The Salutary Effects of Catalpol on Diesel Exhaust Particles-Induced Thrombogenic Changes and Cardiac Oxidative Stress, Inflammation and Apoptosis

Inhaled particulate air pollution exerts pulmonary inflammation and cardiovascular toxicity through secondary systemic effects due to oxidative stress and inflammation. Catalpol, an iridiod glucoside, extracted from the roots of Rehmannia glutinosa Libosch, has been reported to possess anti-inflammatory and antioxidant properties. Yet, the potential ameliorative effects of catalpol on particulate air pollution—induced cardiovascular toxicity, has not been studied so far. Hence, we evaluated the possible mitigating mechanism of catalpol (5 mg/kg) which was administered to mice by intraperitoneal injection one hour before the intratracheal (i.t.) administration of a relevant type of pollutant particle, viz. diesel exhaust particles (DEPs, 30 µg/mouse). Twenty-four hours after the lung deposition of DEPs, several cardiovascular endpoints were evaluated. DEPs caused a significant shortening of the thrombotic occlusion time in pial microvessels in vivo, induced platelet aggregation in vitro, and reduced the prothrombin time and the activated partial thromboplastin time. All these actions were effectively mitigated by catalpol pretreatment. Likewise, catalpol inhibited the increase of the plasma concentration of C-reactive proteins, fibrinogen, plasminogen activator inhibitor-1 and P- and E-selectins, induced by DEPs. Moreover, in heart tissue, catalpol inhibited the increase of markers of oxidative (lipid peroxidation and superoxide dismutase) and nitrosative (nitric oxide) stress, and inflammation (tumor necrosis factor α, interleukin (IL)-6 and IL-1β) triggered by lung exposure to DEPs. Exposure to DEPs also caused heart DNA damage and increased the levels of cytochrome C and cleaved caspase, and these effects were significantly diminished by the catalpol pretreatment. Moreover, catalpol significantly reduced the DEPs-induced increase of the nuclear factor κB (NFκB) in the heart. In conclusion, catalpol significantly ameliorated DEPs–induced procoagulant events and heart oxidative and nitrosative stress, inflammation, DNA damage and apoptosis, at least partly, through the inhibition of NFκB activation.

Source apportionment of ambient fine and coarse aerosols in Embalenhle and Kinross, South Africa

The South African Highveld is recognised as a region having significant negative ambient air quality impacts with its declaration as an Air Quality Priority Area in 2007. Such areas require the implementation of specific air quality intervention strategies to address the air quality situation. A greater understanding of the composition of the atmospheric aerosol loading and the contributing air pollution sources will assist with the formulation and implementation of these strategies. This study aims to assess the composition and sources of the aerosol loading in Embalenhle and Kinross located on the Highveld. Fine (PM2.5) and coarse (PM2.5-10) aerosol samples were collected during summer and winter, which were quantified using the gravimetric method. Wavelength-Dispersive X-Ray Fluorescence (WD-XRF) and Ion Chromatography (IC) analysis were used to determine the chemical composition of aerosols. Mean PM2.5 concentrations in Embalenhle and Kinross ranged from 16.3 to 34.1 µg/m3 during winter and 7.4 to 19.0 µg/m3 during summer. Mean PM10-2.5 concentrations ranged from 10.3 to 114 µg/m3 during winter and 5.9 to 11.2 µg/m3 during summer. Si, Al, S, Na (winter only), Ca (summer only), SO42- and NH4+ were the most abundant species in PM2.5 during both seasons. In PM10-2.5, Si, Al, Na (winter only), SO42- and F- were the most abundant species during both seasons. The elements S and Ca also had high abundances at Embalenhle and Kinross, respectively, during summer. Source apportionment was undertaken using Positive Matrix Factorisation, which identified five sources. Dust, secondary aerosols, domestic combustion, wood and biomass burning, and industry were determined to be the contributing sources. Any measures to mitigate particulate air pollution on the Highveld should consider these key sources.

NeuroSmog: Determining the impact of air pollution on the developing brain: project protocol

Background Exposure to airborne particulate matter (PM) may affect neurodevelopmental outcomes in children. The mechanisms underlying these relationships are not currently known. We aim to assess whether PM affects the developing brains of schoolchildren in Poland, a European country characterized by very high levels of particulate air pollution. Methods Between 2020 and 2022, 800 children aged 10 to 13 years are being recruited as participants in a case-control study. Cases (children with attention deficit hyperactivity disorder (ADHD)) are being recruited from psychology clinics. Population-based controls are being sampled from schools. The study area comprises 18 towns in southern Poland characterized by wide-ranging levels of PM. Comprehensive psychological assessments are being conducted to assess cognitive and social functioning. Cases and controls undergo MRI including T1, T2 and MP2RAGE structural imaging, task (Go/NoGo) and resting-state MRI, and diffusion-weighted imaging (DWI). Concentrations of PM are being assessed using land use regression models, which incorporate data from air monitoring networks, dispersion models, and characteristics of roads and other land cover types. The estimated concentrations will be assigned to prenatal and postnatal residential and preschool/school addresses of all study subjects. We will assess whether long-term exposure to outdoor PM affects brain function, structure, and connectivity in healthy children and those diagnosed with ADHD. Results and Discussion This comprehensive study will provide novel, in-depth understanding of the neurodevelopmental effects of air pollution.

Cardiovascular Effects of Particulate Air Pollution

Inhalation of fine particulate matter (PM2.5), produced by the combustion of fossil fuels, is an important risk factor for cardiovascular disease. Exposure to PM2.5 has been linked to increases in blood pressure, thrombosis, and insulin resistance. It also induces vascular injury and accelerates atherogenesis. Results from animal models corroborate epidemiological evidence and suggest that the cardiovascular effects of PM2.5 may be attributable, in part, to oxidative stress, inflammation, and the activation of the autonomic nervous system. Although the underlying mechanisms remain unclear, there is robust evidence that long-term exposure to PM2.5 is associated with premature mortality due to heart failure, stoke, and ischemic heart disease. Expected final online publication date for the Annual Review of Medicine, Volume 73 is January 2022. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.