Impact of Air Pollution in Children With Wheezing or Asthma
The results of the present study demonstrate that exposure to traffic-related air pollution is associated with an increased risk of respiratory morbidity in children with pre-exisiting asthma or lower respiratory tract disease with wheezing. Our findings are consistent with the results of a recent prospective study in Sweden in which 4,089 children followed from birth to the age of 12 years showed a positive association between exposure to air pollution (PM10 and NO2) during early years of life and asthma exacerbations. Additionally, the association between exposure to particulates and persistent wheezing during infancy was confirmed in the Cincinnati birth cohort study of more than 700 infants born to atopic parents. Furthermore, a cross-sectional study conducted in China of more than 3,000 schoolchildren documented that long-term exposure to high air pollution concentrations was associated with reduction in lung function and that asthmatic children were more susceptible to this effect.
The finding that episodes of bronchial obstruction related to air pollution due to traffic occurs almost exclusively in children born to atopic parents or in children who have been previously diagnosed with wheezing or asthma could be clinically relevant because it could permit the early identification of subjects living in areas with traffic-related air pollution who have an increased risk for the development of respiratory problems later in life. However, this conclusion should be considered with caution for several reasons. Most of the data that lead to this conclusion, such as those regarding home environment and the risk of pollution exposure, were reported by the parents and, consequently, had debatable reliability. Moreover, to be born to atopic parents does not mean that a child is himself atopic and that has an increased risk of development of bronchial hyperresponsiveness. The analysis of the characteristics of the enrolled children revealed that the two groups of subjects were substantially different from a socio-economic point of view. The asthma cohort had parents with lower level of education and lived in less elaborate homes because smaller and more frequently not air conditioned. A number of studies has reported that socio-economic status could condition response to air pollution with the adverse effects greater in individuals in lower social classes. Consequently, it is possible that, at least in part, the results of this study could be due to the difference in socio-economic status of patients in comparison to healthy controls.
Moreover, the period of study was relatively short and it cannot be excluded that a longer study duration could have led to different results.. It has been reported that children with long-term exposure to traffic-related air pollution can develop respiratory disease after several years. Consequently, some of the healthy children included in the present study, particularly the youngest, could have developed bronchial obstruction after the study was concluded. Moreover, the genetic characteristics of the enrolled children, which differ from those that lead to atopy and were not considered in this study, could have reduced or increased susceptibility of the children to wheezing or asthma independently of traffic-related pollutants. The close relationship between genetic variants and increased susceptibility to bronchial obstruction has been repeatedly reported.
In the present study, the risk of developing wheezing or asthma was strictly related to the degree of exposure to traffic-related air pollutants, with fewer incidences occurring in children living in a green area compared with those living in areas with the highest degree of air pollution. This finding is consistent with the results of several studies showing greater evidence of an association between traffic-related air pollutants and respiratory problems in children living near roads with heavy traffic with a higher incidence of exacerbations with increasing concentrations of pollutants.
In this study a close association between paternal smoking during pregnancy, prematurity, respiratory and cardiac diseases at birth with recurrent wheezing or asthma was found, in agreement with previous reports. We did not find any significant differences between the two groups with respect to the duration of breastfeeding, in contrast to the results of some studies showing a protective role of human milk in the development of asthma and consistent with research that failed to demonstrate any long-term protection. In our study, children with recurrent wheezing or asthma had greater exposure than healthy controls to passive smoke in their homes. It is surprising and unfortunate that despite the well-known negative effects of passive smoke on recurrent or chronic respiratory disease, children with recurrent wheezing or asthma continued to be exposed to this risk factor. We did not detect any differences between children with recurrent wheezing or asthma with respect to the presence of domestic pets, particularly cats and dogs. This result appeared to exclude an effect of pet ownership on respiratory symptoms and was consistent with some previous findings. However, it has been reported that exposure to cats during the first year of life is an independent risk factor for wheezing and asthma at the age of 7 years.
