Health effects of air pollution

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Health effects of air pollution

Dra. Patricia Matus Correa

There is great evidence linking outdoor air pollution with mortality and morbidity in the general population (1-7). The public health damage is consistent and shows its adverse effects in urban areas both in developed and developing countries (7).The range of adverse health effects is broad affecting both the respiratory and the cardiovascular system, and young children and older adults were the most susceptible in the general population (7). The risk increases with intensity of exposure. Little information supports the presence of a threshold level for these effects. In fact, effects were found at low levels not much higher than 3 to 5 µg/m3 the U.S. background concentrations. The adverse health effects of air pollution are observed in short-term exposures and also for long time exposures (8-9).

The World Health Organization conducted a study of burden of disease caused by environmental problems attributed to air pollution effects on respiratory diseases, perinatal conditions and birth defects, cancer, cardiovascular diseases, bronchial obstructive disease and asthma. Pruss-Ustun and Corvalan (2006) estimated that in developing countries by 42% (95% CI 32-47) of all respiratory diseases are attributable to air pollution.

Respiratory effects of air pollution have been described mainly for particulate matter and ozone. However, other pollutants such as nitrogen oxides have also been associated with respiratory diseases, mainly in children under 1 year (11). The mechanisms involved in these effects are primarily irritation and inflammation of the airways (12). Studies have shown that particles can trigger inflammation of small airways (diameter <2 mm), which may cause exacerbation of asthma or obstructive bronchitis, airway obstruction and decreased gas exchange (13). Air pollutants such as nitrogen oxides, can also enhance the inflammatory reaction of the airway to allergens in asthmatics (14). The particles can also interfere with the mechanisms of cleansing and destruction of bacteria in lung tissue and this is a very important mechanism to link air pollution to respiratory infections (15).

Pinkerton et al (16) studied the lungs of residents of Fresno (Central Valley) have reported wall thickening and remodeling of the terminal bronchioles, associated with increased collagen, inflammatory cells and interstitial macrophages loaded with particulate matter. These changes were significantly more marked in the first generation of the terminal bronchioles, suggesting that the accumulation of coal and mineral dust in the lung, mainly affects the central acinar zone of the lung.

To live in area with high levels of particulate matter in air produces pulmonary retention of a large numbers of particles, some of which appear to be products of combustion. This was detected by comparing lungs of Mexico City residents with Vancouver residents whose were exposed to an average of 66 and 14 µg/m3 of PM10 in 3 years. Moreover Churg and Brauer have reported that in lung tissue of autopsied human particles is retained providing evidence on the role of PM2.5 (18).

Exposure to complex mixtures of air pollutants, mainly particulate matter and ozone causes lung structural changes that are induced by sustained inflammation, leading to vascular remodeling in the airways of the lung and impaired repair process. It has been suggested that ozone can increase the toxicity of inhaled particles or vice versa, since there were more lung damage in rats, both agents harmful to inhale a whole than separately administered (19). This observation is supported by the study of Vincent et al (20) who exposed rats for 4 hours by inhalation to 0.8 ppm ozone exposure by linking this urban particulate matter. In this study, the effects of O3 (altered epithelial terminal bronchioles and alveolar ducts and increased DNA synthesis) were clearly enhanced by the co-exposure to urban particulate matter. Moreover, it is reported that both urban particulate matter, like particles released from diesel and carbon black, are able to cause mutagenesis by DNA damage in type II alveolar cells in culture (cell line A549) (21).

The mechanisms of damage induced by exposure to air pollutants have been the subject of many studies in order to establish a criterion of biological plausibility, to offer support and substantiate the need for measures to control pollution.

The inflammatory mechanism plays an important role in the exacerbation of respiratory diseases promoted by exposure to respirable particles. It has been suggested that on the surface of the particles produced a series of physical-chemical reactions that cause intracellular oxidative stress. Due to the large contact area between particles and pneumocytes (lungs cells) would be a release of inflammatory mediators in the lung, which would trigger the recruitment of inflammatory cells with a heightened response leading to functional and structural damage in the process of ventilation lung.

