PM2.5 exposure in early life and childhood asthma incidence in a retrospective birth cohort Open Access

Flak, Audrey Lauren (2016)

Permanent URL: https://etd.library.emory.edu/concern/etds/wp988k031?locale=en
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Abstract

It is well established that urban air pollution exacerbates pre-existing asthma, and the literature suggests that it may also play a role in asthma development. This dissertation investigated the association between exposure to PM2.5 (particulate matter ≤2.5µm in diameter) in early life and childhood asthma incidence in the Kaiser Air Pollution and Pediatric Asthma Study (KAPPA). The KAPPA Study is a birth cohort of 24,608 children born between 2000 and 2010 enrolled in Kaiser Permanente Georgia. Asthma case definitions vary widely among studies using medical records to define disease. In Aim 1, we examined 15 case definitions of incident asthma in early life. Choice of case definition had a large impact on the estimate of asthma incidence by age 3 and the ability to predict asthma at school age. These results informed our decision to designate one asthma diagnosis plus one asthma-related medication dispensing as the primary outcome definition in subsequent aims. In Aims 2 and 3 we assessed the association between prenatal and first year of life exposure to PM2.5 and asthma incidence by ages 2 through 6. The impact of exposure to both primary PM2.5 from traffic emissions and total PM2.5 was explored. In adjusted models, an increase of 1 µg/m3 of traffic PM2.5 during the first year of life was associated with a 2.7% to a 5.8% absolute increase in risk of asthma, depending on the follow-up age (Risk Difference(95%CI) age 2=0.027(0.003,0.050); age 3=0.037(0.004,0.070); age 4=0.037(-0.007,0.082); age 5=0.058(0.004,0.112); age 6=0.036(-0.029,0.101)). An increase of 1 µg/m3 of total PM2.5 was associated with a 0.4% to 1.8% increase in risk of asthma (RD(95%CI) age 2=0.008(-0.002,0.017); age 3=0.007(-0.006,0.020); age 4=0.004(-0.014,0.022); age 5=0.018(-0.005,0.041); age 6=0.018(-0.011,0.046)). Risk differences were smaller for the association of PM2.5 exposure during pregnancy. Across aims, we observed little evidence of additive interaction between PM2.5 and child race, child sex, maternal asthma, or city region of residence. This dissertation provides some evidence for an association between PM2.5 exposure in early life and childhood asthma incidence. Our results highlight the impact of case definition on estimates of asthma incidence in early childhood in a medical record setting.

Table of Contents

CHAPTER 1: Introduction. 1

CHAPTER 2: Literature Review. 3

Childhood Asthma. 3

Asthma Diagnosis. 4

Wheeze. 6

Early life respiratory symptoms and future disease. 7

Asthma phenotypes and allergic sensitization. 9

Hygiene hypothesis and asthma. 12

Asthma disparities. 13

Asthma risk factors. 14

Asthma diagnosis for research. 16

Air Pollution. 23

Traffic-related pollutants. 25

Pollution data and health research. 27

Prenatal and early-life air pollution exposure and asthma incidence. 28

Biological susceptibility and potential mechanisms. 28

Conclusions of key review articles. 30

Results of key studies. 32

Effect modification by atopy and socioeconomic status. 34

Limitations of previous research. 36

CHAPTER 3: Methods. 43

Data Sources. 43

Air Pollution Data. 43

Kaiser Permanente Georgia. 46

Georgia Birth Certificates. 47

Data Preparation. 47

Socioeconomic Data. 51

Analytic Methods. 52

CHAPTER 4: Evaluating early-life asthma definitions as a marker for subsequent asthma in an electronic medical record setting. 56

CHAPTER 5: Prenatal and first year of life exposure to primary PM2.5 from traffic and childhood asthma incidence in a birth cohort. 72

CHAPTER 6: Prenatal and first year of life exposure to total PM2.5 and childhood asthma incidence in a birth cohort. 120

CHAPTER 7: Conclusion. 162

APPENDIX A: Additional detail on data sources. 173

APPENDIX B: Additional analyses of prenatal and first year of life exposure to primary PM2.5 from traffic and childhood asthma incidence in a birth cohort. 178

APPENDIX C: Additional analyses of prenatal and first year of life exposure to total PM2.5 and childhood asthma incidence in a birth cohort. 197

CHAPTER 8: References. 213

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