• air pollution;
  • bronchial asthma;
  • airway hyperresponsiveness;
  • hay fever;
  • pollinosis;
  • respiratory allergy;
  • urban pollution


  1. Top of page
  2. Abstract
  3. Introduction
  4. Urban air pollutants
  5. Pollen allergy in urban areas
  6. References

Respiratory allergic diseases such as rhinitis and bronchial asthma appear to be increasing worldwide, affecting in particular subjects living in urban areas, and the reasons for this increase are still largely unknown. Although the role played by air pollution has yet to be clarified, a body of evidence suggests that urbanization, with its high levels of vehicle emissions and a westernised lifestyle are linked to the rising frequency of these diseases observed in most industrialized countries. Laboratory studies confirm the epidemiological evidence that inhalation of some pollutants, either individually or in combination, adversely affect lung function in asthmatics. Air pollutants may not only increase the frequency and intensity of symptoms in already allergic patients but may promote airway sensitization to airborne allergens in predisposed subjects. By attaching to the surface of pollen grains and of plant-derived paucimicronic particles, pollutants can modify the morphology of these antigen-carrying agents and alter their allergenic potential. In addition, by inducing airway inflammation, pollutants may overcome the mucosal barrier and so ‘prime’ allergen-induced responses. In other words airway mucosal damage and impaired mucociliary clearance induced by air pollution may facilitate the access of inhaled allergens to the cells of the immune system.


  1. Top of page
  2. Abstract
  3. Introduction
  4. Urban air pollutants
  5. Pollen allergy in urban areas
  6. References

Respiratory allergic diseases such as rhinits and bronchial asthma are increasing in both prevalence and severity in most industrialized countries (1–13) and subjects living in urban areas are more likely to experience allergic respiratory symptoms than subjects living in rural areas. A number of factors is likely to be important in the increasing prevalence of respiratory allergy and these factors include changes in childhood infections, the sealing up of homes, the food ingested, a lack of physical exercise and airborne materials. Two factors are required for the onset of allergic diseases: sensitizing agents and genetically committed individuals, and various studies suggest that air pollution contributes to the facilitation of allergic sensitization of the airway in predisposed subjects and to the exacerbation of symptoms in already allergic subjects (2, 3, 7, 13–16). In particular it appears that the increase in allergic respiratory disease is paralleled by increasing atmospheric concentration of such pollutants as gases and respirable particulate matter. However, despite evidence of a correlation between the increasing frequency of respiratory allergy and the increasing trend in air pollution, the interrelationship between these two factors is still speculative, since interpretation of studies is confounded by the effect of cigarette smoke, exposure to indoor pollutants and to aeroallergens.

Urban air pollutants

  1. Top of page
  2. Abstract
  3. Introduction
  4. Urban air pollutants
  5. Pollen allergy in urban areas
  6. References

There is evidence that living near roads with high levels of car traffic is associated with impaired respiratory health, since road traffic with its gaseous and particulate emissions is currently, and is likely to remain, the main contributor to air pollution in most urban settings.

Epidemiological and laboratory studies have shown that many common air pollutants are able to induce airway inflammation and airway hyperresponsiveness. A large number of epidemiological studies has been published documenting respiratory effects of major air pollutants (2–5, 9–12). However, because the exposure is always to mixture of pollutants, epidemiological studies may not be able to define the causal agent in the mix. In other words, although it is plausible that ambient air pollution might play a role in the onset and increasing prevalence of asthma and other allergic, respiratory diseases, including pollen allergy, it is difficult to demonstrate that this happens at a public level (13–16).

Although the nature and concentration of outdoor pollutants vary from place to place, the most abundant in the atmosphere of urban areas are respirable particulate matter (PM), NO2 and ozone. In general, the effects of air pollutants on lung function depends on the environmental concentration of the pollutant, the duration of exposure and the total ventilation of exposed persons.

NO2 exerts an oxidizing action that causes lung injury at high concentrations and toxicological studies have shown that NO2 reduces the efficacy of lung defence mechanisms against infection (2). However, the outdoor NO2 levels are not usually associated with notable changes in bronchial obstruction in asthmatic patients, unlike respirable PM, ozone and allergens, which play a significant role in causing lung function impairment in allergic subjects. Ozone is generated at ground level by photochemical reactions involving NO2, hydrocarbons and ultraviolet radiation. This water-insoluble gas is the main component of photochemical urban oxidants and may contribute up to 90% of the total oxidant levels in cities that enjoy a mild, sunny climate (2). The evidence for effects of ozone exposure on the lung function of normal volunteers and asthmatic subjects has raised concern about possible long-term effects of living in cities in the Mediterranean area, southern California and other locations where there is sustained photochemical pollution. Ozone can affect both the upper and lower respiratory tracts and epidemiological studies have demonstrated decrements in pulmonary function of both asthmatics and nonasthmatics associated with increased levels of ambient ozone. Hospital admissions are also increased following increases in ambient ozone (17). Exposure to ozone may increase the risk of sensitization to aeroallergens in predisposed subjects and may enhance the airway responsiveness of already sensitized subjects by lowering the threshold concentration of allergen able to induce the appearance of clinical symptoms (18, 19). Ozone induces inflammatory effects in upper and lower airways favoring the migration in nasal and bronchial mucosa of eosinophils, neutrophils, eosinophil peroxidase, myeloperoxidase, eosinophil cationic protein and other inflammatory mediators (20).

