Jean Curtin-Brosnan
Johns Hopkins University School of Medicine
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Featured researches published by Jean Curtin-Brosnan.
Journal of Urban Health-bulletin of The New York Academy of Medicine | 2007
Elinor Simons; Jean Curtin-Brosnan; Timothy J. Buckley; Patrick N. Breysse; Peyton A. Eggleston
We conducted this study to compare environmental exposures in suburban homes of children with asthma to exposures in inner city homes of children with asthma, to better understand important differences of indoor pollutant exposure that might contribute to increased asthma morbidity in the inner city. Indoor PM10, PM2.5, NO2, O3, and airborne and dust allergen levels were measured in the homes of 120 children with asthma, 100 living in inner city Baltimore and 20 living in the surrounding counties. Home conditions and health outcome measures were also compared. The inner city and suburban homes differed in ways that might affect airborne environmental exposures. The inner city homes had more cigarette smoking (67% vs. 5%, pu2009<u2009.001), signs of disrepair (77% vs. 5%, pu2009<u2009.001), and cockroach (64% vs. 0%, pu2009<u2009.001) and mouse (80% vs. 5%, pu2009<u2009.001) infestation. The inner city homes had higher geometric mean (GM) levels (pu2009<u2009.001) of PM10 (47 vs. 18xa0μg/m3), PM2.5 (34 vs. 8.7xa0μg/m3), NO2 [19xa0ppb vs. below detection (BD)], and O3 (1.9 vs. .015xa0ppb) than suburban homes. The inner city homes had lower GM bedroom dust allergen levels of dust mite (.29 vs. 1.2xa0μg/g, pu2009=u2009.022), dog (.38 vs. 5.5xa0μg/g, pu2009<u2009.001) and cat (.75 vs. 2.4xa0μg/g, pu2009=u2009.039), but higher levels of mouse (3.2 vs. .013xa0μg/g, pu2009<u2009.001) and cockroach (4.5 vs. .42xa0U/g, pu2009<u2009.001). The inner city homes also had higher GM airborne mouse allergen levels (.055 vs. .016xa0ng/m3, pu2009=u2009.002). Compared with the homes of suburban children with asthma, the homes of inner city Baltimore children with asthma had higher levels of airborne pollutants and home characteristics that predispose to greater asthma morbidity.
Maternal and Child Health Journal | 2011
Arlene M. Butz; Patrick N. Breysse; Cynthia Rand; Jean Curtin-Brosnan; Peyton A. Eggleston; Gregory B. Diette; D’Ann L. Williams; John T. Bernert; Elizabeth C. Matsui
The goal of the study was to examine the association between biomarkers and environmental measures of second hand smoke (SHS) with caregiver, i.e. parent or legal guardian, report of household smoking behavior and morbidity measures among children with asthma. Baseline data were drawn from a longitudinal intervention for 126 inner city children with asthma, residing with a smoker. Most children met criteria for moderate to severe persistent asthma (63%) versus mild intermittent (20%) or mild persistent (17%). Household smoking behavior and asthma morbidity were compared with child urine cotinine and indoor measures of air quality including fine particulate matter (PM2.5) and air nicotine (AN). Kruskal–Wallis, Wilcoxon rank-sum and Spearman rho correlation tests were used to determine the level of association between biomarkers of SHS exposure and household smoking behavior and asthma morbidity. Most children had uncontrolled asthma (62%). The primary household smoker was the child’s caregiver (86/126, 68%) of which 66 (77%) were the child’s mother. Significantly higher mean PM2.5, AN and cotinine concentrations were detected in households where the caregiver was the smoker (caregiver smoker: PM2.5 μg/m3: 44.16, AN: 1.79xa0μg/m3, cotinine: 27.39xa0ng/ml; caregiver non-smoker: PM2.5: 28.88xa0μg/m3, AN: 0.71xa0μg/m3, cotinine:10.78xa0ng/ml, all Pxa0≤xa00.01). Urine cotinine concentrations trended higher in children who reported 5 or more symptom days within the past 2xa0weeks (>5xa0days/past 2xa0weeks, cotinine: 28.1xa0ng/ml vs. <5xa0days/past 2xa0weeks, cotinine: 16.2xa0ng/ml; Pxa0=xa00.08). However, environmental measures of SHS exposures were not associated with asthma symptoms. Urban children with persistent asthma, residing with a smoker are exposed to high levels of SHS predominantly from their primary caregiver. Because cotinine was more strongly associated with asthma symptoms than environmental measures of SHS exposure and is independent of the site of exposure, it remains the gold standard for SHS exposure assessment in children with asthma.
