P233 Environmental and occupational exposures in the development of systemic lupus erythematosus in adults: a narrative review
Authors: Monteiro Bárbarah G , Pizarro Cristina B 
Published: April 2022

Background/Aims

Systemic lupus erythematosus (SLE) is a chronic inflammatory disease, of an autoimmune nature, of unknown origin, characterized by loss of tolerance to nuclear antigens and the deposition of immunecomplexes in the tissues leading to inflammation that can affect various organs and systems of the body. This narrative review aims to demonstrate that occupational factors and environmental exposure contribute to the development of SLE in adults.

Methods

This is a narrative review of literature that seeks to analyse the scientific production on environmental and occupational exposure in the development of systemic lupus erythematosus in adults, published in health journals. A literature search was conducted in the period between November 2020 and July 2021, considering the object

of study, initially the articles related to the theme addressed were searched in the PubMed database, in the US National Institutes of Health (NIH) and Scientific Electronic Library Online (SCIELO) portals.

Results

Exposure to respirable silica dust (i.e. the crystalline form of quartz) is an established risk factor for SLE and other systemic autoimmune diseases.

Exposure to toxic components of cigarette smoke (e.g., tar, nicotine, carbon monoxide, polycyclic aromatic hydrocarbons, and free radicals) can induce oxidative stress and directly damage endogenous proteins and DNA, leading to genetic mutations and gene activation, which may be involved in the development of SLE. Smoking stimulates the expression of CD95 on B and CD4 on T-cell surfaces, potentially inducing autoimmunity, and also increases the production of pro- inflammatory cytokines. Exposure to ultraviolet (UV) radiation may exacerbate pre-existing SLE; it is not yet known whether UV exposure plays a role in the pathogenesis of SLE. Thus, UV may result in a redistribution of nuclear antigens to the cell surface or in the production of new forms of autoantigens, effects that may be relevant given the mechanisms believed to be involved in SLE etiology. Several hypotheses have been postulated that air pollution may contribute to autoimmune diseases via oxidative stress, nitrosative stress, and systemic inflammation. Traffic-related air pollutants may cause oxidative stress and and systemic inflammation. The combination of CO with hemoglobin (Hb) to form carboxyhemoglobin (COHb) reduces the oxygen-carrying capacity of the blood and causes tissue hypoxia.

Conclusion

The articles analysed identified risk factors for exposure to current smoking, silica, ultraviolet radiation, and environmental pollution from CO, NO2, and minute particles. These are caused by oxidative stress, apoptosis inducers, systemic inflammation, genetic mutations, and activation of genes that will lead to immunological changes with increased pro-inflammatory cytokines, activation of genes, and increased autoantigens, leading to predisposition of these exposures in the development of systemic lupus erythematosus. In contrast, alcohol has been shown to be a neutralizing factor in systemic inflammation, causing a decrease in cellular responses and suppressing the synthesis of pro-inflammatory cytokines, showing the association of alcohol with a lower risk of developing SLE.

Disclosure

B.G. Monteiro: Grants/research support; FUNADESP. C.B. Pizarro: Grants/research support; FUNADESP.