Air pollution
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.