|Year : 2018 | Volume
| Issue : 1 | Page : 1-3
Air Pollution and Lungs
Internal and Critical Care Medicine, Chittaranjan Advanced Medical Referral Institute, Burdwan, West Bengal, India
|Date of Web Publication||3-Jan-2018|
2 No Ichlabad, Sripally, Barabenepara, Burdwan 713103, West Bengal
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Maji A. Air Pollution and Lungs. J Assoc Chest Physicians 2018;6:1-3
Air pollution first received recognition as an urban problem in England in the 9th century, when coal was discovered, and complaints about foul air began to be heard. The possible menace to human health was recognized in the 17th century by John Evelyn, who dared to ascribe chronic respiratory ailments to the inhalation of coal smoke.
A moderately active adult inhales about 20 m3 of air daily, of varying quality, and weighing more than 24 kg. The respiratory tract itself is protected by various mechanisms. The nose, acting as a coarse pre-filter, traps relatively large particles (>5 μm) and the epithelial lining acts as a filtration mechanism to trap smaller (>3–5 μm) inhaled particles which are then moved out of the airways by the mucociliary process. The layer of mucus within the respiratory bronchioles traps very small particles, and the alveolar fluid also affords a medium, where particles are engulfed and destroyed by macrophages. The coughing and sneezing reflexes both act as protective mechanisms, as well as efficient systems for rapidly cleansing the respiratory tract from relatively large particulate matter (PM). In clinical terms, exposure to polluted air impacts negatively on lung health by causing respiratory symptoms, principally coughing, breathlessness, and chest tightness. It is also a major factor in exacerbating existing respiratory diseases and may also be the potential cause of lung disorders. Children, the elderly and persons with pre-existing cardiovascular disease, respiratory problems, and diabetes mellitus appear to be at a greater risk to develop complications related to air pollution.,
In general context, aerosol particles and to a lesser extent ozone, are the pollutants that mostly compromise lung and cardiovascular health.
| Major Outdoor Air Pollutants|| |
PM, ozone, nitrogen oxides, carbon monoxide (CO), and sulfur dioxide (SO2).
| Particulate Matter|| |
Suspended dusts, pollen and sea spray are the commoner natural PM, while combustion of fossil fuels in vehicles and power-generating plants are the source of most of “man-made” or anthropogenic PM. Particles >10 μm rarely make it past the upper airways, whereas fine particles <2.5 μm can make it as far as the alveoli.
- PM10 particles with a diameter <10 μm.
- PM2.5 particles with a diameter <2.5 μm (fine particulates).
- PM0.1 particles with a diameter <0.1 μm (ultrafine particulates).
Fine particles deposit in distal airways and cause increased acute respiratory morbidity (pneumonia and asthma), increased mortality (from all causes), decreased lung growth and function.
| Ozone|| |
“Good” ozone occurs in the upper atmosphere. Ozone is a naturally occurring form of oxygen that provides a protective layer shielding the Earth from harmful ultraviolet radiation. “Bad” ozone occurs in the lower atmosphere. Ozone is the major component of urban smog and a potent respiratory irritant. One important fact about ozone is that it requires sunlight for its formation, so it tends to peak on hot summer afternoons from 3 to 5 pm. Ozone is formed by photochemical reaction of volatile organic compounds, NO2 + O2 [sources include motor vehicle exhaust and power plants, although natural sources (trees) can also contribute].
Ozone health effects:
- Powerful oxidant.
- Lung irritation and inflammation.
- Impaired pulmonary function.
- Eye, nose, and throat irritation.
Mechanisms of toxicity:
- Oxidant damage.
- Increased neutrophils and inflammatory cytokines (in bronchoalveolar lavage).
Chronic exposure associated with:
- Chronic lung disease.
- Mild pulmonary fibrosis.
- Small airway obstruction.