Mechanisms of lung injury have been proposed. The sequence of events would begin with the activation of the cascade of inflammation, which may explain the molecular events that lead to transcription of pro-inflammatory genes. The respirable particles cause oxidative stress in cells with the generation of lipid peroxidation products such as hydroxynonenal 4 and oxidized glutathione (GSSG). This change in intracellular redox balance, would cause the acetylation of histones and DNA breakdown, encouraging the promotion of mechanisms of gene transcription. Oxidative stress also directly induces the production of NF-kB factor, allowing transcription of pro-inflammatory genes (TNF, IL-8, IL-2, IL-6, GM-CSF, ICAM-1). Furthermore, oxidative stress and / or direct interaction with the particles induce increased concentrations of calcium (Ca +2), which in turn may stimulate the production of NF-kB, with subsequent increased release of pro-inflammatory substances (22).

Studies also suggest that immunological mechanisms may explain the effects of diesel particulate emissions on asthma. The mechanisms of direct damage to the immune system would include increased production of IgE and IgG immunoglobulin, modulating the expression of cytokines with increased levels of interleukins and chemokines. Phenomena that induce the migration of other cell types primarily of eosinophils that are mediators of chronic bronchial inflammation, prolonged contraction of peribronchial muscles, increased bronchial hyper responsiveness and bronchial mucosal damage, clinically relevant aspects bronchial asthma (23).

Children are particularly vulnerable to respiratory problems because of their physical characteristics and behaviour. At this stage of life the lung has not reached its full development: there is less collateral ventilation and airway resistance of small accounts for 50% of the total resistance to airflow (24). Most of the alveoli (80%) develop in the postnatal period. This occurs because a smaller volume and lower pulmonary alveolar surface, so that equal exposure to adults, enter higher dose to the body. The airways continue to develop in childhood. This implies that peripheral airway (<2 mm diameter) for 50% of the airflow resistance, while in adults only corresponds to less than 20%. The absence of collateral ventilation, i.e. presence of pores of Kohn and channels of Lambert, in children, aggravated obstruction of peripheral airways. Children breathe more often and do more physical exercise than adults; this increases the effective dose of air pollutants that captures the lung. In addition, children have less developed respiratory muscles, and cough less effective in cleaning the central airways. Lung defence mechanisms are not fully developed, causing greater difficulty in removing particles reaching the airways. Finally, children spend more time outdoors than adults, so that exposure to air pollutants is greatest. All this makes it more vulnerable to air pollution than adults (25). So the burden of environmental pollution on respiratory health of children is higher, especially in developing countries where coexist several other insults such as indoor air pollution and malnutrition. Hence the importance of establishing monitoring programs and special attention as are the strategies developed within the framework of environmental pediatrics.

In children under 5 years has been estimated globally that acute lower respiratory infections (pneumonia, bronchiolitis and bronchitis) are responsible for about 20% of the 10.6 million deaths annually worldwide. About 90% of these deaths are due to pneumonia (26).

In the last decade some studies also show that both particulate matter and ozone, are increasing the risk of cardiovascular disease (Tsai S. et al, 2003; Kan H. et al, 2003; Hong Y. et al, 2002; Tamagawa E. and Van Eaden, S., 2006 R. Maheswaran et al, 2005; Henrotin J. et al, 2007). An analysis of daily mortality conducted in the 20 largest counties in the United States within the period 1987-1994, showed that there is a 0.68% increase in mortality due to cardiovascular and respiratory problems to an increase of 10 ug/m3 in the concentration of PM10 (Samet JM, 2000). A larger study conducted in 204 U.S. counties for 4 years and another study in the 5 largest cities in Europe indicate that hospital admissions for cardiovascular disease are positively associated with increased levels of air pollution (Dominici F, 2006 and von Kloto S, 2005).

The cardiovascular injury induced by air pollution results in significant changes in many cardiovascular indexes. Some of the effects (changes in the heart rate, or heart rate variability, blood pressure, vascular tone and blood coagulability) are developed in response to increased levels of ambient particles. At the same time a chronic exposure to increased concentration of particulate air pollutant accelerates the progression of atherosclerosis (Simkhovich, 2008).The evidence suggests that stroke mortality and hospital admissions should be higher in areas with elevated levels of outdoor air pollution because of the combined acute and chronic effects of air pollution on stroke risk (Maheswaran, 2005). A number of potential mechanisms could explain the association between air pollution and stroke. Fine particles air pollution provokes alveolar inflammation, causing the release of potential harmful cytokines, which results in elevated coagulability (Seaton, 1995) and this condition increases thrombotic activity in central and peripherical vascular system.


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