ABSTRACT
OBJECTIVES: To assess whether population-level violent (and all) crime rates were associated with population-level child asthma utilization rates and predictive of patient-level risk of asthma reutilization after a hospitalization. STUDY DESIGN: A retrospective cohort study of 4638 pediatric asthma-related emergency department visits and hospitalizations between 2011 and 2013 was completed. For population-level analyses, census tract asthma utilization rates were calculated by dividing the number of utilization events within a tract by the child population. For patient-level analyses, hospitalized patients (n = 981) were followed until time of first asthma-related reutilization. The primary predictor was the census tract rate of violent crime as recorded by the police; the all crime (violent plus nonviolent) rate was also assessed. RESULTS: Census tract-level violent and all crime rates were significantly correlated with asthma utilization rates (both P < .0001). The violent crime rate explained 35% of the population-level asthma utilization variance and remained associated with increased utilization after adjustment for census tract poverty, unemployment, substandard housing, and traffic exposure (P = .002). The all crime rate explained 28% of the variance and was similarly associated with increased utilization after adjustment (P = .02). Hospitalized children trended toward being more likely to reutilize if they lived in higher violent (P = .1) and all crime areas (P = .01). After adjustment, neither relationship was significant. CONCLUSIONS: Crime data could help facilitate early identification of potentially toxic stressors relevant to the control of asthma for populations and patients.
Subject(s)
Asthma/epidemiology , Crime/statistics & numerical data , Exposure to Violence/statistics & numerical data , Child , Child, Preschool , Cohort Studies , Emergency Service, Hospital/statistics & numerical data , Female , Hospitalization/statistics & numerical data , Humans , Male , Ohio/epidemiology , Police , Retrospective StudiesABSTRACT
OBJECTIVE: To examine the association between exposure to traffic-related air pollution (TRAP) and hospital readmission for asthma or bronchodilator-responsive wheezing. STUDY DESIGN: A population-based cohort of 758 children aged 1-16 years admitted for asthma or bronchodilator-responsive wheezing was assessed for asthma readmission within 12 months. TRAP exposure was estimated with a land use regression model using the home address at index admission, with TRAP dichotomized at the sample median (0.37 µg/m3). Covariates included allergen-specific IgE, tobacco smoke exposure, and social factors obtained at enrollment. Associations between TRAP exposure and readmission were assessed using logistic regression and Cox proportional hazards models. RESULTS: The study cohort was 58% African American and 32% white; 19% of the patients were readmitted within 12 months of the original admission. Higher TRAP exposure was associated with a higher readmission rate (21% vs. 16%; P = .05); this association was not significant after adjusting for covariates (aOR, 1.4; 95% CI, 0.9-2.2). Race modified the observed association; white children with high TRAP exposure had 3-fold higher odds of asthma readmission (OR, 3.0; 95% CI, 1.1-8.1), compared with white children with low TRAP exposure. In African American children, TRAP exposure was not associated with increased readmission (OR, 1.1; 95% CI, 0.6-1.8). In children with high TRAP exposure, TRAP exposure was associated with decreased time to readmission in white children (hazard ratio, 3.2; 95% CI, 1.5-6.7) compared with African American children (hazard ratio, 1.0; 95% CI, 0.7-1.4). African American children had a higher readmission rate overall. CONCLUSION: TRAP exposure is associated with increased odds of hospital readmission in white children, but not in African American children.
Subject(s)
Air Pollutants/adverse effects , Asthma/epidemiology , Environmental Exposure/adverse effects , Patient Readmission/statistics & numerical data , Vehicle Emissions/toxicity , Adolescent , Asthma/etiology , Asthma/therapy , Causality , Child , Child, Preschool , Cohort Studies , Environmental Monitoring/methods , Female , Gasoline/toxicity , Hospitalization/statistics & numerical data , Humans , Incidence , Infant , Logistic Models , Longitudinal Studies , Male , Particulate Matter/adverse effects , Prognosis , Proportional Hazards Models , Prospective Studies , Risk Assessment , Socioeconomic FactorsABSTRACT
OBJECTIVE: To examine risk factors for eczema at age 4 years. STUDY DESIGN: Beginning at 1 year of age, infants of atopic parents (n = 636) had annual clinical evaluations and skin prick tests (SPTs) to 15 aeroallergens and milk and egg. Parents completed validated surveys on eczema and environmental exposures. House dust samples were evaluated for allergens and endotoxin. Eczema was defined as a parental report of scratching, and redness, "raised bumps," or dry skin/scaling for 6 of the last 12 months. RESULTS: At age 4 years, a total of 90 children (14%) had eczema. Not having a dog before 1 year of age and being dog SPT+ at 1, 2, or 3 years of age conferred a 4-fold higher risk for eczema at age 4 years (adjusted odds ratio [aOR] = 3.9 [1.6-9.2]; P = .002). Among dog owners, however, dog SPT+ was not associated with significantly increased risk (aOR 1.3 [0.3-6.8]; P = .8). Among children with cats before 1 year of age, cat SPT+ conferred significantly increased risk for eczema (aOR = 13.3 [3.1-57.9]; P < .001). Among non-cat owners, cat SPT+ was not associated with increased risk (aOR = 1.1 [0.5-2.7]; P = .8). CONCLUSION: Dog ownership significantly reduced the risk for eczema at age 4 years among dog-sensitized children, cat ownership combined with cat sensitization significantly increased the risk.
Subject(s)
Animals, Domestic/immunology , Dermatitis, Atopic/immunology , Eczema/immunology , Environmental Exposure/adverse effects , Immunization , Age Factors , Allergens , Analysis of Variance , Animals , Cats , Child, Preschool , Cohort Studies , Confidence Intervals , Dermatitis, Atopic/diagnosis , Dermatitis, Atopic/epidemiology , Dermatitis, Atopic/genetics , Dogs , Eczema/epidemiology , Eczema/genetics , Female , Genetic Predisposition to Disease , Humans , Incidence , Infant , Infant, Newborn , Longitudinal Studies , Male , Odds Ratio , Prognosis , Risk Assessment , Skin TestsABSTRACT
OBJECTIVE: To determine the impact of environmental exposures (diesel exhaust particle [DEP], environmental tobacco smoke [ETS], and mold) that may contribute to oxidative stress on persistent wheezing in the Cincinnati Childhood Allergy and Air Pollution Study (CCAAPS) birth cohort and to determine how the impact of these exposures is modified by the GST-P1 Ile105Val polymorphism. STUDY DESIGN: A land-use regression model was used to derive an estimate of each child's DEP exposure. ETS exposure was determined by questionnaire data. Each child's home was evaluated for visible mold by a trained professional. Children in the CCAAPS cohort were genotyped for the GST-P1 polymorphism (n = 570). Persistent wheezing was defined as wheezing at both 12 and 24 months. RESULTS: High DEP exposure conferred increased risk for wheezing phenotypes but only among the Val(105) allele carriers. Infants with multiple exposures were significantly more likely to persistently wheeze despite their genotype. CONCLUSION: There is evidence for an environmental effect of DEP among carriers of the GST-P1 Val(105) allele in the development of persistent wheezing in children. The protective effect of the GST-P1 Ile(105) genotype may be overwhelmed by multiple environmental exposures that converge on oxidative stress pathways.