And after asking the ICC to revise the rulebook, the Indian Medical Association has now requested the BCCI to look into the matter. The letter to acting president CK Khanna and CoA head Vinod Rai has been penned by IMA president KK Aggarwal.
The Indian Medical Association (IMA) is greatly troubled about the recent cricket match between India and Sri Lanka in Delhi played under conditions of high levels of air pollution.
Air quality in the Delhi-NCR region has been ranging between ‘very poor’ and ‘severe’ since last several days. This has been a cause of great concern to us. Exposure to air pollution increases the risk of lung and heart disease and may precipitate an acute potentially life-threatening event. But, when pollution levels are this high, everyone, including healthy persons may experience some level of discomfort.
Air pollution also reduces performance of the athletes. In a situation where milliseconds and millimetres often determine success of athletes, air pollution can be an important factor in affecting their performance.
Rain and poor light are taken into consideration when determining suitable playing conditions, we suggest that atmospheric pollution should now also be included in the assessing criteria for a match.
The safe levels of atmospheric particulate matter (PM), according to the World Health Organization (WHO) air quality guidelines, are 20 μg/cu mm (annual mean) for PM10 and 10 μg/ cu mm (annual mean) for PM2.5.
If the air quality index (AQI) is between 151 and 200, it is recommended that outdoor exercises should be reduced. If the AQI is between 201 and 300, all outdoor activities and sports should be reduced. If the AQI is more than 300, all outdoor exercise and activities should be avoided as much as possible. If the AQI crosses 400, indoor activities too should be reduced and no exercise even at home is recommended.
The message from the India and Sri Lanka cricket match that has gone home is that it is safe for children to play cricket even when the PM 2.5 levels are more than 300.
There is sufficient evidence in medical literature documenting the adverse effects of air pollution on the human body.
Following are the evidence
• A meta-analysis of seven trials has revealed that a one-unit (μg/m3) increase in ambient PM2.5 concentration in adults is associated with an increase in the odds of physical inactivity by 1.1% (odds ratio = 1.011; 95% confidence interval = 1.001, 1.021; p-value < .001). (Perspect Public Health. 2017 Aug 1:1757913917726567)
• Poor air quality can adversely affect athletes with asthma or other pulmonary disorders. As the AQI rises above 100 to 150, athletes and volunteers can be adversely affected. If the AQI is above 100, it is prudent for race administrators to warn participants and volunteers, particularly those with lung conditions, about the potential risk. (J Am Coll Cardiol. 2005;46(7):1373-4)
• PM10 is associated with decrements in performance of women. For every 10-microg x m (-3) increase in PM10, performance can be expected to decrease by 1.4% (Med Sci Sports Exerc. 2010 Mar;42(3):585-91).
Short-term exposure to air pollutants (both ozone and fine particulate matter) is associated with acute coronary ischemic events
In addition to long-term risk, short-term exposure to air pollutants (both ozone and fine particulate matter) is associated with acute heart attacks (Circulation. 2006; 114:2443; Circulation. 2005;111:563; Eur Heart J. 2013; 34:1306).
• In a study of over 12,000 patients living in a defined geographic area, a short-term increase in fine ambient particulate matter positively correlated with an increase in acute ischemic coronary events (Circulation. 2006;114:2443).
• In a systematic review and meta-analysis of data from 34 studies, carbon monoxide, nitrogen dioxide, sulfur dioxide, and small particulate matter (less than 10 microns and less than 2.5 microns) were all associated with an increased risk of myocardial infarction (MI), with the overall population attributable risk ranging from 1-5% (JAMA. 2012;307:713).
• In a study of 772 patients with an acute myocardial infarction (MI), the risk of an MI was increased in the two hours after exposure to elevated levels of fine particles in the air (odds ratio 1.48 compared to low levels of fine particles); this effect lasted for up to 24 hours after exposure (Circulation. 2001;103:2810).
The possible mechanism by which fine particulate air pollution may increase the risk of cardiovascular disease include
o An increase in mean resting arterial blood pressure through an increase in sympathetic tone and/or the modulation of basal systemic vascular tone (Circulation. 2002;105:1534).
o An increase in the likelihood of intravascular thrombosis through transient increases in plasma viscosity and impaired endothelial dysfunction (Circulation. 2002;106:933).
o The initiation and promotion of atherosclerosis (Circulation. 2010;121:2755; J Am Coll Cardiol. 2010;56:1803).
• There is 0.13% reduction in peak expiratory flow rate (PEFR) per 10 µg/m3 of PM 2.5.
• Asthma is linked to high NO2 (nitrogen dioxide) levels and bronchitis is linked to high levels of SO2 (sulphur dioxide).
• Compared to during rest, the air pollution dosage is much higher during exercise because of a higher ventilatory rate and both nasal and oral breathing. SO2, a highly water-soluble gas, is almost entirely absorbed in the upper respiratory tract during nasal breathing. However, with oral pharyngeal breathing, the amount of SO2 that is absorbed is significantly less, and with exercise and oral pharyngeal breathing a significant decrease in upper airway absorption occurs, resulting in a significantly larger dosage of this pollutant being delivered to the tracheobronchial tree.