In the present study, traffic-related pollutants appeared to play a relevant role in conditioning the incidence of respiratory infections. Children with atopy or recurrent wheezing or asthma presented more respiratory tract infections including pneumonia compared with control subjects. These findings are not surprising as patients with asthma are more susceptible to recurrent viral respiratory infections. Allergic inflammation in the airways leads to an impaired barrier function that facilitates the penetration of infectious particulate allergens, favoring the development of inflammatory responses and impaired interferon responses to viral infection in asthmatic children irrespective of their atopic status. However, in the current study, in children with recurrent wheezing or asthma but not in healthy controls, pneumonia events appeared to be related to the concentrations of PM10 and NO2, clearly supporting the hypothesis that traffic-related air pollution increases the risk of respiratory infections. However, other studies have demonstrated an association between exposure to common air pollutants and susceptibility as well as severity of respiratory infections. In a recent meta-analysis, Dherani et al. documented that the risk of pneumonia nearly doubled in young children exposed to unprocessed solid fuels. Gurley et al. showed that each hour of exposure to PM2.5 concentrations exceeding 100 μg/m was associated with a 7% increase in the incidence of acute lower respiratory infections among children aged 0–11 months. Finally, a study conducted in 33,632 Italian children (aged 6–7 years) and adolescents showed that children living in polluted areas had a great risk of cough or phlegm, whereas traffic pollution was weakly associated with asthmatic symptoms. To the best of our knowledge, the present study is the first to demonstrate that the effects of air pollution on the occurrence of respiratory tract infections are observed only in children with recurrent wheezing or asthma. This finding might be explained by an increase in pollution-induced airway inflammation, genetic susceptibility to oxidative stress and the role of epigenetics in lung damage induced by air pollutants.
A further limitation of the present study is that children suffering from recurrent wheezing and asthma were considered in the same group. The former is not a homogeneous disease, and only a few phenotypes of wheezing can be considered as asthma before the school age. Limiting the analysis to older children would permit a more reliable diagnosis of asthma but would exclude the younger age group in which exposure to air pollution is known to be associated with an increased risk of subsequent asthma onset. Moreover, respiratory diseases were assessed based on a parental questionnaire, which could have been influenced by a number of subjective issues. We tried to limit the bias in responses with weekly telephone calls by medical practitioners. A final limitation is that we focused on traffic pollution in the zone of residence but did not collect information about other outdoor exposures such as those near schools.
Discussion
The results of the present study demonstrate that exposure to traffic-related air pollution is associated with an increased risk of respiratory morbidity in children with pre-exisiting asthma or lower respiratory tract disease with wheezing. Our findings are consistent with the results of a recent prospective study in Sweden in which 4,089 children followed from birth to the age of 12 years showed a positive association between exposure to air pollution (PM10 and NO2) during early years of life and asthma exacerbations. Additionally, the association between exposure to particulates and persistent wheezing during infancy was confirmed in the Cincinnati birth cohort study of more than 700 infants born to atopic parents. Furthermore, a cross-sectional study conducted in China of more than 3,000 schoolchildren documented that long-term exposure to high air pollution concentrations was associated with reduction in lung function and that asthmatic children were more susceptible to this effect.
The finding that episodes of bronchial obstruction related to air pollution due to traffic occurs almost exclusively in children born to atopic parents or in children who have been previously diagnosed with wheezing or asthma could be clinically relevant because it could permit the early identification of subjects living in areas with traffic-related air pollution who have an increased risk for the development of respiratory problems later in life. However, this conclusion should be considered with caution for several reasons. Most of the data that lead to this conclusion, such as those regarding home environment and the risk of pollution exposure, were reported by the parents and, consequently, had debatable reliability. Moreover, to be born to atopic parents does not mean that a child is himself atopic and that has an increased risk of development of bronchial hyperresponsiveness. The analysis of the characteristics of the enrolled children revealed that the two groups of subjects were substantially different from a socio-economic point of view. The asthma cohort had parents with lower level of education and lived in less elaborate homes because smaller and more frequently not air conditioned. A number of studies has reported that socio-economic status could condition response to air pollution with the adverse effects greater in individuals in lower social classes. Consequently, it is possible that, at least in part, the results of this study could be due to the difference in socio-economic status of patients in comparison to healthy controls.
