Systemic sclerosis and organic solvents: early diagnosis in industry.

Garcia-Zamalloa, Alberto; Ojeda, Ernesto; Gonzalez-Beneitez, C; Goñi, José Luis Olcoz; Garrido, Almudena Ortiz

doi:10.1136/ard.53.9.618-a

Cited by 26 publications

(10 citation statements)

References 7 publications

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“…Occurrence of cases of SSc has been reported among workers exposed to organic solvents (Yamakage and Ishikawa 1982;Flindt-Hansen and Isager 1987;Brasington and Thorpe-Swenson 1991;Garcia-Zamalloa et al 1994;Altomonte et al 1996). Among epidemiological studies that evaluated the possible role of solvents in the aetiopathogenesis of SSc, Silman and Jones (1992) found an increased risk of SSc among men with self-reported occupational exposure to organic solvents, but the association was not confirmed when the exposure was expert-assessed on the basis of their job titles.…”

Section: Solventsmentioning

confidence: 83%

“…However, several environmental factors have been suggested to play a role in the causation of SSc. Cases of SSc occurring after occupational exposure to silica dust (Rodnan et al 1967;Sluis-Cremer et al 1985;Cowie 1987;Yanez Diaz et al 1992;Sanchez-Roman et al 1993), hand-arm vibration (Pelmear et al 1992), organic solvents (Yamakage and Ishikawa 1982;Flindt-Hansen and Isager 1987;Brasington and Thorpe-Swenson 1991;Garcia-Zamalloa et al 1994;Altomonte et al 1996), and other chemicals (Yamakage et al 1980;Rush and Chaiton 1986;Owens and Medsger 1988), have been reported.…”

Section: Introductionmentioning

confidence: 95%

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A case?control study of occupational exposures and systemic sclerosis

Bovenzi

Barbone

Pisa

et al. 2004

International Archives of Occupational and Environmental Health

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The findings of this study tend to support the role of organic solvents and certain chemicals in SSc causation. The association with teaching and working in the textile industry suggests that other exposures are involved in the aetiology of SSc among women. However, because of the small number of subjects, particularly in stratified analyses, chance cannot be ruled out as an explanation of some findings of this study.

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Section: Solventsmentioning

confidence: 83%

Section: Introductionmentioning

confidence: 95%

A case?control study of occupational exposures and systemic sclerosis

Bovenzi

Barbone

Pisa

et al. 2004

International Archives of Occupational and Environmental Health

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“…The etiology of SSc remains unknown, but its occurrence has been associated with numerous factors, including various environmental agents, genetic influences, and viruses. Environmental agents associated with SSc or closely related syndromes include organic solvents, such as vinyl chloride and trichloroethylene, adulterated rapeseed oil, certain tryptophan products, bleomycin, and silica (3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13). Vinyl chloride-induced disease (14) has an HLA-DR5 association in those individuals who progress to develop SSc (15), and specific HLA alleles have been associated with autoantibody subgroups expressed in SSc patients (16).…”

Section: Conclusion the Results Suggest That Vinyl Chloride Injectiomentioning

confidence: 99%

Increased numbers of microchimeric cells of fetal origin are associated with dermal fibrosis in mice following injection of vinyl chloride

Christner

Artlett

Conway

et al. 2000

Arthritis & Rheumatism

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Objective. To develop a murine model for use in examining the role of microchimeric cells and certain chemical exposures in the pathogenesis of systemic sclerosis (SSc). Methods. Female BALB/cJ retired breeder mice were bled before and after vinyl chloride injection. The DNA from their white blood cells was obtained, and the number of microchimeric cell equivalents was determined by quantitative polymerase chain reaction using DNA primers specific for the H-2K b gene, a sequence not found in BALB/cJ mice. Skin was obtained at autopsy, embedded in paraffin, sectioned, and stained with Masson's trichrome. Hydroxyproline analyses were performed on 4-mm skin biopsy samples. Results. Microchimeric cells were identified and quantitated before and after 20 daily intraperitoneal injections of vinyl chloride. The number of microchi-meric cells in the peripheral blood increased an average of 48-fold after treatment with vinyl chloride. Histologic examination of the skin of these same mice (which had an increased number of microchimeric cells) showed inflammation, with abundant fibroblasts and a heavy mononuclear infiltration in the dermis. The collagen fibers appeared densely packed and disorganized. His-tologic examination of the skin of untreated retired breeder mice and treated virgin mice appeared normal. Quantitative assays to determine the collagen content of skin biopsy samples obtained from treated microchi-meric mice compared with nontreated microchimeric or with treated nonmicrochimeric mice showed a 2-3-fold increase in collagen content in the treated microchi-meric mice. Extraordinary splenomegaly was present in the vinyl chloride-treated microchimeric mice, accompanied by cellular infiltration and fibrosis. Conclusion. The results suggest that vinyl chloride injections into BALB/cJ retired breeder mice lead to activation of microchimeric cells, which causes the cells to divide and multiply. The correlation between the 48-fold increase in microchimeric cells and the appearance of dermal inflammation and fibrosis similar to that of graft-versus-host disease suggests that activated mi-crochimeric cells may be a necessary factor in the pathogenesis of autoimmune diseases such as SSc.

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“…Infection-caused stimuli, e.g., cytomegalovirus [1], Epstein-Barr virus [2] or parvovirus B19 [3,4], as well as other environmental factors [5] such as exposure to silica [6] or to organic solvents [7,8], but also genotypic modalities comprising certain susceptibility constellations [5,7,[9][10][11] have been discussed to contribute to the development of SSc. Nonetheless, an increasing and yet more detailed knowledge about the true etiology is still to be expected by ongoing studies.…”

Section: Introductionmentioning

confidence: 99%

The Pathogenesis of Systemic Sclerosis Revisited

Geyer

Müller‐Ladner

2010

Clinic Rev Allerg Immunol

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Although infectiological stimuli, environmental factors and genotypic features are known to contribute to the initiation and perpetuation of systemic sclerosis (SSc), its etiology still remains to be enigmatic, and less elusive insights are to be achieved by ongoing and future investigations. Being characterized, however, as chronic autoimmune disease with excessive collagen accumulation in skin, synovia and visceral organs such as lung, heart, and digestive tract along with obliterating angiopathy, the pathophysiology of SSc can be summarized as being based on imbalances of the cellular and humoral immune system, vascular dysfunction and activation of resident connective tissue cells. A complex interplay between these major components manages to establish and maintain the inability of the vasculature to adequately react to the need for dilatation, constriction and growth of new vessels, to cause the increased deposition of extracellular matrix constituents as well as to facilitate immunological disarrangement. Despite parallels to the chicken and egg causality dilemma, all of these account for what later clinicians observe in patients suffering from Raynaud's phenomenon, digital ulcers, sclerodactyly, rigidity of the face, microstomia, sicca syndrome, dyspnea, dry cough, pulmonary hypertension, palpitations, syncopes, renal insufficiency, dysphagia, gastroesophageal reflux, dyspepsia, generalized arthralgias, but also dyspareunia, or erectile dysfunction.

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Systemic sclerosis and organic solvents: early diagnosis in industry.

Cited by 26 publications

References 7 publications

A case?control study of occupational exposures and systemic sclerosis

A case?control study of occupational exposures and systemic sclerosis

Increased numbers of microchimeric cells of fetal origin are associated with dermal fibrosis in mice following injection of vinyl chloride

The Pathogenesis of Systemic Sclerosis Revisited

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