Neurotoxicity of air pollution: Role of neuroinflammation

Costa, Lucio G.; Cole, Toby B.; Dao, Khoi; Chang, Yu‐Chi; Coburn, Jacki; Garrick, Jacqueline M.

doi:10.1016/bs.ant.2018.10.007

Cited by 5 publications

(6 citation statements)

References 182 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Most studies so far have focused mainly on the gestational exposure period, 17,18,[47][48][49] whereas little has been studied about neurodevelopmental mechanisms of early postnatal exposure to air pollution that may lead to ASD. This is true for animal studies as well, since most of them were focused on exposure in developmental periods which are equivalent to the third trimester in humans.…”

Section: Discussionmentioning

confidence: 99%

“…16 During gestation, mechanisms such as maternal immune activation and systemic inflammation or penetration of ultrafine particles to the fetal brain may induce neuroinflammation, 17 which may result in ASD. 18 In the early postnatal exposure period, the infant directly inhales polluted air so that neuroinflammation may be induced through systemic inflammation or particle penetration into the brain, possibly through the olfactory route. 19 A comprehensive investigation of the role of air pollutants in ASD should take into account all these exposure periods, given that each of them represents a distinct mechanistic pathway.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Air Pollution and Autism Spectrum Disorder in Israel

et al. 2021

View full text Add to dashboard Cite

Background: Residual confounding is a major concern for causal inference in observational studies on air pollution-autism spectrum disorder (ASD) associations. This study is aimed at assessing confounding in these associations using negative control exposures. Methods: This nested case-control study included all children diagnosed with ASD (detected through 31 December 2016) born during 2007-2012 in Israel and residing in the study area (N = 3,843), and matched controls of the same age (N = 38,430). We assigned individual house-level exposure estimates for each child. We estimated associations using logistic regression models, mutually adjusted for all relevant exposure periods (prepregnancy, pregnancy, and postnatal). We assessed residual confounding using postoutcome negative control exposure at age 28-36 months. Results: In mutually adjusted models, we observed positive associations with ASD for postnatal exposures to NOx (odds ratio per interquartile range, 95% confidence interval: 1.19, 1.02-1.38) and NO 2 (1.20, 1.00-1.43) , and gestational exposure to PM 2.5-10 (1.08, 1.01-1.15). The result for the negative control period was 1.04, 0.99-1.10 for PM 2.5, suggesting some residual confounding, but no associations for PM 2.5-10 (0.98, 0.81-1.18), NOx (1.02, 0.84-1.25), or NO 2 (0.98, 0.81-1.18), suggesting no residual confounding. Conclusions: Our results further support a hypothesized causal link with ASD that is specific to postnatal exposures to traffic-related pollution.

show abstract

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Air Pollution and Autism Spectrum Disorder in Israel

et al. 2021

View full text Add to dashboard Cite

show abstract

“…As such, the aim of our study was to evaluate whether perinatal DE exposure alone is sufficient to impact markers of neurodegenerative disease later in life in aged mice. Specifically, our study focused on markers relevant to AD 43 and neuroinflammation, an important mechanism by which DE exerts neurotoxicity 44 …”

Section: Introductionmentioning

confidence: 99%

“…Specifically, our study focused on markers relevant to AD 43 and neuroinflammation, an important mechanism by which DE exerts neurotoxicity. 44 All qPCR primers were purchased from Integrated DNA Technologies (Newark, NJ, USA).…”

mentioning

confidence: 99%

Perinatal diesel exhaust exposure causes persistent changes in the brains of aged mice: An assessment of behavioral and biochemical endpoints related to neurodegenerative disease

Garrick

Cole

Dao

et al. 2023

Environmental Toxicology

View full text Add to dashboard Cite

Epidemiological studies support an association between air pollution exposure, specifically particulate matter (PM), and neurodegenerative disease. Diesel exhaust (DE) is a principal component of ambient air pollution and a major contributor of PM. Our study aimed to examine whether early‐life perinatal DE exposure is sufficient to affect behavioral and biochemical endpoints related to Alzheimer's disease later in life. To achieve this, mice were perinatally exposed (embryonic day 0–postnatal day 21) to DE (250–300 μg/m3) or filtered air (FA), and allowed to reach aged status (>18 months). Mice underwent behavioral assessment at 6 and 20 months of age, with tissue collected at 22 months for biochemical endpoints. At 6 months, minimal changes were noted in home‐cage behavior of DE treated animals. At 20 months, an alternation deficit was noted with the T‐maze, although no difference was seen in the object location task or any home‐cage metrics. DE exposure did not alter the expression of Aβ42, phosphorylated tau S199, or total tau. However, IBA‐1 protein, a microglial activation marker, was significantly higher in DE exposed animals. Further, lipid peroxidation levels were significantly higher in the DE exposed animals compared to FA controls. Cytokine levels were largely unchanged with DE exposure, suggesting a lack of inflammation despite persistent lipid peroxidation. Taken together, the findings of this study support that perinatal exposure alone is sufficient to cause lasting changes in the brain, although the effects appear to be less striking than those previously reported in younger animals, suggesting some effects do not persist over time. These findings are encouraging from a public health standpoint and support the aggressive reduction of DE emissions to reduce lifetime exposure and potentially reduce disease outcome.

show abstract

“…Although numerous investigations have been devoted to the elucidation of the ND pathologies, their primary causes continue elusive. Some interrelated crucial aspects on the progression of these disorders are proteopathy [6–8], metal ion dyshomeostasis [9–32], environmental pollutants [33–47], and neurotransmitter deficiencies. A chemical phenomenom shared by all these diseases is oxidative stress (OS).…”

Section: Introductionmentioning

confidence: 99%

Computational design of rasagiline derivatives: Searching for enhanced antioxidant capability

Reina

Guzmán‐López

Galano

2022

Int J of Quantum Chemistry

View full text Add to dashboard Cite

A set of new rasagiline derivatives is presented. They were designed to be antioxidant compounds with the potential to be used for treating neurodegenerative disorders. They are expected to be multifunctional molecules that can help reduce oxidative stress, which is thought to contribute to neurodegenerative disorders. The CADMA‐Chem computational protocol was used to produce rasagiline derivatives and to evaluate their likeliness as oral drugs and antioxidants. Three of them were identified as the most promising ones. They are proposed to be better free radical scavengers than rasagiline. In addition, they are expected to keep the parent's molecule neuroprotective capability. Hopefully, the results presented here would promote further experimental and theoretical investigations on these compounds.

show abstract

Neurotoxicity of air pollution: Role of neuroinflammation

Cited by 5 publications

References 182 publications

Air Pollution and Autism Spectrum Disorder in Israel

Air Pollution and Autism Spectrum Disorder in Israel

Perinatal diesel exhaust exposure causes persistent changes in the brains of aged mice: An assessment of behavioral and biochemical endpoints related to neurodegenerative disease

Computational design of rasagiline derivatives: Searching for enhanced antioxidant capability

Contact Info

Product

Resources

About