Sunday, 9 October 2011

A matter of the heart

Some years ago, I accompanied a young relative, a very eager science graduate working on particulate matter, as she conducted her research survey on public perception of particulate matter and its effects in a certain borough of London. Particulate matter (PM) is used to describe solid matter suspended in a gas or liquid phase. In the environment, particulates may occur naturally (as consequence of forest fires, volcanoes, dust storm, sea sprays etc) or via anthropogenic activities, such as the burning of fossil fuels in automobile exhausts and other industrial processes. PM10 is used to describe particles of 10 micrometres or less. Unsurprisingly, densely populated metropolitan areas in developing countries are hot spots for PM. The exercise with my relative was an eye-opener, and also quite fun as we pounced on shoppers, city workers on lunch breaks, pedestrians in Central London etc., armed with our clip boards and ticking or crossing their responses. I enjoyed being the magician’s assistant….but that is another story.

All this came back to me as I read the recent article by Bhaskaran et al, of the London School of Tropical Medicine and Hygiene, who studied the effects of air pollution on the risk of heart attack- specifically whether alterations in pollution levels on an hourly timescale affects the short-term risk in urban settings of England and Wales, So what is the novelity in this study? The links between particular matter and heart and lung diseases is documented and there are several publications in these topics.In an earlier post in this site, David discussed a study where PM10 caused increase in blood pressure in traffic controllers in the metropolitan area of Sao Paolo. However, there is a wee difference in what this paper covered: This work considered the overall risk of heart attack in urban settings of England and Wales over very short time frames and it involved a large population size. In essence, this study looked at effects of very short-term exposure (which was not, previously possible due to technology limitations). In this mega-study of over 79000 individuals with a diagnosis of heart attack over three years from 15 cities( including Greater London, Greater Manchester, West Yorkshire, Bristol, Cardiff, Southampton) the team looked at PM10 and other pollutants such as ozone, carbon monoxide, nitrogen dioxide, and sulphur dioxide over five short periods of up to 72 hours. For the analysis of their results they used statistical modelling approach for single pollutant and multiple pollutants where they adjusted for factors that could influence and otherwise confuse data including ambient temperature, humidity, virus in the atmosphere ( both that for flu and for other infections- respiratory syncytial virus). The researchers found that increase in PM10 levels & NO2 levels was associated increase in risk for heart attacks 1-6 hours post-exposure;.The source of PM10 & NO2 in urban areas is largely from automobile exhausts. Interestingly the increase in immediate risks was followed by reduction in risks at longer lags and therefore they found no net risk increase over 72 hour periods. They found a protective effect for increase in CO & ozone however; there was no change in overall risk over 72 hours leading the team to speculate that ischaemic events that would have occurred soon were advanced by a few hours. Most studies so far had shown the effects after years of chronic exposure and herein lies the difference of this study. A previous small study in Greater Boston with less than 1000 subjects showed an increased risk 1-3 hours after exposure of PM10. The risk was 11% which is higher than that observed in the current study. What do the results mean cumulatively? Remember this was a statistical exercise, though a worthy one. It would still be interesting to explore the physiological, cellular, & molecular basis of organ responses to short-term exposure to PM10 which will further our understanding. It might also be interesting to pursue questions such as, are there individuals of a particular genetic signature who might be prone to the effects of short-term exposure and low doses of PM more than others? the effect of age etc. Are similar trends seen in respiratory disorders? Does PM exposure compound the effects in vulnerable populations? All these questions remain.

But what does the study mean to the society as a whole and what can we do? The results in addition to the existing body of evidence should send warning bells to the world but emerging economies that are mushrooming urban sprawls. The recent UN summit highlighted the importance of non-communicable diseases including cardiovascular disease on the global health. With NCDS (CVDS and cancer) accounting to 36 million of global deaths in 2008 WHO stats, the UN draft resolutionon (dated 16 September 2011) submitted by the President of the General Assembly - political declaration of the high level meeting of the general assembly on the prevention and control of non-communicable diseases -concedes the gravity of the situation and ‘recognizes that prevention must be the cornerstone of the global response to NCDS’ and identified several modifiable factors including diet and tobacco smoke that results in the rise of NCDS and called for ‘reducing their exposures’. These are valid and commendable. However, a glaring omission is the lack of mention of air pollutants contributing to NCDs. In the UN document, the closest air pollution is touched upon is with the reference to pollution from cooking stoves used for indoor cooking and heating. In essence, the enumerated risk factors do not include particulate matter from vehicles!!.

The results in this paper and the other background research cannot be ignored and should prompt usto push for measures for cutting down particulate matter emissions. Prevention is certainly a better option than treatment and cure as the UN draft declaration as well as common sense dictate. Importantly, prevention is something that is easy to achieve, but requires efforts starting from the individual to local to the global.

Bhaskaran K, Hajat S, Armstrong B, Haines A, Herrett E, Wilkinson P, & Smeeth L (2011). The effects of hourly differences in air pollution on the risk of myocardial infarction: case crossover analysis of the MINAP database. BMJ (Clinical research ed.), 343 PMID: 21933824








