Short-term and long-term exposures to fine particulate matter constituents and health: A systematic review and meta-analysis

Yang, Yang; Ruan, Zengliang; Wang, Xiaojie; Yang, Yin; Mason, Tonya G.; Lin, Hualiang; Tian, Linwei

doi:10.1016/j.envpol.2018.12.060

Cited by 304 publications

(171 citation statements)

References 70 publications

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“…Pb also results in oxidative stress by depleting GSH [86,89], decreasing superoxide dismutase activity [86,89], and increasing malondialdehyde [89], ROS production [85], and catalase expression [89]. PM 2.5 also contains other toxic and nutrient metals including cadmium, iron and nickel which can have detrimental effects on the mitochondria [6,90]. Interestingly, we have recently found that prenatal exposure to nutrient metals Zinc and Manganese, both of which are contained in air pollution, modulate long-term mitochondrial function in children with ASD and NDR [91].…”

Section: Elements Of Air Pollution Can Directly Affect Mitochondrial mentioning

confidence: 99%

Prenatal air pollution influences neurodevelopment and behavior in autism spectrum disorder by modulating mitochondrial physiology

et al. 2020

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We investigate the role of the mitochondrion, an organelle highly sensitive to environmental agents, in the influence of prenatal air pollution exposure on neurodevelopment and behavior in 96 children with autism spectrum disorder (ASD) [45 with neurodevelopmental regression (NDR); 76% Male; mean (SD) age 10 y 9 m (3 y 9 m)]. Mitochondrial function was assessed using the Seahorse XFe96 in fresh peripheral blood mononuclear cells. Second and third trimester average and maximal daily exposure to fine air particulate matter of diameter ≤2.5 µm (PM2.5) was obtained from the Environmental Protection Agency’s Air Quality System. Neurodevelopment was measured using the Vineland Adaptive Behavior Scale 2nd edition and behavior was assessed using the Aberrant Behavior Checklist and Social Responsiveness Scale. Prenatal PM2.5 exposure influenced mitochondrial respiration during childhood, but this relationship was different for those with (r = 0.25–0.40) and without (r = −0.07 to −0.19) NDR. Mediation analysis found that mitochondrial respiration linked to energy production accounted for 25% (SD = 2%) and 10% (SD = 2%) of the effect of average prenatal PM2.5 exposure on neurodevelopment and behavioral symptoms, respectively. Structural equation models estimated that PM2.5 and mitochondrial respiration accounted for 34% (SD = 4%) and 36% (SD = 3%) of the effect on neurodevelopment, respectively, and that behavior was indirectly influenced by mitochondrial respiration through neurodevelopment but directly influenced by prenatal PM2.5. Our results suggest that prenatal exposure to PM2.5 disrupts neurodevelopment and behavior through complex mechanisms, including long-term changes in mitochondrial respiration and that patterns of early development need to be considered when studying the influence of environmental agents on neurodevelopmental outcomes.

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Section: Elements Of Air Pollution Can Directly Affect Mitochondrial mentioning

confidence: 99%

Prenatal air pollution influences neurodevelopment and behavior in autism spectrum disorder by modulating mitochondrial physiology

et al. 2020

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“…Some uncertainty in our risk estimate also arises with the use of effect estimates derived from a single study. Surveying several meta-analyses [28,51] yielded no additional studies providing suitable effect estimates corresponding to long-term exposure specifically for BC and the CHD endpoint. More information was available from a similar survey of NO 2 studies [27].…”

Section: Discussionmentioning

confidence: 99%

A risk-based model to assess environmental justice and coronary heart disease burden from traffic-related air pollutants