Annals of Allergy Asthma & Immunology | 2011
Meredith C. McCormack; Patrick N. Breysse; Elizabeth C. Matsui; Nadia N. Hansel; Roger D. Peng; Jean Curtin-Brosnan; D'Ann L. Williams; Marsha Wills-Karp; Gregory B. Diette
BACKGROUNDnCompared with atopic asthma, fewer environmental modifications are recommended for non-atopic asthma in children.nnnOBJECTIVEnTo better understand the role of indoor pollutants in provoking non-atopic asthma, we investigated the effect of in-home particulate matter on asthma symptoms among non-atopic and atopic children living in inner-city Baltimore.nnnMETHODSnA cohort of 150 children ages 2 to 6 years with asthma underwent home environmental monitoring for 3-day intervals at baseline, 3, and 6 months. Children were classified as non-atopic if they were skin test negative to a panel of 14 aeroallergens. Caregivers completed questionnaires assessing symptoms and rescue medication use. Longitudinal data analysis included regression models with generalized estimating equations.nnnRESULTSnChildren were primarily African American from lower socioeconomic backgrounds and spent most of their time in the home. Thirty-one percent were non-atopic, and 69% were atopic. Among non-atopic and atopic children, increased in-home fine (PM2.5) and coarse (PM2.5-10) particle concentrations were associated with significant increases in asthma symptoms and rescue medication use ranging from 7% (95% confidence interval [CI], 0-15) to 14% (95% CI, 1-27) per 10 μg/m(3) increase in particle concentration after adjustment for confounders.nnnCONCLUSIONSnIn-home particles similarly cause increased symptoms of asthma in non-atopic and atopic children. Environmental control strategies that reduce particle concentrations may prove to be an effective means of improving asthma outcomes, especially for non-atopic asthma, for which there are few environmental control practice recommendations.
Annals of Allergy Asthma & Immunology | 2006
Tamara T. Perry; Robert A. Wood; Elizabeth C. Matsui; Jean Curtin-Brosnan; Cynthia Rand; Peyton A. Eggleston
BACKGROUNDnRoom characteristics predicting indoor allergen exposure in suburban homes have not been clearly identified.nnnOBJECTIVEnTo examine relationships between room characteristics and concentrations of indoor allergens in homes of suburban asthmatic patients.nnnMETHODSnThe homes of 339 asthmatic children ages 6 to 17 years were studied. Home inspections were conducted by a trained technician, and dust samples were analyzed for indoor allergen content. A high allergen concentration was defined as 8 microg (U)/g or more of fine dust.nnnRESULTSnInfrequent sheet washing and wall-to-wall carpet were risk factors for high bedroom dust mite concentrations. Infrequent sheet washing was also a risk factor for high Fel d 1 concentrations. Food remains in the bedroom was a risk factor for high bedroom Bla g 1 levels, and exposed food, leaks, and dirty pots were all risk factors for high kitchen Bla g 1 levels. The combination of lack of mattress or pillow encasements, infrequent sheet washing, and carpeting was associated with a 24-fold increase in odds of a high dust mite concentration (odds ratio [OR], 24.1; 95% confidence interval [CI], 3.2-181.4). Among non-cat owners, the combination of stuffed toys on the bed, lack of mattress or pillow encasements, and infrequent sheet washing was associated with a 49-fold increase in odds of a high Fel d 1 level (OR, 49.4; 95% CI, 2.8-887.3). The combination of leaks, exposed food, and dirty pots was associated with a high kitchen Bla g 1 concentration (OR, 10.6; 95% CI, 2.8-40.5).nnnCONCLUSIONSnSpecific room characteristics predict high indoor allergen exposure among children with asthma, and a combination of these characteristics may further increase the risk of high allergen exposure.
The Journal of Allergy and Clinical Immunology | 2002
Sally H Joo; Robert A. Wood; Elizabeth C. Matsui; Tamara T. Perry; Jean Curtin-Brosnan; Sukon Kanchanaraksa; Cynthia Rand; Karen Callahan; Lee Swartz; Peyton A. Eggleston
The Journal of Allergy and Clinical Immunology | 2018
Suzanne Rossi; Torie L. Grant; Wanda Phipatanakul; Matthew S. Perzanowski; Susan L. Balcer-Whaley; Jean Curtin-Brosnan; Michelle Newman; Amparito Cunningham; Mary Beth Bollinger; Elizabeth C. Matsui
The Journal of Allergy and Clinical Immunology | 2018
Ammara G. Ahmed; Torie L. Grant; Wanda Phipatanakul; Matthew S. Perzanowski; Susan L. Balcer-Whaley; Roger D. Peng; Jean Curtin-Brosnan; Michelle Newman; Amparito Cunningham; Adnan Divjan; Mary Beth Bollinger; Robert A. Wise; Rachel L. Miller; Ginger L. Chew; Elizabeth C. Matsui
The Journal of Allergy and Clinical Immunology | 2018
Sara C. Sadreameli; Jean Curtin-Brosnan; Ammara G. Ahmed; Matthew S. Perzanowski; Wanda Phipatanakul; Susan L. Balcer-Whaley; Adnan Divjan; Elizabeth C. Matsui
The Journal of Allergy and Clinical Immunology | 2007
Kim Mudd; M. Paterakis; Jean Curtin-Brosnan; Robert A. Wood
The Journal of Allergy and Clinical Immunology | 2006
Karen Callahan; Elizabeth C. Matsui; Jean Curtin-Brosnan; Peyton A. Eggleston; Gregory B. Diette