Effect Of Early Life Exposure To Air Pollution On Development Of Childhood Asthma

Project and Seminar Material for Environmental Science

Effect Of Early Life Exposure To Air Pollution On Development Of Childhood Asthma


Abstract


There is increasing recognition of the importance of early environmental exposures in the development of childhood asthma. Outdoor air pollution is a recognized asthma trigger, but it is unclear whether exposure influences incident disease. We investigated the effect of exposure to ambient air pollution in utero and during the first year of life on risk of subsequent asthma diagnosis in a population-based nested case-control study.

Methods:

We assessed all children born in southwestern British Columbia in 1999 and 2000 (n = 37,401) for incidence of asthma diagnosis up to 34 years of age using outpatient and hospitalization records. Asthma cases were age- and sex-matched to five randomly chosen controls from the eligible cohort. We estimated each individual’s exposure to ambient air pollution for the gestational period and first year of life using high-resolution pollution surfaces derived from regulatory monitoring data as well as land use regression models adjusted for temporal variation. We used logistic regression analyses to estimate effects of carbon monoxide, nitric oxide, nitrogen dioxide, particulate matter

Results:

A total of 3,482 children (9%) were classified as asthma cases. We observed a statistically significantly increased risk of asthma diagnosis with increased early life exposure to CO, NO, NO2, PM10, SO2, and black carbon and proximity to point sources. Traffic-related pollutants were associated with the highest risks: adjusted odds ratio = 1.08 (95% confidence interval, 1.041.12) for a 10-microg/m3 increase of NO, 1.12 (1.071.17) for a 10-microg/m3 increase in NO2, and 1.10 (1.061.13) for a 100-microg/m3 increase in CO. These data support the hypothesis that early childhood exposure to air pollutants plays a role in development of asthma.


Chapter One


Introduction

1.1 Background of the Study

Earlier studies have generally relied on simple measures of traffic proximity and density to estimate exposure and have not found an association between air pollution and asthma incidence (Ciccone et al. 1998; English et al. 1999; Wjst et al. 1993). More recent studies have used modeling approaches that provide high -resolution estimates of neighborhood-scale variations in air pollution. Several studies using this approach have observed increases in asthma incidence or asthma symptoms for children exposed to higher levels of traffic­-related air pollution (Brauer etal. 2002, 2007; Gauderman et al. 2005; McConnell et al. 2006; Morgenstern et al. 2008; Zmirou et al. 2004). However, not all such studies of this type have reported consistent associations (Gehring et al. 2002; Zmirou et al. 2004).

Pre- and postbirth exposures to environmental tobacco smoke (ETS) are inde-pendently associated with increased asthma incidence (Haberg et al. 2007). Although air pollution exposures before 2–3 years of age appear to be most important for asthma devel-opment (McConnell et al. 2006; Zmirou et al. 2004), the effect of prebirth (or in utero) expo-sure has not to our knowledge been examined. One exception is a study of polyclyclic aro-matic hydrocarbon exposure, which has been examined in conjunction with ETS (Miller et al. 2004).

In the first population-based birth cohort study to explore the relationship between ambient air pollution exposure and the risk of asthma incidence, we examined the effect of in utero and first-year exposures to ambi-ent air pollutants, estimated at the individual level, on the risk of asthma diagnosis in chil-dren up to 3 and 4 years of age. Pollutant exposures investigated were carbon monoxide(CO), nitrogen oxides [nitric oxide (NO) and nitrogen dioxide (NO2 )], particulate matter [≤ 10 µm and ≤ 2.5 µm in aerodynamic diam-eter (PM10 and PM 2.5)], ozone (O3), sulfur dioxide (SO2), black carbon, woodsmoke, and proximity to roads and point sources.


1.2 Statement of the Problem

Asthma is the most common chronic disease in childhood [World Health Organization (WHO) 2006]. Its prevalence is high and has generally increased worldwide over the latter part of the 20th century (Asher et al. 2006; WHO 2006). Although explanations for relatively rapid changes in prevalence are unknown, environmental factors, independently and jointly with genetic factors, are thought to be responsible. Although air pollution has been consistently shown to exacerbate existing asthma (English et al. 1999; Lipsett et al. 1997; McConnell et al. 1999, 2006; Nicolai et al. 2003; Norris et al. 1999), there are few investigations of asthma onset and air pollution despite the hypothesized link with exposure to outdoor air pollution (Institute of Medicine 2000; von Mutius 2000).


