Air pollution
Direct effects
Air pollutants considered major risk factors for the development of allergic diseases are ground-level ozone, particulate matter (PM), carbon monoxide (CO), sulfur dioxide (SO2), and nitrogen dioxide (NO2).15, 16 CO, SO2, and NO2 are released from combustion of fossil fuels. Ground-level ozone is a secondary pollutant that is produced when nitrogen oxides and volatile organic compounds released from industrial sources react in the presence of sunlight.
PM with diameters ≤10µm or smaller (e.g. PM10 and PM2.5) can carry organic and inorganic components such as heavy metals and penetrate deeply into the respiratory tract and skin barrier. In a prospective birth cohort study of over 5,000 children during the first 6 years of life, strong positive associations were found between the distance to the nearest main road and asthmatic bronchitis, hay fever, eczema, and sensitization.17 An association between eczema and traffic-related pollutants was also found in children from small towns, where exposure to was much lower than in urban areas.18 Some studies speculate that ultrafine particles (UFPs) with diameter ≤ 100nm may have greater effects due to their increased capacity to penetrate the lung alveoli and cardiovascular system.19 A recent meta-analysis estimated that increases in UPFs per 10000 particles/cm3 were associated with 7%, 11%, and 5% increase in exacerbations, emergency department visits, and hospital admissions for asthma, respectively.20
A recent study estimated that exposure to ambient NO2may cause 4 million new cases of pediatric asthma per year, with over 60% occurring in urban areas.21 Norbäck et al. observed robust relationships between lifetime exposure to NO2 and allergic diseases including asthma, eczema, wheeze and rhinitis for children ages 3–6 years in China.22 Similar associations have been observed with SO2 and CO. A study by Penard–Morand et al. found that SO2 exposure significantly increases the prevalence of asthma in children.23 Similarly, Samoli et al. found an association between SO2 and PM10exposure and the number of pediatric asthma hospital admissions among children aged 0 to 14 years in Athens, Greece.24Several time-series studies in China reported positive associations between exposure to CO within a few days and the risk of hospital admission/mortality from asthma.25Another Korean study found that for children aged 6–7 years, the odds ratio (OR) for life-time allergic rhinitis was 1.10 per 100 ppb increase in CO concentration during the first year of life. In addition, the OR for current atopic dermatitis was 8.11 for every 1 ppb increase in the average CO concentration during the preceding 12 months.26 In the US, the risk for emergency department visits was estimated to increase by 0.8% for asthma or wheeze and 3.7% for bronchitis per IQR increase in the preceding 3-day average concentration of CO.27
Ozone in the stratosphere is protective as it shields living things from ultraviolet radiation from the sun. However, ground-level ozone, which forms just above the earth’s surface has been associated with adverse health effects. A birth cohort study in Canada reported that ozone exposure at birth was associated with the onset of asthma and allergic rhinitis during a follow-up at age 17.28 In France, a higher annual outdoor concentration of ozone was associated with increased total IgE levels.29 A study estimated that 7-day exposure to ozone was associated with significant increase in physician visits for atopic dermatitis, contact dermatitis and urticaria.30
The pathophysiological mechanisms by which air pollution mediates allergic disease are poorly understood; however, oxidative stress, enhanced sensitization to allergens, inflammatory and immunological responses, and epigenetic modifications have been suggested as possible mechanisms. 31-33 Exposure of human nasal epithelium cells to PM2.5 was found to decrease loss of barrier function, as determined by measures of transepithelial resistance, permeability, decreased expression of tight junction proteins, and production of proinflammatory cytokines, such as thymic stromal lymphopoietin (TSLP).34 A genome-wide DNA methylation study found that long-term ambient air pollution exposure impacts DNA methylation of a number of genes, some of which play a role in inflammatory responses.35 Short-term and long-term exposures to high levels of CO, NO2, and PM2.5 were associated with alterations in differentially methylated regions of Foxp3.36
Indirect effect on plants and ecosystemsThe effects of air pollution reported above on the increase in allergies are direct the immune system or barrier function in humans. However, there is also an indirect effect: air pollution as well as other effects of climate change affect pollen, plants and biodiversity per se. Air pollution (and climate change) affect not only plant growth, pollen and flower production, and duration of the whole pollen season but can also display more indirect health effects by increasing the amount of allergenic encoding transcripts and proteins of the pollen.37, 38 When ragweed plants were grown in climate chambers under controlled conditions and fumigated with enhanced levels of NO2, transcript levels of amb were up-regulated, indicating potentially higher allergenicity due to NO2.37 On exposure of ragweed to varying NO2 levels during the growing season, a significantly higher allergenicity for Amb a 1 was observed.38 Elevated CO2 levels and drought stress was also found to increase allergenic ragweed proteins (Amb a).39Therefore, under global change scenarios the allergenic potential of pollen is also expected to change. Epidemiologic studies have demonstrated that urbanization, high levels of vehicle emissions, and westernized lifestyle are correlated to an increase in the frequency of pollen-induced respiratory allergy prevalent in people who live in urban areas compared to those who live in rural areas – this can in part be due to the effects of pollution on the pollen and plants themselves and therefore indirectly impacting human health.