Influence of air pollution on airway inflammation and disease activity in childhood-systemic lupus erythematosus

Abstract

Exposure to fine particles may trigger pulmonary inflammation/systemic inflammation. The objective of this study was to investigate the association between daily individual exposure to air pollutants and airway inflammation and disease activity in childhood-onset systemic lupus erythematosus (cSLE) patients. A longitudinal panel study was carried out in 108 consecutive appointments with cSLE patients without respiratory diseases. Over four consecutive weeks, daily individual measures of nitrogen dioxide (NO), fine particulate matter (PM), ambient temperature, and humidity were obtained. This cycle was repeated every 2.5 months along 1 year, and cytokines of exhaled breath condensate-EBC [interleukins (IL) 6, 8, 17 and tumoral necrose factor-α (TNF-α)], fractional exhaled NO (FeNO), and disease activity parameters were collected weekly. Specific generalized estimation equation models were used to assess the impact of these pollutants on the risk of Systemic Lupus Erythematous Disease Activity Index 2000 (SLEDAI-2K) ≥ 8, EBC cytokines, and FeNO, considering the fixed effects for repetitive measurements. The models were adjusted for inflammatory indicators, body mass index, infections, medication, and weather variables. An IQR increase in PM 4-day moving average (18.12 μg/m) was associated with an increase of 0.05 pg/ml (95% CI 0.01; 0.09, p = 0.03) and 0.04 pg/ml (95% CI 0.02; 0.06, p = 0.01) in IL-17 and TNF-α EBC levels, respectively. Additionally, a short-term effect on FeNO was observed: the PM 3-day moving average was associated with a 0.75 ppb increase (95% CI 0.38; 1.29, p = 0.03) in FeNO. Also, an increase of 1.47 (95% CI 1.10; 1.84) in the risk of SLEDAI-2K ≥ 8 was associated with PM 7-day moving average. Exposure to inhalable fine particles increases airway inflammation/pulmonary and then systemic inflammation in cSLE patients.

Can atmospheric pollution be considered a co-factor in extremely high level of SARS-CoV-2 lethality in Northern Italy?

“…All these modifications are well known to contribute to atherogenesis, chronic respiratory diseases and cardiovascular events, the latter strictly correlated with IL-6 serum levels (Aromolaran et al, 2018). Nevertheless, aside of "classical" pollution-related conditions, several recent studies have pointed out a possible correlation between poor air quality and development and worsening of chronic inflammatory disease, such as systemic lupus erythematous (Alves et al, 2018;Gulati and Brunner, 2018) and rheumatoid arthritis (Sigaux et al, 2019).…”

Precision Medicine: The Role of the MSIDS Model in Defining, Diagnosing, and Treating Chronic Lyme Disease/Post Treatment Lyme Disease Syndrome and Other Chronic Illness: Part 2

“…Autoimmunity can result from antibodies produced against Borrelia that cross react with our own tissue antigens (molecular mimicry), while bacteria activate Toll-like receptor 2 (TLR-2), [160,161] furthering increases in the pro-inflammatory cytokines, TNF-alpha and IL-17. Similarly, mercury (Hg), bisphenol A (BPA), asbestos, and small particle pollution have now been published in the medical literature as potential factors increasing autoimmune reactions [37,51,101,102]. Over 84% of patients had evidence of exposure to at least one heavy metal, with 68% had evidence of mercury exposure; 100%, 46.5%, and 82% of patients had evidence of exposure to Borrelia , Bartonella , and Mycoplasma spp., respectively; and 72.5% of our patients in this study had evidence of immune dysfunction, including production of positive antinuclear antibodies and rheumatoid factors.…”

“…Any of these chronic disease manifestations may be worsened and/or due to one or multiple factors. This is the case with autoimmune reactions, which the scientific literature has shown can be affected by exposure to borrelia and other infections [100] (including, but not limited to, Bartonella and Mycoplasma species) [30,32,33], environmental toxin exposure (i.e., mercury, bisphenol A, asbestos, and/or small particle pollution) [50,51,101,102], imbalances in the microbiome of the gut, and/or from a genetic predisposition [103]. We therefore collected data from an online survey, which evaluated the efficacy of dapsone combined with other antibiotics and agents that disrupt biofilm for the treatment of chronic Lyme disease/PTLDS, along with information data mined directly from 200 patient records detailing abnormalities on the MSIDS model.…”

Understanding COVID-19 diffusion requires an interdisciplinary, multi-dimensional approach

“…Indeed, COVID-19 infection can cause pneumonia and acute respiratory syndrome, i.e., symptoms that can be exacerbated by air pollution. Although not directly connected to COVID-19 diffusion, previous research has suggested a correlation between poor air quality and development and worsening of chronic inflammatory disease (Alves et al, 2018). Since COVID-19 is mainly a respiratory syndrome, polluted air was supposed to increase the risk of death of infected patients, mainly due to the high concentrations of airborne PM (Paital, 2020, in press).…”