Measuring the Effects of Mouse Allergen and Black Carbon Exposure on Children Living in New York City with Allergic Diseases
By: Medina Samira Jackson-Browne
Publisher: [publisher not identified]
Published: 2016
Place of publication: [New York, N.Y.?]
Language: eng
Description: Measuring the Effects of Mouse Allergen and Black Carbon Exposure on Children Living in New York City with Allergic Diseases Medina Samira Jackson-Browne Background: Exposure to allergens and combustion by-products are risk factors for allergic health outcomes in children. The connection between exposure to allergens and allergic diseases such as asthma, in some children, is through the development of a biological condition known as allergic sensitization. In susceptible children, sensitization may occur when early-life exposure to an allergen causes the production of immunoglobulin E (IgE) antibodies. In asthmatic children, repeated exposures to this allergen may lead to clinical manifestations including airway inflammation, airway mucous production, bronchospasms, and bronchial hyper-responsiveness. Sensitization and repeated exposure to allergens may, therefore, be important risk factors for asthma morbidity in children. Findings from a cross-sectional asthma study of children living in NYC published previously by our group found a positive association between cockroach and dust-mite allergens measured in bed dust and sensitization risk to these allergens consistent with other studies.

However, contrary to previously published research, no association was observed between mouse allergen measured in bed dust and mouse sensitization risk in our study. In urban areas such as New York City (NYC), exposure to combustion by-products, including black carbon (BC), has been shown to be associated with both asthma development and asthma morbidity. BC has been proposed to exacerbate asthma symptoms directly through airway irritation or by behaving as an adjuvant, enhancing the production of IgE antibodies following exposure to an allergen in sensitized individuals. Our group previously observed an association between indoor measured BC concentrations and airway inflammation, however no association was found between BC and asthma symptoms for children living in NYC. In the present study, we sought to address some of the limitations of the previous work. These limitations included a singular measurement of mouse allergen exposure, a shorter-term BC exposure measurement, and a cross-sectional study design for asthma symptom risks.

My overarching hypothesis for this dissertation is that exposures to mouse allergen and BC are significant risk factors for allergic sensitization and asthma morbidity, respectively, for children living in NYC. I tested these hypotheses in three separate manuscripts by assessing multiple mouse exposure measurements with the risk for mouse sensitization (Chapter 2), testing the correlation between 7-day measured indoor BC and particulate matter smaller than 2.5 microns (PM2.5) concentrations with annual modeled outdoor BC and PM2.5 concentrations (Chapter 3), and determining whether annual modeled outdoor BC concentration is associated with persistent asthma symptoms, over a three-year period, for asthmatic children in NYC (Chapter 4). Methods: For all manuscripts, data from an asthma case-control cohort of children (age 7-8 years) previously established by our group, the NYC Neighborhood Asthma and Allergy Study (NAAS), was utilized for analysis (n=350). Kitchen floor and bed settled dust samples were collected from the children’s home during the initial home visit.

Mouse allergen concentrations were quantified from both kitchen floor and bed dust samples using an enzyme-linked immunosorbent assay (ELISA). Blood samples were also collected during this visit. IgE antibodies to mouse allergens were measured by ImmunoCAP (Phadia, Uppsala, Sweden) from these blood samples. Information on the frequency of mouse sightings in the previous 12 months was extracted from a questionnaire administered to parents of NAAS children. Neighborhood and school mouse sightings were collected from reports from the NYC Department of Health and Mental Hygiene (DOHMH). Indoor PM2.5 and BC samples were collected from air samplers placed in NAAS children’s home for an average of 7 days. In collaboration with the NYC DOHMH, we were given access to 2-year averaged modeled outdoor PM2.5 and BC concentrations collected from air monitors at 124 street-level locations throughout NYC from 2008-2010. After the initial home visit, asthmatic NAAS children were followed-up annually for asthma symptoms.

The questionnaire data collected from the asthmatics followed were used to evaluate the persistence or remittance of asthma symptoms over the 3-years following the initial home visit. Results: In our mouse study we found that increasing mouse allergen measured from kitchen floor dust and children whose parents reported greater than weekly mouse sightings in the previous 12 months has an increased risk of mouse sensitization (prevalence risk (PR) = 1.09 [1.02-1.17], p=0.04 and PR= 3.84 [1.95-6.97], p=0.001 respectively). Neither mouse allergen measured from settled bed dust (PR = 1.06 [0.95-1.19], p=0.46) nor neighborhood rodent reports (PR = 1.25 [0.94-1.68], p=0.16) were significantly associated with an increased risk of sensitization to mouse. Exposure to mouse at school was also not associated with an increased risk of mouse sensitization (PR=0.66 [0.35-1.26], p=0.30). Results from the correlation study indicated both annual modeled outdoor PM2.5 and BC concentrations were weakly correlated with 7-day measured indoor PM2.5 and BC concentrations (r = 0.21 and 0.39, respectively, p < 0.01).

However, annual modeled outdoor BC concentrations predicted almost 20% of the variability of 7-day measured indoor BC (R2=0.19, p<0.001) compared to only 4% of the variability of 7-day indoor PM2.5 explained by annual modeled outdoor PM2.5, which predicted measured indoor PM2.5 (R2 = 0.04, p < 0.001). Our regression analysis of the asthma morbidity study found no significant association between longer-term neighborhood modeled BC concentrations at study participant’s home (PR = 0.87 [0.58-1.29, p=0.49] and school addresses (PR =1.09 [0.77-1.56], p=0.60) and persistent asthma symptoms. Conclusions: My findings suggest that mouse allergen measured from kitchen floor dust and parent reported mouse sightings are important risk factors of mouse sensitization for children living in urban areas such as NYC. The results of the BC analysis indicate a moderate correlation between annual modeled outdoor BC concentrations and 7-day measured indoor BC concentrations. The annual modeled outdoor BC also predicted 20% of the variability in 7-day measured indoor BC.

Conversely, PM2.5 analysis indicate that annual modeled outdoor PM2.5 is not correlated with 7-day measured indoor PM2.5 concentrations. Finally, regression analysis of BC exposure and asthma morbidity indicate that annual modeled outdoor BC is not predictive of persistent asthma symptoms in our cohort.
Notes: Department: Environmental Health Sciences.

Thesis advisor: Matthew S. Perzanowski.

Thesis (Ph.D.)--Columbia University, 2016.