Analysis of autoantibody profiles in two asbestiform fiber exposure cohorts

Pfau, Jean C.; Barbour, Christopher; Black, Brad; Serve, Kinta M.; Fritzler, Marvin J.

doi:10.1080/15287394.2018.1512432

Cited by 13 publications

(12 citation statements)

References 64 publications

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“…One occupational agent of particular interest is asbestos, which is known to cause inflammation and increase the risk of fibrosis and cancer in the lungs 12. However, the knowledge regarding any association between exposure to asbestos and RA is scarce 4 5 13 14. Both asbestos and silica are naturally occurring silicon-containing compounds.…”

Section: Introductionmentioning

confidence: 99%

Occupational exposure to asbestos and silica and risk of developing rheumatoid arthritis: findings from a Swedish population-based case-control study

et al. 2019

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ObjectiveAirborne agents including cigarette smoke associate with an increased risk of rheumatoid arthritis (RA). We analysed to which extent occupational exposure to asbestos and silica confers an increased risk of developing serologically defined subsets of RA.MethodsThis Swedish population-based case-control study enrolled incident RA cases between 1996 and 2013 (n=11 285), identified through national public authority and quality registers, as well as from the Epidemiological Investigation of Rheumatoid Arthritis (EIRA) Study. Controls (n=1 15 249) were randomly selected from Sweden’s population register and matched on sex, age, index year and county. Occupational histories were obtained from national censuses. Exposure to asbestos and silica was assessed by job-exposure matrices. Logistic regression was used to calculate ORs adjusted for age, sex, county, index year, alcohol use and smoking.ResultsResults showed that male workers exposed to asbestos had higher risk of seropositive RA (OR=1.2, 95% CI 1.0 to 1.4) and seronegative RA (OR=1.2, 95% CI 1.0 to 1.5) compared with unexposed workers. The risk was highest among workers exposed to asbestos from 1970, before a national ban was introduced. Male workers exposed to silica also had higher risk of RA (seropositive RA: OR=1.4, 95% CI 1.2 to 1.6; seronegative RA: OR=1.3, 95% CI 1.0 to 1.5). For the largest subset, seropositive RA, the OR increased with the number of years exposed to silica, up to OR=2.3 (95% CI 1.4 to 3.8, p for trend <0.0001). Women overall had lower ORs than men, but the duration and intensity of their exposure were lower.ConclusionsIn conclusion, we observed an association between asbestos exposure and risk of developing RA and extended previous findings of an association between silica exposure and RA risk, where a dose-response relationship was observed.

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Section: Introductionmentioning

confidence: 99%

Occupational exposure to asbestos and silica and risk of developing rheumatoid arthritis: findings from a Swedish population-based case-control study

et al. 2019

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“…Libby amphibole (LA) asbestos is highly inflammatory and has been linked to the development of various asbestos-related diseases (ARDs), as well as autoimmune disease [14,29,40]. Development of ARDs and autoimmunity may be due to chronic, non-resolving inflammation and immune activation perpetuated by LA fiber deposition.…”

Section: Discussionmentioning

confidence: 99%

Late Inflammation Induced by Asbestiform Fibers in Mice Is Ameliorated by a Small Molecule Synthetic Lignan

Badger

Park

Pietrofesa

et al. 2021

IJMS

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Exposure to Libby amphibole (LA) asbestos-like fibers is associated with increased risk of asbestosis, mesothelioma, pulmonary disease, and systemic autoimmune disease. LGM2605 is a small molecule antioxidant and free radical scavenger, with anti-inflammatory effects in various disease models. The current study aimed to determine whether the protective effects of LGM2605 persist during the late inflammatory phase post-LA exposure. Male and female C57BL/6 mice were administered daily LGM2605 (100 mg/kg) via gel cups for 3 days before and 14 days after a 200 µg LA given via intraperitoneal (i.p.) injection. Control mice were given unsupplemented gel cups and an equivalent dose of i.p. saline. On day 14 post-LA treatment, peritoneal lavage was assessed for immune cell influx, cytokine concentrations, oxidative stress biomarkers, and immunoglobulins. During the late inflammatory phase post-LA exposure, we noted an alteration in trafficking of both innate and adaptive immune cells, increased pro-inflammatory cytokine concentrations, induction of immunoglobulin isotype switching, and increased oxidized guanine species. LGM2605 countered these changes similarly among male and female mice, ameliorating late inflammation and altering immune responses in late post-LA exposure. These data support possible efficacy of LGM2605 in the prolonged treatment of LA-associated disease and other inflammatory conditions.

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“…Anti-mesothelial cell antibodies, and ANA, have been linked to pleural abnormalities (85). Autoantibodies against cyclic citrullinated peptide (CCP) and RF are not elevated (86) even though there is evidence of increased PAD2/4 and citrullination in the lung following asbestos exposure (87). ANA have also been found in subjects exposed to asbestos without systemic autoimmune diseases (75).…”

Section: Fibrous Materials Asbestosmentioning

confidence: 99%

Perspective: The Lung, Particles, Fibers, Nanomaterials, and Autoimmunity

Pollard

2020

Front. Immunol.

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Studies have shown that a wide range of factors including drugs, chemicals, microbes, and other environmental agents can induce pre-clinical autoimmunity. However, only a few have been confidently linked to autoimmune diseases. Among these are exposures to inhaled particulates that are known to be associated with autoimmune diseases such as lupus and rheumatoid arthritis. In this article, the potential of particle, fiber, and nanomaterial exposures to induce autoimmunity is discussed. It is hypothesized that inhalation of particulate material known to be associated with human autoimmune diseases, such as cigarette smoke and crystalline silica, results in a complex interplay of a number of pathological processes, including, toxicity, oxidative stress, cell and tissue damage, chronic inflammation, post-translational modification of self-antigens, and the formation of lymphoid follicles that provide a milieu for the accumulation of autoreactive B and T cells necessary for the development and persistence of autoimmune responses, leading to disease. Although experimental studies show nanomaterials are capable of inducing several of the above features, there is no evidence that this matures to autoimmune disease. The procession of events hypothesized here provides a foundation from which to pursue experimental studies to determine the potential of other environmental exposures to induce autoimmunity and autoimmune disease.

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Analysis of autoantibody profiles in two asbestiform fiber exposure cohorts

Cited by 13 publications

References 64 publications

Occupational exposure to asbestos and silica and risk of developing rheumatoid arthritis: findings from a Swedish population-based case-control study

Occupational exposure to asbestos and silica and risk of developing rheumatoid arthritis: findings from a Swedish population-based case-control study

Late Inflammation Induced by Asbestiform Fibers in Mice Is Ameliorated by a Small Molecule Synthetic Lignan

Perspective: The Lung, Particles, Fibers, Nanomaterials, and Autoimmunity

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