Moreover, the period of study was relatively short and it cannot be excluded that a longer study duration could have led to different results.. It has been reported that children with long-term exposure to traffic-related air pollution can develop respiratory disease after several years. Consequently, some of the healthy children included in the present study, particularly the youngest, could have developed bronchial obstruction after the study was concluded. Moreover, the genetic characteristics of the enrolled children, which differ from those that lead to atopy and were not considered in this study, could have reduced or increased susceptibility of the children to wheezing or asthma independently of traffic-related pollutants. The close relationship between genetic variants and increased susceptibility to bronchial obstruction has been repeatedly reported.
In the present study, the risk of developing wheezing or asthma was strictly related to the degree of exposure to traffic-related air pollutants, with fewer incidences occurring in children living in a green area compared with those living in areas with the highest degree of air pollution. This finding is consistent with the results of several studies showing greater evidence of an association between traffic-related air pollutants and respiratory problems in children living near roads with heavy traffic with a higher incidence of exacerbations with increasing concentrations of pollutants.
In this study a close association between paternal smoking during pregnancy, prematurity, respiratory and cardiac diseases at birth with recurrent wheezing or asthma was found, in agreement with previous reports. We did not find any significant differences between the two groups with respect to the duration of breastfeeding, in contrast to the results of some studies showing a protective role of human milk in the development of asthma and consistent with research that failed to demonstrate any long-term protection. In our study, children with recurrent wheezing or asthma had greater exposure than healthy controls to passive smoke in their homes. It is surprising and unfortunate that despite the well-known negative effects of passive smoke on recurrent or chronic respiratory disease, children with recurrent wheezing or asthma continued to be exposed to this risk factor. We did not detect any differences between children with recurrent wheezing or asthma with respect to the presence of domestic pets, particularly cats and dogs. This result appeared to exclude an effect of pet ownership on respiratory symptoms and was consistent with some previous findings. However, it has been reported that exposure to cats during the first year of life is an independent risk factor for wheezing and asthma at the age of 7 years.
In the present study, traffic-related pollutants appeared to play a relevant role in conditioning the incidence of respiratory infections. Children with atopy or recurrent wheezing or asthma presented more respiratory tract infections including pneumonia compared with control subjects. These findings are not surprising as patients with asthma are more susceptible to recurrent viral respiratory infections. Allergic inflammation in the airways leads to an impaired barrier function that facilitates the penetration of infectious particulate allergens, favoring the development of inflammatory responses and impaired interferon responses to viral infection in asthmatic children irrespective of their atopic status. However, in the current study, in children with recurrent wheezing or asthma but not in healthy controls, pneumonia events appeared to be related to the concentrations of PM10 and NO2, clearly supporting the hypothesis that traffic-related air pollution increases the risk of respiratory infections. However, other studies have demonstrated an association between exposure to common air pollutants and susceptibility as well as severity of respiratory infections. In a recent meta-analysis, Dherani et al. documented that the risk of pneumonia nearly doubled in young children exposed to unprocessed solid fuels. Gurley et al. showed that each hour of exposure to PM2.5 concentrations exceeding 100 μg/m was associated with a 7% increase in the incidence of acute lower respiratory infections among children aged 0–11 months. Finally, a study conducted in 33,632 Italian children (aged 6–7 years) and adolescents showed that children living in polluted areas had a great risk of cough or phlegm, whereas traffic pollution was weakly associated with asthmatic symptoms. To the best of our knowledge, the present study is the first to demonstrate that the effects of air pollution on the occurrence of respiratory tract infections are observed only in children with recurrent wheezing or asthma. This finding might be explained by an increase in pollution-induced airway inflammation, genetic susceptibility to oxidative stress and the role of epigenetics in lung damage induced by air pollutants.
A further limitation of the present study is that children suffering from recurrent wheezing and asthma were considered in the same group. The former is not a homogeneous disease, and only a few phenotypes of wheezing can be considered as asthma before the school age. Limiting the analysis to older children would permit a more reliable diagnosis of asthma but would exclude the younger age group in which exposure to air pollution is known to be associated with an increased risk of subsequent asthma onset. Moreover, respiratory diseases were assessed based on a parental questionnaire, which could have been influenced by a number of subjective issues. We tried to limit the bias in responses with weekly telephone calls by medical practitioners. A final limitation is that we focused on traffic pollution in the zone of residence but did not collect information about other outdoor exposures such as those near schools.
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