1.3 Objectives of the Study

The primary objective of this study is to study the effect of early life exposure to air pollution on development of childhood asthma. Specifically, the study seeks to:

  1. To assess all children born in southwestern British Columbia in 1999 and 2000 for incidence of asthma diagnosis up to 34 years of age using outpatient and hospitalization records.
  2. To estimate each individual’s exposure to ambient air pollution for the gestational period and first year of life using high-resolution pollution surfaces derived from regulatory monitoring data.
  3. To estimate the effect of carbon monoxide, nitric oxide, nitrogen dioxide, particulate matter.

1.4 Research Hypothesis

The following hypotheses were formulated to be tested in this study:

  • H0: Early childhood exposure to air pollutants does not plays a role in development of asthma.
  • HA: Early childhood exposure to air pollutants plays a role in development of asthma.

1.5 Scope of the Study

This study is limited to all children born in southwestern British Columbia in 1999 and 2000 with population of 37,401for incidence of asthma diagnosis up to 34 years of age using outpatient and hospitalization records.


1.6 Significance of the Study

This study will be of significance to the general public and will expose them to the effect of early life exposure to air pollution on development of childhood asthma. This study will also bring to the notice of health practitioners and mothers to know the necessary precaution to take to avoid childhood asthma.


Chapter Five


Discussion of Finding and Conclusion

5.1 Discussion of Findings

We found that higher exposure to ambient air pollution in early life was associated with elevated risks of asthma diagnosis in preschoolage children based on clinical records. Traffic related pollutants (NO, NO2, CO, and black carbon) were associated with the highest risk estimates. PM10, SO2, and residence near industrial point sources were also associated with elevated asthma risk, whereas PM2.5, wood smoke, and road proximity did not show elevated risks. The results from this population-based study strengthen the emerging evidence that air pollution exposure plays a role in childhood asthma development, although these findings should be confirmed in additional cohorts of children, particularly as they reach school age and asthma diagnosis is more robust. The risk estimates we found were similar to the results of other birth cohort studies investigating respiratory outcomes. Morgenstern et al. (2008) also estimated air pollution exposure using LUR modeling and examined effects on risk of asthma diagnosis in 6-year-old children in Germany. They found ORs of 1.12 per 1-µg/m3 increase in PM2.5, 1.56 per 0.2 × 10–5/m increase in filter absorbance measure of black carbon, and 1.04 per 6.4-µg/m3 increase in NO2. Nordling et al. (2008) prospectively followed children in Stockholm, Sweden, from birth until 4 years of age and found that exposure to traffic-related air pollution during the first year of life was associated with an excess risk of persistent wheezing of 1.60 (95% CI, 1.09–2.36) for a 44-µg/m3 increase in traffic NOx. Brauer et al. (2007) used LUR models to estimate the effect of traffic-derived pollutants on asthma incidence among 4-year-old children in the Netherlands. They found ORs of 1.20 per 10-µg/m3 increase in NO2 and 1.30 per 0.6 × 10–5/m increase in filter absorbance (black carbon). They also found an elevated risk of 1.20 per 3.3-µg/m3 increase in PM2.5, which we did not identify in this study, although the composition of PM2.5 and the relationship between PM2.5 and other pollutants are likely to differ across locations. Compared with other studies/locations, PM2.5 in this study area was quite low and less variable. PM2.5 exposure estimates were also subject to more error because they were based on fewer monitors than other pollutants. To our knowledge, this was the largest study and one of the few to examine the effects of in utero air pollution exposure on pediatric asthma risk. Mortimer et al. (2008) found that in utero exposure to air pollution was associated with negative effects on lung function in asthmatic children. Other effects of air pollution on the developing fetus include lower birth weight (Bobak 2000; Slama et al. 2007), small size for gestational age (Brauer et al. 2008b), preterm births (Bobak 2000; Brauer et al. 2008b; Ritz et al. 2000), and intrauterine mortality (Pereira et al. 1998). Because of relatively high correlation between in utero and first-year exposures for many pollutants, we are unable to discern the relative importance of these exposure periods. Mutually adjusted models for NO, NO2, PM10, and black carbon did not consistently identify either period as more significant but did suggest that in utero exposures have an effect independent from postbirth exposures for NO and PM10. We cannot eliminate the possibility that these results were influenced by misclassification bias associated with a lack of temporal precision in the residential histories; in utero exposures were more likely to have been misclassified than first-year exposures because of greater confidence in residential postal code (which can be confirmed against the mother’s data after birth) and likely greater time spent at the residence after birth than during pregnancy. These exposure assessment errors would be expected to lead to a bias to the null for the intrauterine period. Further work is necessary to elucidate the relative importance of pre- and postbirth exposures. Asthma risks due to air pollution were generally larger for girls for both in utero and first-year exposures. As expected, girls had a lower incidence of asthma (making up 36% of cases), but despite the smaller numbers, associations with pollutants were significantly elevated (except for woodsmoke, PM2.5, and road proximity). Several previous studies have also found that girls are more susceptible to air pollution, with higher risks of asthma (McConnell et al. 2006; van Vliet et al. 1997) and greater effects on lung function (Peters et al. 1999). However, this is not an entirely consistent finding (Gehring et al. 2002). Proximity to roads is commonly used to approximate exposure because of its relative ease compared with monitoring methods. Although many studies have found asthma symptoms to be associated with proximity to major roads (Gauderman et al. 2005; McConnell et al. 2006; Morgenstern et al. 2007), this is also not a consistent finding (English et al. 1999). Simple proximity measures may not capture exposure accurately because they lack information on traffic density, vehicle mix, wind patterns, topography, land use characteristics, and other influences on pollution levels (Brauer et al. 2003; Henderson et al. 2007; Jerrett et al. 2005). This may explain why we did not find proximity to roads to be associated with increased asthma risk in this study. Our study was further challenged by the small number of children residing in proximity to major roads. Nonetheless, we did observe consistently elevated risks with measured and modeled values of traffic-derived pollutants, suggesting that traffic-related exposure is important. The industrial point source index is subject to many of the same limitations as the road proximity measure. Despite these limitations, we observed elevated asthma risks associated with the point source index. This may partially indicate a socioeconomic effect; the point source index was among the only exposure indices that were reduced after adjustment for covariates, primarily as a result of adjustment for income and education status. Residential woodsmoke contributes a considerable fraction of PM exposure in portions of the study area in the winter months (Ries et al. 2009). Despite this, woodsmoke exposure was not found to be associated with increased asthma risk.

