Environmental Science Project Topics

Effect of Early Life Exposure to Air Pollution on Development of Childhood Asthma

Effect of Early Life Exposure to Air Pollution on Development of Childhood Asthma

Effect of Early Life Exposure to Air Pollution on Development of Childhood Asthma

Chapter One

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.



 Coal mine fire smoke exposure and human health

Coal mine fires are widespread and currently active around the world, generating air pollutants including particulate matter, gases and condensation by-products[1]. In February 2014, an opencut coal mine fire (Hazelwood coal mine fire) was ignited by embers from wildfires and lasted for 45 days in the Latrobe Valley, Victoria, Australia. Several regional towns near the mine were affected by smoke during the fire period with air quality impacts ranging from minor to severe. The nearest town of Morwell experienced severe air pollution exposure with a peak 24hour average PM2.5 concentration of 731 µg/m3, which is remarkably higher than the Australian air quality standard of 25 µg/m3[2-3]. However, the potential health effects of coal mine fire smoke exposure have been poorly investigated[4].

Air pollutants generated from coal mine fire emissions are thought to be similar to those from landscape fires including burning forest, grass and peat[4], which make a significant contribution to air pollution[5] and is an increasing global concern because of the rising frequency and severity of fires resulting from climate change[6]. Exposure to air pollutants from landscape fire smoke has been demonstrated to adversely affect human health, especially the respiratory and immune systems. For example, epidemiological studies have consistently found that short-term fire smoke exposure is significantly associated with decreased lung function among nonasthmatic children, and increased hospitalisations, physician and emergency department visits for respiratory problems and asthma among general population[7-8]. There is also strong evidence suggesting an association between fire smoke exposure and increased respiratory infections[8-9]. However, evidence on the health effects from early life fire smoke exposure is very limited[7]. A study of rhesus macaque monkeys suggested that infant exposure to fire smoke was associated with immune dysregulation and reduced lung volume in adolescence[10] indicating that further work is warranted.

Particulate matter with an aerodynamic diameter < 2.5 micrometers (PM2.5) is one of the primary emissions from landscape fires[11-12]. PM2.5 from other sources such as traffic and industrial emissions is well known to be harmful to respiratory and immune health, both for short-term and long-term exposures. For example, daily exposure to PM2.5 has been found to be positively associated with increased hospital admissions and/or emergency department visits for pneumonia and asthma in children and adolescents[13-15], while long-term exposure has also been associated with asthma development during childhood[16]. There is a small, but growing, body of evidence indicating an association between short-term fire smoke-related PM2.5 exposure and adverse health outcomes. A study of the 2007 San Diego landscape fires observed a significant association between daily fire smoke-related PM2.5 exposure and increased emergency department presentations for respiratory issues such as asthma, respiratory infections and other symptoms[17]. In line with this, similar associations were also found in studies of landscape fires from other areas of America and Canada between short-term exposure to PM2.5 from fire emissions and respiratory diseases including asthma/wheezing and bronchitis[18-21]. However, the effects of fire smoke PM2.5 exposure in later life have not been well documented. Additionally, despite the similarity in toxic components from coal mine fire and landscape fire emissions, individual fire emissions vary significantly depending on the substrate burned, the nature of combustion and meteorological conditions[4]. Coal mine fires are often of a longer duration than landscape fires, and are characterised by predominantly smouldering combustion. Therefore, it is important to understand the association between coal mine fire smoke exposure and human health to guide public health responses.

Developmental susceptibility to the effects of air pollution

The development and growth of human respiratory and immune systems starts in utero and lasts throughout the whole childhood. For the respiratory system, the prenatal period is critical for cellular differentiation and branching morphogenesis[22]. The embryonic stage starts from the first week of pregnancy and lasted for nearly 7 weeks, followed by the pseudoglandular stage (5-17 weeks of pregnancy), the canalicular stage (16-26 weeks of pregnancy) and the saccular stage (24-38 weeks of pregnancy) successively[23]. The alveoli develop and grow from 36 weeks of pregnancy to 1-2 years after birth, which is known as the alveolar proliferation stage[22-23]. Development of the human immune system begins with the formation and migration of hematopoietic stem cells, followed by the expansion of progenitor cells and the colonisation of the bone marrow and thymus. All these processes occur during the in utero period[22, 24]. After birth, the immune system matures to immunocompetence during the first year of life[22].

Infants and young children have higher oxygen consumption rates compared with adults[25]. On a body weight basis, the rate of oxygen consumption of a resting infant is nearly twice the rate of a resting adult. Therefore, the volume of air pollutants reaching the lung of an infant, per body weight, are likely to be much higher than that of an adult under the same conditions[25].

Therefore, the in utero and early post-natal periods (i.e. first two years of life) may be periods of heightened susceptibility to adverse health outcomes resulting from air pollution exposure due to the developing respiratory and immune systems, and the faster breathing rates of infants.

