| Summary: | Chapter 1. Background: Asthma is the most common chronic childhood disease and is characterized by recurrent airway obstruction, bronchial hyper-responsiveness, and airway inflammation. Asthma is the leading cause of childhood hospitalization and school absenteeism in the United States. The associations between adverse respiratory effects and exposure to indoor nitrogen dioxide (NO2) and other byproducts of combustion such as particulate matter (PM) in particular ultrafine particulates (UFP), Ozone (O3) and Sulfur Dioxide (SO2), have been the focus of many epidemiological studies in recent years. Indoor exposure to NO2 and other pollutants from combustion may increase the risk of acute and chronic respiratory disease, reduce lung function, initiate and exacerbate asthma in children.
The levels of exposure to NO2 indoors are of public health concern because children spend nearly 70% of their time indoors at home. According to the 2010 US Census report, approximately 39% of US households use natural gas for cooking, and the primary source of residential NO2 is a gas-fuel cooking appliance. Indoor levels of NO2 where NO2 sources are present can be much higher than outdoors, where the primary source of NO2 is vehicular traffic. Epidemiological studies in developed countries suggest that gas stoves used for cooking and/or heat are associated with an increased risk of asthma and respiratory symptoms in children. While there are numerous, epidemiological studies supporting an association between increased NO2 levels and gas stoves and asthma symptom severity in children, there are other studies that have examined the relationship in homes that did not observe significant associations.
A better understanding of how NO2 and other indoor environmental (e.g., environmental tobacco smoke (ETS), allergens) exposures contribute to asthma morbidity in inner city preschool children will allow interventions to more effectively designed and implemented. To date, there are conflicting results on the role of exposure to indoor NO2 and its association with new-onset asthma in young inner-city children. The recent studies assessing the effects of indoor NO2 on asthma morbidity were limited to inner-city children, largely older, who were diagnosed with asthma. A gap in knowledge remains regarding the role indoor NO2 plays on the development of asthma in children not previously diagnosed. The scientific and public health rationale for conducting this dissertation was to describe the association of exposure to indoor NO2 and primary sources with the initiation and exacerbation of asthma symptoms among pre-school children with and without diagnosed asthma. The data analyzed in the current research come from a larger study of Endotoxin, Obesity, and Asthma (EOA) in the New York City Head Start Program, funded in the summer of 2002. The primary research objective of that study was to identify modifiable risk factors associated with asthma and asthma persistence among preschool children from low-income families living in select New York City neighborhoods with high pediatric asthma hospitalization rates.
We conducted a cross-sectional analysis of data collected from the study questionnaire and home visit sampling at study enrollment. The analyses were performed in two phases: the first phases used data collected at study enrollment and the second phase used data collected 12-months after study baseline. Henceforth, the dissertation will refer to the first analyses as the baseline study and the second as the follow-up study. The research evaluated the association of NO2 exposure with asthma status among New York City Head Start children with and without asthma at study enrollment and with respiratory symptoms among children with asthma at 12-month follow-up.
Chapter 2. Baseline Study: We conducted a cross-sectional analysis of data collected from the study questionnaire and home visit sampling at study enrollment. Specifically, the research sought to evaluate the association of NO2 exposure with asthma status among New York City Head Start children with and without asthma at study enrollment and with respiratory symptoms among children with asthma at enrollment. A total of 503 children were included in the baseline study. A total of 105 children (20.9%) met the criteria for both asthma and allergy, and 67 (13.3%) met the criteria for asthma alone. Girls made up 51.7% and boys, 48.3% of the 503 study participants. Descriptive analyses suggested that asthma/allergy status was associated with: male gender, non-Mexican ethnicity/national origin, presence of a smoker in the child’s home, number of smokers in the child’s home, self-reported parental history of asthma, mother’s education level and sensitization to one or more of the four allergens. Logistic regression models were used to investigate the magnitude and direction (as well as trend) of the association between childhood asthma and indoor NO2 sources in the child’s home.