- Asthma exacerbation and clinic visits.
| Nitrogen Oxide|| |
It’s derived from power plants, motor vehicles, and natural sources (volcanoes, lightning, and bacteria). Most combustion processes produce nitrogen monoxide which through oxidation processes results in nitrogen dioxide (NO2). NO2 combines with oxygen in the presence of sunlight to form ozone. It causes emphysema in animals decrements in lung function, increased airway reactivity and increased susceptibility to infection.
| Carbon Monoxide|| |
It is produced from incomplete combustion of fuels, vehicle exhaust, industry, and fires. CO combines with hemoglobin in blood and reduces oxygen-carrying capacity. Children with anemia, heart disease or chronic lung disease, and fetuses are the high-risk population. Infants and children have an increased susceptibility to CO toxicity because of their higher metabolic rates.
| Sulfur Dioxide|| |
It is produced from combustion of sulfur-containing coal or oil industrial processes, smelting of sulfur-containing ores natural sources (volcanoes), and combines with water to form H2SO4 (acid aerosol and acid rain). SO2 gas is upper airway irritant primarily affects nasopharynx and proximal airways. Acid aerosol particles reach distal airways and causes bronchoconstriction, slowing of bronchial mucociliary clearance, and chronic bronchitis.
Several large epidemiological studies have documented a link between air pollution and lung cancer in nonsmokers. Recent evidence shows a clear relationship between concentrations of ambient PM2.5 over a 26-year period and mortality from lung cancer among persons who never smoked. Arsenic, chromium, nickel, polycyclic aeromatic hydrocarbon, and radon are carcinogens to lung. These cancers usually present during adulthood.
Moulds are an important pollutant of the outdoor air. Exposure to moulds can cause severe asthma morbidity and mortality. Daily increases in mould spore counts are associated with daily increases in hospital admissions for asthma. There may also be a synergistic effect between ozone and some mould spores. That is, the combined effects of exposure to ozone and mould spores are greater than the effects of either exposure alone.
Pollen is the male reproductive structure of flowering plants. Pollen exposure has long been recognized as a stimulant for symptoms of allergic disease, especially for allergic rhinitis (hay fever). There is an association between grass pollen counts and admissions of patients with asthma in Mexico City in both dry and wet seasons.
| Air Pollution and Obstructive Airway Diseases|| |
Air pollution is a recognized cause for destabilizing well-controlled asthma, and for exacerbating this inflammatory condition. This is especially so among children, who are more susceptible to air pollution than adults, even when levels of pollution are relatively low and within "acceptable" ranges., There is a clear relationship between ambient ozone concentrations and increased symptoms of asthma. Persons with asthma might be more sensitive to ozone, and may, therefore, develop respiratory symptoms either at lower concentrations of the gas, or with greater magnitude than persons, who do not have this condition. Exposure to traffic-related air pollution over a long period also increases the risk of hospitalization because of unstable asthma among older persons; however, children are probably at an even higher risk.
A large Danish cohort study suggests that exposure to high levels of air pollution in the long-term may itself contribute to the development of chronic obstructive pulmonary disease (COPD). Persons, who were exposed for more than 25 years, ran a 7% higher risk, while the impact of air pollution on persons, who also had asthma and diabetes was greater. The role of air pollution as a complicating factor in COPD as a preexisting lung condition is, however, not in any doubt, and the relationship has been well-defined.
| Indian Data|| |
A recent most study on ambient air quality, respiratory symptoms, and lung function of children in Delhi revealed:
- The prevalence of respiratory and associated symptoms was investigated in 11,628 children from 36 schools in Delhi and 4536 control children from two schools in Uttaranchal and 15 from rural West Bengal. The children were aged between 4 and 17 years, and 55% of them were 12–14 years old. Two-third of the children were boys, and one-third was girls.
- Upper respiratory symptoms namely sinusitis, running or stuffy nose, sneezing, sore throat, and common cold with fever were 1.8-times more (23.1% vs. 14.6%) prevalent in Delhi than in controls.
