Exposure to Air Pollutants and Disease Activity in Juvenile-Onset Systemic Lupus Erythematosus Patients
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Citações na Scopus
48
Tipo de produção
article
Data de publicação
2015
Título da Revista
ISSN da Revista
Título do Volume
Editora
WILEY-BLACKWELL
Citação
ARTHRITIS CARE & RESEARCH, v.67, n.11, p.1609-1614, 2015
Resumo
ObjectiveTo investigate the association between exposure to air pollutants in the Sao Paulo metropolitan area and disease activity in juvenile-onset systemic lupus erythematosus (SLE) patients. MethodsA longitudinal panel study based on 409 consecutive visits of juvenile-onset SLE patients living in the Sao Paulo metropolitan area was carried out. Disease activity was evaluated in accordance with the Systemic Lupus Erythematosus Disease Activity Index 2000 (SLEDAI-2K), and the patients were divided into 2 groups: those with SLEDAI scores 8 and those with SLEDAI scores >8. Daily concentrations of inhaled particulate matter (PM10), sulfur dioxide, nitrogen dioxide (NO2), ozone, and carbon monoxide (CO) were evaluated on the 21 days preceding the medical visits. A generalized estimation equation model was used to assess the impact of these measurements on SLEDAI-2K scores, considering the fixed effects for repetitive measurements. The models were adjusted for erythrocyte sedimentation rate, corticosteroid use (daily and cumulative doses), antimalarial use, the use of immunosuppressive agents, the presence of infection 20 days preceding the medical appointment, and the minimum temperature and relative humidity outdoors. ResultsPM(10), NO2, and CO were risk factors for juvenile-onset SLE disease activity (SLEDAI-2K score >8) approximately 2 weeks after exposure. A 13.4 g/m(3) increase in the PM10 moving average (from lag 12 to lag 15) was associated with a 34% increase (95% confidence interval 7.0-68.0) in the risk of a SLEDAI-2K score >8. ConclusionThis is the first study to show that exposure to inhaled pollutants may increase the risk of disease activity in children with juvenile-onset SLE in a large urban center.
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Referências
- Pfau JC, 2008, J IMMUNOTOXICOL, V5, P129, DOI 10.1080/15476910802085756
- Brown JM, 2003, CLIN EXP IMMUNOL, V131, P415, DOI 10.1046/j.1365-2249.2003.02094.x
- Vidotto JP, 2012, LUPUS, V21, P526, DOI 10.1177/0961203312437806
- Farhat SCL, 2013, CHEST, V144, P1186, DOI 10.1378/chest.12-2414
- Brook RD, 2010, CIRCULATION, V121, P2331, DOI 10.1161/CIR.0b013e3181dbece1
- Farhat SCL, 2011, AUTOIMMUN REV, V11, P14, DOI 10.1016/j.autrev.2011.06.008
- Hochberg MC, 1997, ARTHRITIS RHEUM, V40, P1725, DOI 10.1002/art.1780400928
- Bernatsky S, 2011, ENVIRON HEALTH PERSP, V119, P45, DOI 10.1289/ehp.1002123
- Ghaussy NO, 2003, J RHEUMATOL, V30, P1215
- Pfau JC, 2004, TOXICOLOGY, V195, P167, DOI 10.1016/j.tox.2003.09.011
- Boghdadi G, 2014, RHEUMATOL INT, V34, P1217, DOI 10.1007/s00296-014-3020-4
- Zeft AS, 2009, CLIN EXP RHEUMATOL, V27, P877
- Santos UP, 2008, J EPIDEMIOL COMMUN H, V62, P267, DOI 10.1136/jech.2006.058123
- Campos LMA, 2013, ARTHRIT CARE RES, V65, P1121, DOI 10.1002/acr.21948
- Gladman DD, 2002, J RHEUMATOL, V29, P288
- Calderon-Garciduenas L, 2009, TOXICOL PATHOL, V37, P161, DOI 10.1177/0192623308329340
- Calderon-Garciduenas L, 2008, INHAL TOXICOL, V20, P499, DOI 10.1080/08958370701864797
- Ekblom-Kullberg S, 2014, RHEUMATOL INT, V34, P341, DOI 10.1007/s00296-013-2889-7
- Ganguly K, 2009, PART FIBRE TOXICOL, V6, DOI 10.1186/1743-8977-6-31
- Umare V, 2014, MEDIAT INFLAMM, V2014
- World Health Organization, 2005, AIR QUAL GUID GLOB U