Chapter 3. Follow-up Study: Our follow-up study involved the analysis of the 12-month follow-up data from the study of Endotoxin, Obesity, and Asthma in the New York City Head Start Program funded in the summer of 2002. We focused on assessing the magnitude and direction of the associations of exposure to indoor NO2 levels (based on baseline NO2 measurements) with children’s asthma status and with symptom severity among asthmatics at 1-year follow-up. For the follow-up study, we categorized children by whether their asthma status had changed since baseline. Descriptive analyses were performed looking at key characteristics by “change in asthma status.” Children’s asthma status at baseline and at follow-up, were based on responses to the questionnaire. We analyzed indoor NO2 level measurements at baseline in relation to asthma outcomes on follow-up. We did not have enough data on NO2 levels at follow-up to analyze them in relation to asthma status on follow-up. Unless the family had relocated since baseline and/or reported changes since baseline in the use of gas appliances or the number of smokers in the home, we assumed that baseline NO2 levels in the participating children’s homes were reasonable proxies for current exposures. We looked at the number of children who moved since baseline and whether the move (for example, looking at gas stove status, age of new building) may have impacted indoor NO2 levels. Of the 503 children who were included in the baseline analyses, 47.3% had data on asthma status on follow-up. A total of 238 children (111 male, 127 female) were grouped into the four mutually exclusive outcome categories: 122 (51.3%) did not have asthma at baseline or on follow-up, 34 (14.3%) had asthma on follow-up but not at baseline, 65 (27.3%) had asthma at baseline but not on follow-up, and 17 (7.1%) had asthma at baseline and on follow-up. The mean age at 1-year follow-up was 59.5 months (6.95), and neither age nor gender was associated with asthma. The distribution of ethnicity/national origin among the 238 children remained the same as at baseline; no one ethnicity group experienced disproportionate loss to follow-up, and asthma status remained associated with non-Mexican ethnicity/national origin, although 44.1% with new-onset asthma were of Mexican background. Asthma was also associated with self-reported parental history of asthma and allergy in children, but nearly 80% of children with new-onset asthma had no such parental history of asthma. More parents of children with new-onset (35.3%) or persistent asthma (23.5%) than of other children reported making efforts to reduce risk factors or triggers for asthma exacerbations in the past 12 months.
Chapter 4. Dissertation Conclusion : The primary objective of the dissertation research was the examination of the relationship between asthma and asthma severity and exposure to gas cooking and residential NO2. In both our baseline and 12-month follow-up studies, exposure to indoor NO2 was represented by the baseline measurement of NO2 and the NO2 surrogate, gas stove. Asthma status of children was based on parental responses on the questionnaire regarding asthma symptoms and urgent care visits due to respiratory distress over the course of each 12-month period prior to the conducting study questionnaires. For both studies, we did not find an association between exposure to NO2 levels at baseline and asthma status or severity. Our findings contradict the results of most recent studies of both NO2 levels and residential sources of NO2 and their effects on asthma symptoms in very young children. However, it remains difficult to compare our results we those of previous published studies because those studies primarily focused on children who were diagnosed with asthma, whereas our research included preschool aged children with and without asthma. Based on our findings and the fact they conflict with other epidemiological studies, of which there were also conflicting results, we feel that the relationship between asthma symptoms and NO2 exposures remains ambiguous. The lack of consistent results of epidemiological research raises questions that should be the focus of future epidemiological studies. What are the roles of co-pollutants and co-risk factors? Does NO2 work alone or in concert with other indoor pollutants? There exists a real lack of understanding on the possible synergistic effects of exposure to NO2 and other combustion byproducts. Important to furthering our knowledge of the role of exposure to indoor NO2 and asthma is determining whether NO2 acts as a surrogate for co-pollutants that are considered risk factors for asthma and other respiratory conditions. Another focus of future indoor pollution studies should be the development of effective methods and technologies for measuring the constituents of the complex mixture of pollutants in indoor air; these methods and technologies can then be applied in personal monitoring of exposure to indoor pollutants in epidemiological studies that would help to determine with much more accuracy the effects of individual indoor pollutants on asthma and other respiratory symptoms. This knowledge would help in the development of more effective public health and environment policies towards reducing the burden of childhood asthma.
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