Atmospheric dry and wet deposition of sulphur and nitrogen species and assessment of critical loads of acidic deposition exceedance in South Africa

We tested the hypothesis that acidic atmospheric pollution deposition, originating from the South African central industrial area, poses an environmental threat across a larger region within the dispersal footprint. A network of 37 passive monitoring sites to measure SO2 and NO2 was operated from August 2005 to September 2007. The area extended over the entire northern and eastern interior of South Africa. Monitoring locations were chosen to avoid direct impacts from local sources such as towns, mines and highways. Dry deposition rates of SO2 and NO2 were calculated from the measured concentrations. Concentrations of sulphur and nitrogen species in wet deposition from a previous study were used in conjunction with measured rainfall for the years 2006 and 2007 to estimate the wet deposition over the region. The calculated total (non-organic) acidic deposition formed the basis for an assessment of exceedance of critical loads based on sensitivity of the regional soils. Regional soil sensitivity was determined by combining two major soil attributes available in the World Inventory of Soil Emission Potentials (International Soil Reference and Information Centre). Results indicate that certain parts of the central pollution source area on the South African Highveld have the potential for critical load exceedance, while limited areas downwind show lower levels of exceedance. Areas upwind and remote areas up and downwind, including forested areas of the Drakensberg escarpment, do not show any exceedance of the critical loads

Do Early Relapses Predict the Risk of Long-Term Relapsing Disease in an Adult and Paediatric Cohort with MOGAD?

OBJECTIVE: Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) can be monophasic or relapsing, with early relapse being a feature. However, the relevance of early relapse on longer-term relapse risk is unknown. Here, we investigate whether early relapses increase longer-term relapse risk in patients with MOGAD. METHODS: A retrospective analysis of 289 adult- and pediatric-onset patients with MOGAD followed for at least 2 years in 6 specialized referral centers. "Early relapses" were defined as attacks within the first 12 months from onset, with "very early relapses" defined within 30 to 90 days from onset and "delayed early relapses" defined within 90 to 365 days. "Long-term relapses" were defined as relapses beyond 12 months. Cox regression modeling and Kaplan-Meier survival analysis were used to estimate the long-term relapse risk and rate. RESULTS: Sixty-seven patients (23.2%) had early relapses with a median number of 1 event. Univariate analysis revealed an elevated risk for long-term relapses if any "early relapses" were present (hazard ratio [HR] = 2.11, p < 0.001), whether occurring during the first 3 months (HR = 2.70, p < 0.001) or the remaining 9 months (HR = 1.88, p = 0.001), with similar results yielded in the multivariate analysis. In children with onset below aged 12 years, only delayed early relapses were associated with an increased risk of long-term relapses (HR = 2.64, p = 0.026). INTERPRETATION: The presence of very early relapses and delayed early relapses within 12 months of onset in patients with MOGAD increases the risk of long-term relapsing disease, whereas a relapse within 90 days appears not to indicate a chronic inflammatory process in young pediatric-onset disease. ANN NEUROL 2023