While the National Environment Agency (NEA) has traditionally reported the Pollutant Standards Index (PSI) which measures the concentration of Particulate Matter less than 10 microns in size (PM 10), experts over the years have been warning that the smaller particles smaller than 2.5 microns or PM 2.5 are actually more dangerous to health.
The physiological reasons are straightforward: at sizes larger than 2.5 microns, the respiratory tract can quite effectively trap and filter away particles. However, at sizes lesser than 2.5 microns, PM 2.5, particles breach these defenses and penetrate deeply into the alveoli of the lungs and may even enter the blood stream. The subsequent effects are still the subject of intense study and a recent article in the Proceedings of the National Academy of Sciences provides a very nice overview. The adverse effects on the lungs are well-known but what is less publicized is the impact on heart disease, stroke and other vascular conditions. The exact mechanism is not clear but one theory is that PM 2.5 triggers an inflammatory response leading to oxidative damage. Similar to the risks from chronic inflammation of any part of the body from any source, a complex cascade of bodily responses then occurs, leading finally to increased plaque formation in the blood vessels.
Thresholds and Dose-Effects
Is there a threshold effect? Is there a dose-effect response? In simple English, these two key concepts in toxicology mean “Is there a minimum level of PM 2.5 below which there is no noticeable physiological effect?” and “Are the harmful effects proportional to the total level of exposure?”
For the former, the answer is unfortunately ‘No’ at the population level. Researchers from the Harvard School of Public Health analyzed data from a study of death rates and PM 2.5 levels in six American cities and concluded there was “no evidence of a threshold down to the lowest levels of PM 2.5”. In fact, the researchers noted that the relationship or curve was quite linear between 0 to 35 micrograms/ m3.
It should be noted there is no firm evidence either way at the individual level. A useful but imperfect analogy is that of smoking. At the population level, we know the harmful effects of smoking, but can we predict with certainty for any given individual cancer or chronic lung disease? No.
With regards to dose-effect response, Chen from McGill University in Canada reviewing the scientific literature concludes:
“The latter long-term exposure to PM2.5 increases the risk of non-accidental mortality by 6% per a 10 micrograms/m3 increase, independent of age, gender, and geographic region. Exposure to PM2.5 was also associated with an increased risk of mortality from lung cancer (range: 15% to 21% per a 10 micrograms/m3 increase) and total cardiovascular mortality (range: 12% to 14% per a 10 micrograms/m3 increase).”
In a nutshell: ‘Yes’, the greater the long term exposure, the higher the risk. Again, these numbers reflect observations at the population rather than the individual level.
What are the ‘safe’ levels then? Below is the guidance from the American Environmental Protection Agency (EPA):
“With regard to primary (health-based) standards for fine particles (generally referring to particles less than or equal to 2.5 micrometers (mm) in diameter, PM2.5), the EPA is revising the annual PM2.5 standard by lowering the level to 12.0 micrograms per cubic meter so as to provide increased protection against health effects associated with long- and short-term exposures (including premature mortality, increased hospital admissions and emergency department visits, and development of chronic respiratory disease), and to retain the 24-hour PM2.5 standard at a level of 35 micrograms per cubic meter.” [Emphasis added]
In plain English, the EPA recognizes there is an ‘average’ annual as well as a more volatile ’24 hour’ value and both are important in risk assessment.
Singapore’s PM 2.5 levels have in the first 12 days of June been below the EPA 24 hour standard of 35 micrograms/m3. Beginning 13 June, PM 2.5 crossed 35 micrograms/m3 but remained below 100 micrograms/m3 until 18 June when it jumped to 149-169 micrograms/m3, peaking at 304 micrograms/m3 on 20 June and coming down to 71-94 micrograms/m3 yesterday (23 June 2013). Source: NEA
The last 6 days have been above the daily threshold set by the American EPA. This is cause for concern and should warrant precautionary measures as Singaporeans have already taken. Are the numbers cause for alarm? We don’t know but the graph below from Bloomberg which shows Beijing’s PM 2.5 levels in January 2013 help put things into perspective.
What’s salient to note for Singaporeans living with PM 2.5 values generally in the 100-200 range during this period? Firstly, the average PM 2.5 measured across airport smoking lounges in the USA is 166.6 micrograms/m3. Secondly, Chinese in Beijing live with PM 2.5 levels virtually always above the World Health Organization’s ‘Healthy Level’ and the peak of 886 micrograms/m3 is almost three times Singapore’s highest ever of 304 micrograms/m3.
‘Keep calm and carry on’
What should Singaporeans do then? Various government agencies such as the Ministry of Health have issued guidance which should be heeded. I would encourage adhering to the guidance and not being alarmist. Check the daily PSI and the PM 2.5 levels and decide on what precautionary measures to take for that day. The London Smog of 1952 which saw cows keeling over had PM 2.5 levels as high as 4,500 micrograms/m3 which Singapore is a long way from.
Given the science including the papers cited above, I do wish the MOH would issue advice based on PM 2.5 levels too. The Americans have moved away from PM 10 and instead use PM 2.5 in computing their Air Quality Index (AQI). It should be noted also that PM 2.5 refers only to the size of the particles and not what the particles are made of. The hazardous effects of PM 2.5 would naturally depend also on what particles make up PM 2.5. AQI in addition to PM 2.5 also factors in carbon monoxide, ozone, sulfur dioxide and nitrogen dioxide and it is the composite that makes up AQI. PSI comprises five components (PM 10, SO2, CO, ozone, NO2) but the NEA only reports levels of the individual components without annotation.
An EPA guideline dated May 2006 recommends reporting both the AQI and the responsible pollutant, e.g. AQI: 162, Responsible Pollutant: Ozone. This helps as different pollutants affect the body in different ways- the report lists people with asthma as “the group most at risk from sulfur dioxide” and people with heart disease as “group most at risk from carbon monoxide”. In some of the papers cited above, the particles arising from traffic seem more hazardous than those emanating from say pollen, and it would be wonderful if the relevant government agency could provide the public with some indication on what the ‘haze’ chemically comprises of.
[24 June 2013 7.25 am:
Microns/m3 replaced by micrograms/m3 as unit of measurement for PM 2.5. Apologies for the confusion. A micron is one millionth of a meter
Edited to include component measurements of PSI and EPA recommendations for reporting of AQI]
[25 June 2013 2.40 pm:
Correction: NEA does list in table form without annotation the levels of individual components and has also stated that PM 10 is the dominant pollutant- “During haze, the pollutant that records the highest concentration is PM10.”. It is not clear what chemical substances make up PM 10. The blog post has been amended]