical pollutants associated with sleep outcomes? A systematic review

Wallace

Gallagher

Peterson

et al. 2022

Preprint

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Background: Sleep disruption is a public health concern and environmental exposures that influence the biological processes underpinning sleep may contribute to impaired sleep health. However, the contributions of environmental chemical pollutants to sleep health have not been systematically investigated. Objectives: This systematic literature review sought to identify, evaluate, summarize, and synthesize the existing evidence between environmental chemical pollutant exposure and dimensions of sleep health in humans. We sought to evaluate potential mechanisms underlying exposure-outcome relationships and recommend areas for future research. Methods: Databases were searched for peer-reviewed published research on chemical environmental pollutants and sleep health and disorders with no date restriction up to the last search date of April 2021 (registered protocol PROSPERO # CRD42021256918), resulting in 9,918 records. Two reviewers independently screened identified records against inclusion and exclusion criteria, extracted study information, and performed risk of bias assessments. Results: We identified 204 studies of exposure to air pollution, exposures related to the Gulf War and other conflicts, endocrine disruptors, metals, pesticides, and solvents with dimensions of sleep health (architecture, duration, quality, timing) and sleep disorders (sleeping pill use, insomnia, sleep-disordered breathing) for inclusion in this review. Metals were the most frequently evaluated pollutants, while sleep maintenance/insomnia and quality were the most reported sleep outcomes. Synthesis of the evidence suggests mechanisms related to cholinergic signaling, neurotransmission, and inflammation as the most shared pathways. Discussion: Evidence indicates that exposure to particulate matter, secondhand smoke, dioxins and dioxin-like compounds, lead, mercury, pesticides, solvents, and exposures related to the Gulf War are associated with worse sleep health and disorders. Chemical pollutants are likely key environmental determinants of sleep health and disorders; thus, there is a need to improve measurement of pollutants and sleep, study rigor, and determine the populations most vulnerable to the effects of exposure.

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Ozone-induced paradoxical sleep decrease is related to diminished acetylcholine levels in the medial preoptic area in rats

Cited by 12 publications

References 25 publications

Episodic ozone exposure in adult and senescent Brown Norway rats: acute and delayed effect on heart rate, core temperature and motor activity

Episodic ozone exposure in adult and senescent Brown Norway rats: acute and delayed effect on heart rate, core temperature and motor activity

Prenatal Exposure to Ozone Disrupts Cerebellar Monoamine Contents in Newborn Rats

Is exposure to chemical pollutants associated with sleep outcomes? A systematic review

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