- Children in Delhi had two-times more (17 % vs. 8%) lower respiratory symptoms such as frequent dry cough, sputum-producing cough, wheezing breath, breathlessness on exertion, chest pain or tightness, and disturbed sleep due to breathing problems.
- Prevalence of current asthma was present in 4.6% children of Delhi against 2.5% of controls. Similarly, the instance of physician-diagnosed asthma was two times more in Delhi (1.7% vs. 0.9%). The difference in asthma prevalence between control and Delhi’s school children was significant (P < 0.001).
| Conclusion|| |
Lung function and structure may be compromised by repeated exposure to contaminated air. Exposures to both PM and ozone have a negative impact on lung. Air pollution frequently causes exacerbation and deterioration of both asthma and COPD, and may be a potential cause for lung cancer.
Hence lung health is varying from minor discomfort to serious disability. Control of airborne pollution requires effective health education and preventive strategies, through combined community, administrative, and political approaches.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Miller GT. Living in the Environment: An Introduction to Environmental Science. Wadsworth Publishers; 1998.
Perez L, Rapp R, Künzli N. The year of the lung: Outdoor air pollution and lung health. Swiss Med Wkly 2010;140:w13129.
Brook RD, Franklin B, Cascio W, Hong Y, Howard G, Kipsett M et al.
American Heart Association scientific statement: Air pollution and cardiovascular disease. Circulation 2004;109:2655-71.
European Environment Agency. Air Quality in Europe − 2011 Report. EEA Technical Report 12/2011. Copenhagen: EEA; 2011.
Gauderman WJ, McConnell R, Gilliland F, London S, Thomas D, Avol E et al.
Association between Air Pollution and Lung Function Growth in Southern California Children. Am J Respir Crit Care Med 2000;162:1383-90.
O’Connor GT. Acute respiratory health effects of air pollution on children with asthma in US inner cities. J Allergy Clin Immunol 2008;121:1133-9.e1.
Kind T. Carbon monoxide. Pediatr Rev 2005;26:150-1.
Pikhart H, Bobak M, Gorynski P, Wojtyniak B, Danova J, Celko MA et al.
Outdoor sulfur dioxide and respiratory symptoms in Czech and Polish school children: A small-area study (SAVIAH). Small-Area Variation in Air Pollution and Health. Int Arch Occup Environ Health 2001;74:574-8.
Dales RE, Cakmak S, Judek S, Dann T, Coates F, Brook JR et al.
Influence of outdoor aeroallergens on hospitalization for asthma in Canada. J Allergy Clin Immunol 2004;113:303.
Turner MC, Krewski D, Pope CA, Chen Y, Gapstur SM, Thun MJ. Longterm ambient fine particulate matter air pollution and lung cancer in a large cohort of never-smokers. Am J Respir Crit Care Med 2011;184:1374-81.
Chew FT, Goh DY, Ooi BC, Saharom R, Hui JK, Lee BW. Association of ambient air-pollution levels with acute asthma exacerbation among children in Singapore. Allergy 1999;54:320-9.
Pönkä A, Virtanen M. Asthma and ambient air pollution in Helsinki. J Epidemiol Community Health 1996;50(Suppl 1):s59–62.
Andersen ZJ, Bønnelykke K, Hvidberg M, Jensen SS, Ketzel M, Loft S et al.
Long-term exposure to air pollution and asthma hospitalisations in older adults: A cohort study. Thorax 2012;67:6-11.
Andersen ZJ, Hvidberg M, Jensen SS, Ketzel M, Loft S, Sørensen M et al.
2010. Chronic obstructive pulmonary disease and longterm exposure to traffic-related air pollution: A cohort study. Am J Respir Crit Care Med 2011;183:455-61.
Sint T, Donohue JF, Ghio AJ. Ambient air pollution particles and the acute exacerbation of chronic obstructive pulmonary disease. Inhal Toxicol 2008;20:25-9.