PM2.5 in Beijing – temporal pattern and its association with influenza – Environmental Health
Many studies, in particular epidemiological studies, have demonstrated strong evidence for the association between particulate air pollution (from both PM10 and PM2.5) and human illness, in particular cardiovascular and respiratory disease. Both short- and long-term exposures to ambient particulate matters have implications for different health impacts [13, 27–31]. In China, much attention on air pollution has been focused on PM10, and the studies about PM2.5 exposure on health impact in China have just started. In this study, we report a five-year period of PM2.5 measurements from an urban site of Beijing and its possible association with human influenza. To our knowledge, this is the first study reporting comprehensive measurements of PM2.5 related to influenza in Beijing, China.
Although the present study only used data from one monitoring site in Beijing, it certainly reflects the unacceptably high air pollution occurring in one of the most populated cities in the world. From the monitoring records, on average, more than 81% of days each year, people live in the environment with polluted air exceeding US EPA and Chinese health standards. PM2.5 has increasingly been shown to be more harmful to human health than bigger particles since the smaller particles have more potential to be deposited in the alveoli and even penetrate the blood-gas barrier [32]. However, China has only been recently releasing PM2.5 concentrations to the public in major cities. We all recognize that significant efforts have been made, but record-breaking pollution levels were recorded in the winter of 2013 in Beijing, China [33]. This indicates that more comprehensive efforts still are needed so that the air quality improvements during the Beijing Olympic Games in 2008 could be sustainable [34, 35].
Air pollution has been implicated in respiratory illness infections [36]. Moreover, many reports are related to indoor air pollution (e.g. combustion) which has been related to acute lower respiratory infections [37–40] and this has been a concern in many developing countries. There are not many studies related to ambient air pollution and infections, although there are reports on association between air pollution and pneumococcal disease related to respiratory viruses [41]. In this study, we chose to explore the potential linkage between exposure to PM2.5 and human influenza, given the consideration of nature of the disease, biological plausibility, and availability of the influenza data. Using three-year’s data, our study suggested that human influenza cases were correlated to PM2.5 concentrations in Beijing and the finding is in general agreement with other studies [42]. This seems to have a time lag while peaks of PM2.5 levels were followed by peaks of influenza in 2009 and 2010. Interestingly, the peak of PM2.5 levels were not obvious in 2008, so was relatively moderate for influenza cases during the same year, which further strengthens the correlation between PM2.5 exposure and influenza occurrence. The underlying possible mechanisms related to this are complex. There are some reports about ambient air pollution on respiratory infections in humans [43, 44] and it is likely that air pollution exposure causes host defense disorders, including both innate and cell-mediated immune responses against bacterial and viral infections [45, 46]. Various experimental studies have suggested that the deposition of particulates on epithelial cells that line the airways activates inflammatory signaling cascades [47, 48]. In addition, high PM2.5 levels could precipitate inflammatory and tissue remodeling changes in the lungs [49].
The study is also subject to some limitations. First, we only used one measurement source from the US Embassy, limiting spatial representativeness of the present work. Second, our data suffer from under-reporting of influenza cases; however, the under-reporting tends to occur in consistent pattern throughout the country and we believe that the relative pattern (e.g. seasonal variations in influenza) still holds. Third, the observational time periods of five years for PM2.5 levels and three years for influenza cases are relatively short, especially when a definite, strong correlation is concluded. Fourth, one kind of infectious disease, such as influenza in our study, may not be ideal, and more similar respiratory infectious diseases should be included in the future to demonstrate strong and broad correlation between PM2.5 and infectious diseases. Nevertheless, this study demonstrates a temporal correlation between PM2.5 pollution and influenza peak occurrence in Beijing, which provides significant impact on both environmental policy-making and public health preparedness.
In conclusion, despite the limitations, our study has indicated severity of PM2.5 pollution in urban Beijing and health implications associated with human influenza. Further studies are in urgent need to understand the mechanisms underlying the potential association as well as public health and environmental policy implications.