High serum levels of silica nanoparticles in systemic sclerosis patients with occupational exposure: Possible pathogenetic role in disease phenotypes.

Abstract:

BACKGROUND:Systemic sclerosis (SSc) is an autoimmune systemic disease characterized by diffuse fibrosis of skin and visceral organs due to different genetic, infectious, and/or environmental/occupational causative factors, including the inhalation of silica dust. OBJECTIVES:To investigate serum trace elements including silicon (s-Si) levels in SSc patients living in a restricted geographical area with high density of worksites with silica exposure hazard. METHODS:This case-control study included 80 SSc patients (M:F 10:70; aged 58.4 ± 11.9SD years, mean disease duration 10.1 ± 7.8SD) and 50 age-/sex-matched healthy control subjects consecutively investigated at our University-based Rheumatology Unit. Patients and controls were evaluated for environmental/occupational exposure categories (structured questionnaire), morphological characterization of serum micro-/nanoparticles (Environmental Scanning Electron Microscopy and Energy Dispersive X-ray Spectroscopy microanalysis), and quantitative assessment of trace elements (inductively coupled plasma atomic emission spectroscopy). RESULTS:Among various categories, only occupational exposure to silica dust was recorded in a significant proportion of SSc patients compared to controls (55% vs. 11%; p < .0001). Qualitative analysis showed serum silica micro- and nanoparticles in all exposed patients. Quantitative evaluation evidenced significantly higher s-Si levels in SSc patients versus controls (p < .0001); in addition, higher s-Si levels were detected in patients with occupational exposure (p < .0001), diffuse cutaneous SSc (p = .0047), myositis (p = .0304), and/or lung fibrosis (p = .0004) compared to those without; notably, the severity of lung fibrosis scoring positively correlated with s-Si levels (p < .0001). CONCLUSIONS:The study first demonstrated high s-Si levels in exposed SSc patients; this element might represent a pathogenetic co-factor of more severe clinical phenotypes, mainly diffuse scleroderma with lung fibrosis.

journal_name

Semin Arthritis Rheum

authors

Ferri C,Artoni E,Sighinolfi GL,Luppi F,Zelent G,Colaci M,Giuggioli D

doi

10.1016/j.semarthrit.2018.06.009

subject

Has Abstract

pub_date

2018-12-01 00:00:00

pages

475-481

issue

3

eissn

0049-0172

issn

1532-866X

pii

S0049-0172(17)30700-X

journal_volume

48

pub_type

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