Respiratory and immune effects of early life PM2.5 exposure

Current literature on the respiratory and immune health outcomes resulting from early life ambient PM2.5 exposure have focussed on wheezing/asthma, lung function, respiratory mortality, respiratory symptoms (e.g. cough), allergy and infections. A few studies have suggested that early life immune responses, that shape conditions such as lower respiratory infections, are associated with reduced lung function and increased risk of asthma development during childhood[26-28]. Early life allergic sensitisation to mold could also increase the risk of childhood asthma[28]. There are limited, but increasing, studies investigating the associations between PM2.5 exposure during in utero or the first two years of life and respiratory and immune health.




 Cohort identification

 The cohort comprised all 1999 and 2000 births in southwestern British Columbia (BC) identified by linking administrative data sets from the BC Ministry of Health Services, the BC Vital Statistics Agency, and the BC Perinatal Database Registry (described by Brauer et al. 2008b). The study region includes the metropolitan centers of Vancouver (population 2,250,000) and Victoria (population 325,000) as well as the surrounding areas within the same airshed. To be eligible, children and their mothers had to be registered for the provincial medical plan (because registration is mandatory for provincial residents under a universal health care system, the entire resident population is effectively included) and reside in the study area for the duration of pregnancy and the first year of life. Children were excluded for low birth weight (< 2,500 g), preterm birth (< 37 weeks of gestation), or multiple births, given that these conditions are known strong risk factors for development of chronic respiratory conditions.

In addition, these factors may confound the association between air pollution and asthma; low birth weight and gestational period have been found to be associated with both asthma and air pollution exposure in this cohort (Brauer et al. 2008b), as well as in other studies (Bobak 2000; Dik et al. 2004; Salam et al. 2005; Wang and Pinkerton 2007). Because low birth weight and gestational period may also act in the causal pathway between air pollution and lung effects, this exclusion may also bias the results to the null.

We used a nested case–control design to examine the association of air pollutants and incident asthma. Each asthma case was randomly matched to five controls from the birth cohort by sex and age (month and year of birth).

Chapter four


 Study cohort description

BC Vital Statistics data identified 59,917 births in the region in 1999 and 2000. Of these, 41,565 (69.4%)  children met the inclusion criteria of living in the study area during gestation and the first year of life and having complete medical plan registration through to 2003. We excluded 2,967 births because of low birth weight or preterm birth, 216 for multiple births, and 981 because of missing covariate information. Thus, we included 37,401 children (90%) in the final cohort from which we drew cases and controls. We excluded additional subjects for specific analyses where exposure information was not available.

A total of 3,482 children (9.3%) met the case definition for asthma and were included in the nested case–control analysis. Table 1 provides covariate information for the whole birth cohort, stratified by asthma status. Children meeting the case definition of asthma differed from the rest of the birth cohort for certain covariates: They tended to be born to mothers of younger age, lower education and income.

Chapter Five

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 0to 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.


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.


  • Allen RW, Mar T, Koenig J, Liu LJ, Gould T, Simpson C, et al. 2008. Changes in lung function and airway inflammation among asthmatic children residing in a woodsmokeimpacted urban area. Inhal Toxicol 20(4):423–433.
  • Asher MI, Montefort S, Bjorksten B, Lai CKW, Strachan DP, Weiland SK, et al. 2006. Worldwide time trends in the prevalence of symptoms of asthma, allergic rhinoconjunctivitis, and eczema in childhood: ISAAC phases one and three repeat multicountry cross-sectional surveys. Lancet 368(9537):733–743.
  • Bobak M. 2000. Outdoor air pollution, low birth weight, and prematurity. Environ Health Perspect 108:173–176.
  • Brauer M, Ainslie B, Buzzelli M, Henderson S, Larson T, Marshall J, et al. 2008a. Models of exposure for use in epidemiological studies of air pollution health impacts. In: Air Pollution Modelling and Its Application XIX (Borrego C, Miranda AI, eds). New York:Springer, 589–604.
  • Brauer M, Hoek G, Smit HA, de Jongste JC, Gerritsen J, Postma DS, et al. 2007. Air pollution and development of asthma, allergy and infections in a birth cohort. Eur Respir J 29(5):879–888.
  • Brauer M, Hoek G, Van Vliet P, Meliefste K, Fischer PH, Wijga A, et al. 2002. Air pollution from traffic and the development of respiratory infections and asthmatic and allergic symptoms in children. Am J Resp Crit Care Med 166(8):1092–1098.
  • Brauer M, Hoek G, van Vliet P, Meliefste K, Fischer P, Gehring U, et al. 2003. Estimating long-term average particulate air pollution concentrations: application of traffic indicators and geographic information systems. Epidemiology 14(2):228–239.
  • Brauer M, Lencar C, Tamburic L, Koehoorn M, Demers P, Karr C. 2008b. A cohort study of traffic-related air pollution impacts on birth outcomes. Environ Health Perspect 116:680–686.
WeCreativez WhatsApp Support
Our customer support team is here to answer your questions. Ask us anything!