In the urban atmosphere the respirable PM, which derives prevalently from car exhaust emissions, also plays a significant role in causing lung function impairement. It is usually a mixture of solid and liquid particles that vary in size, composition and origin. Penetration of PM into the tracheobronchial tract is related to its size and to the efficiency of the airways defence mechanisms. Respirable PM could induce adverse effects on airways not only acting directly, inducing inflammation of the mucous membranes, but also acting as a carrier of other pollutants or allergens or by potentiating their effects. The latter effect could contribute to explain the increase of cases of sensitization to pollen allergens in urban areas.

As for the health effects of air pollution in subjects living in polluted urban areas, it has been found, both in US (11, 12) and in Europe (21) an association of daily concentrations of particulates and other components of urban air pollution (NO2 and SO2) and daily mortality. In this context Seaton et al. (22) hypothesized that fine particulate of urban areas, penetrating deep into airways, is able to induce alveolar inflammation which is responsible for variation in blood coagulability and release of mediators which induce acute episodes of respiratory and cardiovascular diseases.

A study from the Netherlands (7) demonstrated that children with atopy and bronchial hyperresponsiveness are at risk of increased symptoms during episodes of air pollution. The children with bronchial hyperresponsiveness and high levels of serum total IgE had an increase in respiratory symptoms up to 139% for every 100 µg/m3 increase in particulate matter. However, a potential confounding factor is the content of allergen in air during most of these episodes.

Pollen allergy in urban areas

  1. Top of page
  2. Abstract
  3. Introduction
  4. Urban air pollutants
  5. Pollen allergy in urban areas
  6. References

Aeroallergens derived from pollen grains, lead to bronchial obstruction in predisposed subjects and pollen allergy is a frequent model used to study the interrelationship between air pollution and respiratory allergy (13–16). In other words, biological aerosols such as pollen grains or other pollen allergen carrying particles can act as aerocontaminants and can induce symptoms in predisposed subjects (23–27). They may interact in atmosphere with airborne chemical contaminants and it has been suggested that air pollutants may promote airway sensitization by modulating the allergenicity of airborne allergens (14, 28). Climatic factors (wind speed, temperature, humidity) can affect biological and chemical components of this interaction.

There is also evidence that the airway mucosal damage and the impaired mucociliary clearance induced by air pollution may facilitate the access of inhaled allergens to the immune system (14).

Pollinosis patients can experience symptoms even out of the pollen season, when there is no presence of a relevant quantity of pollen grains and symptoms can be induced by the same pollen allergens carried by airborne particles, much smaller than pollen grains, deriving from allergenic plants (23–27). Some of these paucimicronic particles are plant debris, such as fragments of leaves and stems (27). However, during thunderstorms and after rupture by osmotic shock, pollen grains may release tiny starch granules of mean diameter less than 5 µm which can be responsible for epidemics of asthma attacks (27–30). Also aeroallergens released by pollen grains can be transferred to other small, nonbiological particles of air pollution such as those of the diesel exhaust particulate (DEP) acting as biological aerocontaminants of the inhaled air, which can penetrate deep into the airways inducing allergic symptoms in sensitized subjects (31).

The effects of DEP on IgE production have been studied both in vivo and in vitro (31–34). DEP exerts its effects by way of chemical agents, i.e. polyaromatic hydrocarbons and it has been observed that combined exhaust particulate and ragweed allergen challenge markedly enhances human in vivo nasal ragweed-specific IgE and skews cytokine production to a T-helper cell 2-type pattern (33). A pollutant such as DEP can influence the way a pollen, once inhaled, is processed. In particular, T-cell responses to aeroallergens may be skewed in a Th2 direction in the presence of pollutants such as DEP. In other words DEP increases in vivo IgE and cytokine production at the human respiratory mucosa, exacerbating allergic inflammation (32–34).

In this context the city of Naples provides a tool with which to study the interrelationship between urban air pollution and pollen-derived allergens due to its heavy urban traffic with a high production of photochemical smog and sunny days for most of the year. The climate also favors the pollination of Parietaria, which grows in abundance throughout the city (16, 35, 36); indeed, about 30% of Neapolitans are allergic to this plant and more than 50% of these Parietaria pollen-allergic subjects experience bronchial asthma and its equivalent, with high levels of bronchial hyperresponsiveness. We have observed that cases of pollen-induced respiratory disorders tend to increase when there is a parallel increase in the atmosphere of ozone, PM and Parietaria pollens. This parallel increase usually starts in February and reach its peak in June or July, after which the production and release of Parietaria pollen usually decreases while ozone and PM remain high into the autumn. In addition, Parietaria pollen and ozone reach their highest levels in morning. Parietaria peaks earlier than ozone because of the time required for the photochemical reaction to develop.

To test the hypothesis regarding the interaction between air pollution and allergens released by pollen grains, we examined in different tubes separately the effect of various polluting agents (gas from car powered by normal and catalysed petrol, diesel car and motorcycle) on the pollen of Parietaria and we have found, by using the RAST inhibition, that exhaust emissions from noncatalytic cars increased the allergenic potency of Parietaria pollen as compared with exhaust emissions from noncatalytic cars (16, 36).


  1. Top of page
  2. Abstract
  3. Introduction
  4. Urban air pollutants
  5. Pollen allergy in urban areas
  6. References
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