Background
Authors | Year | Methods | Main conclusion |
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Nordling et al. [12] | 2007 | The spatial distribution of nitrogen oxides from traffic (traffic-NOx) and inhalable particulate matter from traffic (traffic-PM10) in the study area was assessed with emission databases and dispersion modeling. Estimated levels were used to assign first-year exposure levels for children in a prospective birth cohort (n = 4089), by linking to geocoded home addresses. Parents in 4 Swedish municipalities provided questionnaire data on symptoms and exposures when the children were 2 months and 1, 2, and 4-year-old. At 4 years, 73% of the children underwent clinical examination including peak expiratory flow and specific IgE measurements. | Exposure to traffic pollution in early childhood is associated with an excess risk of persistent wheezing and sensitisation to inhaled allergens at the age of four years. |
Brauer et al. [13] | 2008 | The development of asthmatic/allergic symptoms and respiratory infections during the first 4 yrs of life was assessed in a birth cohort study (n = approximately 4,000). Outdoor concentrations of traffic-related air pollutants were assigned to birthplace home addresses with a land-use regression model. They were linked by logistic regression to questionnaire data on doctor-diagnosed asthma, bronchitis, influenza and eczema and to self-reported wheeze, dry night-time cough, ear/nose/throat infections and skin rash. | Air pollution exposure in early childhood is associated with sensitisation to food allergens and respiratory symptoms at the age of four years. |
Gehring et al. [14] | 2009 | Annual questionnaire reports of asthma, hay fever, and related symptoms during the first 8 years of life were analyzed for 3,863 children. At age 8, measurements of allergic sensitization and bronchial hyperresponsiveness were performed for subpopulations (n = 1,700 and 936, respectively). Individual exposures to NO2, PM2.5, and soot at the birth address were estimated by land-use regression models. Associations between exposure to traffic-related air pollution and repeated measures of health outcomes were assessed by repeated-measures logistic regression analysis. | Exposure to traffic-related air pollution seems to cause asthma in children monitored from birth to eight years of age. |
Gruzieva et al. [15] | 2013 | The Swedish birth cohort BAMSE (Children, Allergy, Milieu, Stockholm, Epidemiological Survey) includes 4,089 children who were followed up with repeated questionnaires and blood samples for up to 12 years of age. Residential, daycare, and school addresses, time-activity patterns, emission databases, and dispersion models were used to estimate individual exposure to PM10 and NOx from traffic. | There is a moderate positive association between exposure to traffic-related air pollution in infancy and asthma in children aged up to 12 years, which is possibly stronger in the case of non-allergic asthma. |
Review
Pollution-induced airway inflammation
Authors | Year | Methods | Main conclusion |
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Becker et al. [37] | 2002 | Stimulation of interleukin-8 release from normal human airway epithelial cells with coarse PM2.5-10, fine PM2.5, and ultrafine particle fractions has shown that the coarse particle fraction has the greatest effect on the epithelial cells as well as alveolar macrophages. Since this fraction concentrates fugitive dusts and particle-associated microbial matter, it was hypothesized that epithelial cells may recognize PM through microbial pattern recognition receptors TLR2 and TLR4, as has been previously shown with alveolar macrophages. | Microbial components and TLRs are important players in alveolar macrophage-dependent inflammatory responses to PM. |
Becker et al. [38] | 2004 | The hypothesis behind the present study was that not only particle-bound LPS, but also Gram-negative and Gram-positive bacteria are responsible for PM-induced stimulation of alveolar macrophage, and therefore that PM are likely to activate receptors involved in recognition of microbes. | Both airway epithelial cells and macrophages involve TLRs in recognising the molecules present in PM; epithelial cells use TLR2 and TLR4. |
Hollingsworth et al. [40] | 2007 | Because ozone also alters clearance of pulmonary bacterial pathogens, the authors hypothesized that inhalation of ozone modifies innate immunity in the lung. To address our hypothesis, they exposed C57BL/6 J mice to either free air or ozone, and then subsequently challenged with an aerosol of Escherichia coli LPS. | Ozone exposure increases the pulmonary and systemic biological responses to inhaled LPS by priming the innate immune system. |
Williams et al. [41] | 2007 | The authors investigated the sensing of ozone by TLR2, TLR4, and MyD88. Moreover, they evaluated the expression of inflammatory cytokines and TLR2, TLR4, and MyD88 in these mice. | TLR2- and TLR4-mediated inflammation induced by oxidative stress and the adapter protein MyD88, but not by TLR2 or TLR4, is important in mediating ozone-induced neutrophilia. |