• Combination of exercise and pollutant exposure (SO2 or ozone [O3]) leads to marked bronchoconstriction and reduced ventilatory flow when compared to pollution exposure at rest.
• Each 10 mcg/m3 increase in PM 2.5 levels can increase the chances of death from heart disease by 1.76 times and each decrease in PM 2.5 levels by 10 mcg/m3 life can increase life expectancy by 0.77 year.
• A PM <2.5 reduction of 6.8 mcg/m3 can decrease asthma prevalence by 15.4% and a median reduction in NO2 of 4.9 parts per billion can decrease asthma prevalence by 10%.
• The Women's Health Initiative Observational study database of more than 65,000 postmenopausal women without prior CVD was used to evaluate the relation between a woman's long-term exposure to air pollutants and the risk for a first cardiovascular event . Unlike prior studies, potential confounding factors such as age, body mass index (BMI), and traditional cardiovascular risk factors were taken into account. The principle findings were that for each 10 mcg/m3 increase in pollution concentration, there were significant increases in the risk of any cardiovascular event (hazard ratio [HR] 1.24), death from CVD (HR 1.76), and cerebrovascular events (HR 1.35) (N Engl J Med. 2007;356:447).
• For every increase of 10 μg/m3 in PM10, the lung cancer rate rises by 22% and for PM 2.5 by 36%
• By reducing particulate (PM10) pollution from 70 to 20 μg/m, air pollution-related deaths could be reduced by roughly 15%.
• Mortality in Utah Valley decreased by 3% when average particulate air pollution (PM10) concentrations decreased by 15 µg/m3 as the result of a 13-month strike at a local steel mill (Arch Environ Health. 1992;42:211-7).
Air pollution and the heart
• Air pollution, and specifically fine particulate matter, is associated with increased cardiovascular mortality.
• Air pollution has emerged as a potentially modifiable risk factor for the development of cardiovascular disease.
• The association of air pollution with episodes of atrial fibrillation (AF) was evaluated in a study of 176 patients with dual chamber implantable cardioverter-defibrillators (ICDs) that were capable of detecting episodes of AF. After follow-up of nearly two years, there were 328 episodes of AF lasting 30 seconds or more found in 49 patients. The potential impact of multiple parameters of air pollution, (measured hourly) on the development of AF was examined. The odds of AF increased significantly as the concentration of particulate matter increased in the two hours prior to the event (J Am Coll Cardiol. 2013;62:816).
• Multiple observational studies have demonstrated an association between fine particulate air pollution (primarily from the use of fossil fuels in automobiles, power plants, and for heating purposes) and cardiovascular and cardiopulmonary mortality as well as an increased risk for the development of acute coronary syndromes
• Mortality data from nearly 450,000 patients in the American Cancer Society Cancer Prevention Study II data base were correlated to air pollution data, including average concentrations of ozone and fine particulate matter (≤2.5 micrometers in diameter [PM2.5]). In multivariate analysis PM2.5, but not ozone, concentration was significantly associated with the risk of death from cardiovascular causes (relative risk 1.2) (N Engl J Med. 2009;360:1085).
• Further support for the significance of air pollution comes from a study of death rates in Dublin, Ireland before and after a ban on coal sales that led to a 70 percent reduction in black smoke concentrations (Lancet. 2002; 360:1210). Adjusted cardiovascular deaths fell by 10.3 percent in the six years after the ban.
• Both the American Heart Association (2010) and the European Society of Cardiology (2015) have issued official statements discussing the association between long-term exposure to fine particulate air pollution and increased risk of developing cardiovascular disease (Circulation. 2010;121:2331; Eur Heart J. 2015;36:83).
• Multiple observational studies have demonstrated an association between fine particulate air pollution and distance from a major urban road or freeway and cardiovascular and cardiopulmonary mortality. However, there is conflicting evidence concerning whether air pollution is (J Thromb Haemost. 2010;8:669) or is not (J Thromb Haemost. 2011;9:672), causally related to development of venous thromboembolism (VTE).
• In a multivariate analysis PM2.5 was significantly associated with the risk of death from cardiovascular causes (relative risk 1.2) (N Engl J Med. 2009;360:1085).
• In the prospective MESA Air cohort study involving 6795 participants in six US metropolitan areas, each increase in PM2.5 of 5 mcg/m3was associated with 4.8 Agatston units per year progression of coronary calcification (Lancet. 2016; 388:696).
• American Heart Association (AHA), European Society of Cardiology (ESC), Indian Medical Association (IMA) and Heart Care Foundation of India (HCFI) have issued official statements discussing the association between long-term exposure to fine particulate air pollution and increased risk of developing cardiovascular disease.
Dr KK Aggarwal
Indian Medical Association and Heart Care Foundation of India
Vice President CMAAO.
First Published: December 7, 2017, 11:13 AM IST