Previous studies have associated woodsmoke with adverse respiratory effects in children, including exacerbation of asthma (Allen et al. 2008; Zelikoff et al. 2002); however, its role in asthma development requires more research. The use of linked administrative data sets presents some limitations, such as the lack of clinical details and information on asthma severity. However, our estimates of asthma incidence are consistent with previous findings in similar age ranges (Dik et al. 2004; Jaakkola et al. 2005). Furthermore, the validity of our findings is supported by a recent validation study of administrative data in a similar health care setting. It found that asthma codes were a highly sensitive and specific measurement of asthma in 0- to 5-yearolds compared with experts’ review of medical charts (To et al. 2006). Because of universal and free access to physician visits, we also believe that any misclassification of asthma status was nondifferential and therefore would be expected to bias the results to the null. Limitations of the BC Perinatal Database Registry likely underlie the reason that we did not observe an expected effect of maternal smoking on asthma risk. The variable relies on maternal self-report and therefore likely includes some misclassified exposures due to a healthy reporting bias (e.g., Derauf et al. 2003). An additional limitation of this study was the young age of the children. Wheezing illnesses in early childhood represent multiple phenotypes. Transient wheezing is common in infants and often resolves as the children age (Martinez et al. 1995; To et al. 2007). To et al. (2007) found that among children diagnosed with asthma before 6 years of age, 48.6% were in remission by 12 years of age. Children with a hospitalization for asthma or many physician visits for asthma were at greater risk of persistent asthma by 12 years of age (To et al. 2007). We have addressed this issue by restricting our asthma cases to children with a hospital admission or at least two outpatient diagnoses of asthma, because these indicate severe or ongoing symptoms, respectively. Sensitivity analyses requiring three outpatient diagnoses only made the resulting ORs larger, indicating that air pollution is associated with ongoing respiratory symptoms consistent with asthma. This indicates that adverse respiratory effects do occur with air pollution exposure, but to ensure associations with persistent asthma, the results must be confirmed when the children are older. We were able to correct for a number of individual-level variables, but socioeconomic variables could be adjusted only at the neighborhood level. This is imperfect and may have led to some misclassification of socioeconomic status for individuals (Hanley and Morgan 2008); however, the adjustment generally had small, and often strengthening, effects on ORs. We also had no information on the child or family history of atopy, an important risk factor for asthma development and a potential effect modifier.


5.2 Conclusion

In this population-based study, children with higher early life air pollution exposures, particularly to traffic-derived pollutants, were observed to have an increased risk of asthma diagnosis in the preschool years. This adds to evidence that outdoor air pollution not only exacerbates asthma but also may be associated with development of new disease. The risk increase is small at an individual level but presents a significant increase in burden of disease on a population level because in most urban and suburban settings, traffic-derived air pollution exposure is ubiquitous.


Effect Of Early Life Exposure To Air Pollution On Development Of Childhood Asthma


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