et al. 2020

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Background: Communities need to efficiently estimate the burden from specific pollutants and identify those most at risk to make timely informed policy decisions. We developed a risk-based model to estimate the burden of black carbon (BC) and nitrogen dioxide (NO 2) on coronary heart disease (CHD) across environmental justice (EJ) and non-EJ populations in Allegheny County, PA. Methods: Exposure estimates in census tracts were modeled via land use regression and analyzed in relation to US Census data. Tracts were ranked into quartiles of exposure (Q1-Q4). A risk-based model for estimating the CHD burden attributed to BC and NO 2 was developed using county health statistics, census tract level exposure estimates, and quantitative effect estimates available in the literature. Results: For both pollutants, the relative occurrence of EJ tracts (> 20% poverty and/or > 30% non-white minority) in Q2-Q4 compared to Q1 progressively increased and reached a maximum in Q4. EJ tracts were 4 to 25 times more likely to be in the highest quartile of exposure compared to the lowest quartile for BC and NO 2 , respectively. Pollutantspecific risk values (mean [95% CI]) for CHD mortality were higher in EJ tracts (5.49 × 10 − 5 [5.05 × 10 − 5-5.92 × 10 − 5 ]; 5.72 × 10 − 5 [5.44 × 10 − 5-6.01 × 10 − 5 ] for BC and NO 2 , respectively) compared to non-EJ tracts (3.94 × 10 − 5 [3.66 × 10 − 5-4.23 × 10 − 5 ]; 3.49 × 10 − 5 [3.27 × 10 − 5-3.70 × 10 − 5 ] for BC and NO 2 , respectively). While EJ tracts represented 28% of the county population, they accounted for about 40% of the CHD mortality attributed to each pollutant. EJ tracts are disproportionately skewed toward areas of high exposure and EJ residents bear a greater risk for air pollution-related disease compared to other county residents. Conclusions: We have combined a risk-based model with spatially resolved long-term exposure estimates to predict CHD burden from air pollution at the census tract level. It provides quantitative estimates of effects that can be used to assess possible health disparities, track temporal changes, and inform timely local community policy decisions. Such an approach can be further expanded to include other pollutants and adverse health endpoints.

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“…Skin is the largest organ in humans and the primary organ exposed to PM. A long-term exposure to PM causes many negative effects on the skin, such as oxidative stress, inflammatory response, atopic dermatitis, aging, and skin carcinoma [12][13][14][15][16]. In recent years, the related studies have been done to investigate the relationship between PM and skin health, as well as to discover the agents that could protect or improve PM-induced skin damages.…”

Section: Introductionmentioning

confidence: 99%

Protective Effect of Diphlorethohydroxycarmalol Isolated from Ishige okamurae Against Particulate Matter-Induced Skin Damage by Regulation of NF-κB, AP-1, and MAPKs Signaling Pathways In Vitro in Human Dermal Fibroblasts

Wang

Kim

et al. 2020

Molecules

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Particulate matters (PM), the main contributor to air pollution, have become a serious issue that threatens human’s health. Skin is the largest organ in humans, as well as the primary organ exposed to PM. Overexposure of PM induces skin damage. Diphlorethohydroxycarmalol (DPHC), an algal polyphenol with the potential of skin protection, has been isolated from the edible brown seaweed Ishige okamurae. The purpose of the present study is to investigate the protective effect of DPHC against PM (ERM-CZ100)-induced skin damage in human dermal fibroblasts (HDF) cells. The results indicated that DPHC significantly and dose-dependently reduced intracellular reactive oxygen species generation in HDF cells. In addition, DPHC significantly induced collagen synthesis and inhibited collagenase activity in ERM-CZ100-stimulated HDF cells. Further study demonstrated that DPHC remarkably reduced the expression of human matrix metalloproteinases through regulation of nuclear factor kappa B, activator protein 1, and mitogen-activated protein kinases signaling pathways in ERM-CZ100-stimulated HDF cells. This study suggested that DPHC is a potential candidate to protect skins against PM-induced damage, and it could be used as an ingredient in pharmaceutical and cosmeceutical industries.

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Short-term and long-term exposures to fine particulate matter constituents and health: A systematic review and meta-analysis

Cited by 304 publications

References 70 publications

Prenatal air pollution influences neurodevelopment and behavior in autism spectrum disorder by modulating mitochondrial physiology

Prenatal air pollution influences neurodevelopment and behavior in autism spectrum disorder by modulating mitochondrial physiology

A risk-based model to assess environmental justice and coronary heart disease burden from traffic-related air pollutants

Protective Effect of Diphlorethohydroxycarmalol Isolated from Ishige okamurae Against Particulate Matter-Induced Skin Damage by Regulation of NF-κB, AP-1, and MAPKs Signaling Pathways In Vitro in Human Dermal Fibroblasts

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