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Rheumatoid arthritis and the impact of microplastics on inflammation
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A review of evidence links microplastic and nanoplastic exposure to immune activation — including oxidative stress, macrophage stimulation, and pro-inflammatory cytokine production — and proposes that microplastics may exacerbate rheumatoid arthritis by increasing intestinal permeability and acting as carriers for chemical additives like phthalates and bisphenols. This mechanistic framework connecting microplastic-induced inflammation to autoimmune disease progression underscores the urgency of understanding human health consequences of chronic microplastic exposure.
Background: In recent decades, the use of plastic in our society has grown exponentially thanks to its practical properties in our daily lives. Unfortunately, these characteristics also bring certain disadvantages, such as its great durability. Consequently, inefficient recycling management leads to its accumulation in the environment, which slowly degrades into microplastics. In addition to the environmental consequences, the impacts on human health due to constant exposure are also significant. Recent evidence demonstrates the presence of microplastics and nanoplastics in air, water, and the food chain. Once they are absorbed by the human body, primarily through ingestion and inhalation, these particles can cross biological barriers, such as the alveolar and intestinal linings. This is especially relevant, as increased intestinal permeability (the "leaky gut" theory) has been identified as a critical factor in triggering systemic autoimmunity. Several studies indicate that microplastics induce innate immune responses, characterized by oxidative stress, macrophage activation, and the production of pro-inflammatory cytokines such as TNF-α, IL-6 and IL-1β. They also act as "Trojan horses” by serving as vectors for hazardous chemical additives (like phthalates, bisphenols) and environmental contaminants (like pesticides), exacerbating chronic inflammatory processes. Rheumatoid arthritis is a systemic autoimmune disease characterized by chronic synovitis and joint destruction, driven by the same mediators (TNF-α and IL-6) that are activated upon microplastic exposure. Like the pathogenic role of tobacco smoke, which triggers inflammation and loss of self-tolerance in the lungs, the cumulative burden of microplastics may represent a novel and underestimated environmental risk factor for disease activity and inflammatory flares in patients with rheumatoid arthritis. Objectives: The main objective is to compare the concentration and composition of polymers in biological samples between patients diagnosed with Rheumatoid arthritis and healthy controls. The secondary objectives include investigating the correlation between polymers levels and disease severity, as measured by indices such as DAS28-ESR, DAS28-CRP, CDAI, SDAI, ESR and CRP. Additionally, the study aims to analyze whether specific characteristics of the polymers (size, shape, or chemical composition) are associated with higher degrees of joint destruction or functional disability. Finally evaluate the influence of environmental and lifestyle factors, such as occupation, diet, use of plastic packaging, on polymers load and inflammatory activity
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