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Environmental Factors and Systemic Lupus Erythematosus

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This article explores the relationship between environmental factors and Systemic Lupus Erythematosus (SLE).

Written by

Dr. Leenus A. E

Medically reviewed by

Dr. Kaushal Bhavsar

Published At November 15, 2023
Reviewed AtNovember 15, 2023

Introduction

Currently, research indicates that environmental factors, such as harmful chemicals, food ingredients, gut dysbiosis, and infections, cause 70% of diseases. In addition to infection, several other environmental factors, such as climate, stress, occupation, smoking, and food, have been shown to increase autoimmune diseases like multiple sclerosis. There is compelling evidence connecting environmental factors such as crystalline silica, mercury, pesticides, solvents, smoking, and pollution with the emergence of many autoimmune disorders. The immune system must carefully discriminate between self and non-self to protect the host's integrity. When this narrow line is crossed, self-antigens can become overactive and cause autoimmunity. And research supports that this crossing can be due to the contribution of environmental factors.

How Do Environmental Factors Trigger Autoimmunity?

Numerous experimental research and clinical reports have demonstrated that persistent exposure to numerous substances in animal models and people can cause autoimmune disorders. Either toxicant-induced aberrant cell death, which makes the concealed cellular material accessible to antigen-presenting cells, or immunological responses to xenobiotics (organisms having a chemical that is not natural) and the development of neoantigens (new proteins that form cancer cells) are used to define the mechanism of toxicant-induced autoimmunity.

Xenobiotics are normally unable to bind to proteins when they enter the body, but after becoming reactive metabolites, they can, or they would activate toll-like receptors. Another way environmental cues cause gene expression changes is by altering DNA methylation. For instance, because of their connections to the induction of DNA methylation, environmental contaminants, cigarette smoke, and alcohol intake have been suggested as risk factors for autoimmunity.

What Is Systemic Lupus Erythematosus?

Chronic autoimmune disease Systemic Lupus Erythematosus (SLE) has a complicated etiology and pathophysiology. It is characterized by immune dysregulation, which frequently involves multiorgan systems. About 90% of SLE cases in women are diagnosed during the reproductive years. Due to the variable character of SLE, its complex and multifaceted etiology is supported by interactions between genetic and environmental factors throughout life.

What Is the Role of Environmental Factors in Systemic Lupus Erythematosus?

  • Cigarette Smoking

Numerous potentially harmful substances can be found in cigarette smoke, including tars, nicotine, carbon monoxide, and polycyclic aromatic hydrocarbons. There are two types of cigarette smoke: tar, or particulate, and gaseous, both of which have incredibly high levels of free radicals and also cause the activation of endogenous sources of free radicals. Smoking reduces both humoral and cell-mediated immunity by altering the inflow and activation of neutrophils, macrophages, and monocytes and producing tissue-damaging matrix metalloproteinases. A correlation between current smoking and the existence of anti-dsDNA antibodies (related to lupus) was one biological mechanism that might be implicated in the connection between smoking and SLE. Therefore, it is assumed that smoking results in DNA adduct formation and DNA damage, producing anti-dsDNA antibodies.

  • Alcohol Consumption

Alcoholic beverages contain substances (such as ethanol and antioxidants) that may reduce cellular reactions to immunogens (substances generating immune response) and suppress the production of pro-inflammatory cytokines like tumor necrosis factor (TNF), interleukin (IL)-6, and IL-8 in alveolar macrophages and human blood monocytes, both in vivo and in vitro. Additionally, consuming alcohol in moderation may lower IgG serum levels, making people more susceptible to infections.

  • Diet

Due to the diet's effects on metabolism, oxidative stress, and gut microbiome modification, it constitutes a potentially significant environmental exposure, but it is still understudied in SLE etiology and pathophysiology. However, vitamin D and complete dietary patterns remain the main dietary determinants of interest in the research of SLE risk. Diet and SLE-based investigations have primarily focused on food consumption after the SLE disease starts. Through epigenetic mechanisms and interactions with the gut microbiota, dietary variables may affect the risk of SLE. Dietary habits and SLE associations, however, are still poorly known.

  • Silica Dust

Silicates are made up of metal ions that are typically found in rocks and silicon-based minerals. When ingested as dust, silicates pose a pulmonary threat. One of the most frequent silicate exposures, crystalline silica (quartz) dust, has been shown in North American and European cohorts to be a known risk factor for systemic autoimmune disorders. Although there are also case series and cohort studies from other countries, most current research on the relationship between respirable silica exposure and the risk of SLE comes from North America. SLE and other systemic autoimmune illnesses, including asbestos, have been linked to silicates. However, there isn't much evidence on human populations.

  • Air Pollution

The term "particulate air pollution" refers to tiny airborne particles that come from both "natural" causes (such as forest fires) and other sources (such as industry and traffic). Even while air pollution is a universal risk, its geographic distribution differs due to the effects of climate change, the degree of urbanization, and the proximity to major thoroughfares, potentially adding to the uneven burden of socially disadvantaged communities. People predisposed to developing autoimmune diseases may be further vulnerable to the dangers associated with elevated exposure to particulate air pollution. However, additional research is necessary to fully understand particle air pollution as a potential cause of SLE onset.

  • Ultraviolet (UV) Exposure

The immune system is known to be severely suppressed by UV light. Perhaps the greatest place to understand this is in the skin, where local UV radiation from sunlight increases the risk of skin cancer by locally suppressing skin immunity. Similarly, UV radiation is thought to aggravate SLE symptoms in sufferers; however, it is uncertain whether UV exposure plays a causal role in the development of SLE. Some proposed mechanisms are the formation of autoantigens and autoreactive T cells, the creation of reactive oxygen species and the resulting DNA damage, and impacts on T cells and cytokine production.

  • Agricultural Exposures

For those raised on a farm, exposures during childhood are often more significant than those of the general population. Agricultural exposures also frequently coexist with other potentially significant chemical or physical exposures and factors, such as silica, solvents, infections (such as arboviruses), and UV light. Additional exploration of individual chemicals, timing, and potential interactions or confounding factors is necessary to research pesticides and SLE.

Conclusion

It is significant that environmental factors play a significant influence in Systemic Lupus Erythematosus (SLE). Numerous studies have demonstrated the critical impact of environmental triggers in the onset and progression of this challenging autoimmune disease. Understanding and reducing these triggers is essential for better SLE management and prevention. Reducing the prevalence of SLE requires public health measures emphasizing lifestyle changes, sun protection, and quitting smoking. Furthermore, raising knowledge among medical staff and patients about environmental risk factors can help with early detection and individualized treatment plans, enhancing the quality of life for those with SLE.

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Dr. Kaushal Bhavsar
Dr. Kaushal Bhavsar

Pulmonology (Asthma Doctors)

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