Particulate Matter (PM), particularly fine/ultrafine PM, has been associated with an increasing number of adverse short- and long-term health effects, particularly morbidity and mortality from cancer and cardiopulmonary diseases [1-3]. It has become evident that systemic inflammation and oxidative stress play key roles in the pathogenesis of these diseases and may serve as the common mechanisms by which PM potentiates these diseases. However, in vitro and in vivo studies can only provide indirect evidence due to the inherent uncertainty in the approaches when extrapolating their results to humans. An air quality improvement initiative in Beijing during the 2008 Olympics created a unique natural experiment with an initial dramatic decline in air pollution concentrations followed by a return to pre- Olympic concentrations. We took advantage of this unique opportunity, and designed a prospective cohort study in Beijing to investigate the acute biological response to changes in human exposure to PM and to better understand the critical pathways through which PM operates in these diseases.
The specific aims of the proposed study are to examine whether changes in PM exposure over the course of the Olympics are related to changes in selected markers of DNA/lipid/protein damage and antioxidant defense, or to changes in respiratory and systemic inflammatory response. To achieve the proposed aims, we enrolled 201 adult males and females prior to the air quality improvement initiative in Beijing, China and followed these individuals over the course of the Olympics. One hundred eighty participants completed a series of three interviews: before, during and after the Olympics. Each interview consisted of an in-person interview, physical examination, and biospecimen collection (blood, urine and sputum). Ambient PM concentration in the study area was measured throughout the study period. Multianalyte multiplexed assays are proposed to analyze the selected inflammatory markers. Automated enzyme kinetic analysis, HPLC, ELISA and EIA will be used to assess oxidative DNA/lipid/protein damage and antioxidant defense. We predict that we will observe a decrease in the levels of markers for systemic inflammation and oxidative damage in response to improvements in air quality, and an increase in the levels of anti- inflammatory cytokines and antioxidant enzymes in the first follow-up period. Our hypotheses will be further evaluated by examining changes in inflammation and oxidative damage as air quality in Beijing returns to pre-Olympic levels in the second follow-up period.

Public Health Relevance

Our proposal is highly relevant to the mission of the NIH/National Institute of Environmental Health Sciences. Air pollution is a ubiquitous, worldwide exposure hypothesized to induce oxidative stress and immune responses that have been linked to cancer and cardiopulmonary disease. Our study will provide insight on these potential mechanisms through which air pollution may increase the risk of cancer and cardiopulmonary diseases;moreover, the epidemiologic nature of our proposed research ensures that the data generated will be directly applicable to humans.

National Institute of Health (NIH)
National Institute of Environmental Health Sciences (NIEHS)
Research Project (R01)
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Infectious Diseases, Reproductive Health, Asthma and Pulmonary Conditions Study Section (IRAP)
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Dilworth, Caroline H
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State University of New York at Buffalo
Public Health & Prev Medicine
Schools of Allied Health Profes
United States
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Farhat, Zeinab; Browne, Richard W; Bonner, Matthew R et al. (2018) How do glutathione antioxidant enzymes and total antioxidant status respond to air pollution exposure? Environ Int 112:287-293
Glasgow, Mark L; Rudra, Carole B; Yoo, Eun-Hye et al. (2016) Using smartphones to collect time-activity data for long-term personal-level air pollution exposure assessment. J Expo Sci Environ Epidemiol 26:356-64
Li, Yanli; Browne, Richard W; Bonner, Matthew R et al. (2014) Positive relationship between total antioxidant status and chemokines observed in adults. Oxid Med Cell Longev 2014:693680
Epplein, Meira; Bostick, Roberd M; Mu, Lina et al. (2014) Challenges and opportunities in international molecular cancer prevention research: An ASPO Molecular Epidemiology and the Environment and International Cancer Prevention Interest Groups Report. Cancer Epidemiol Biomarkers Prev 23:2613-7
Mu, Lina; Deng, Furong; Tian, Lili et al. (2014) Peak expiratory flow, breath rate and blood pressure in adults with changes in particulate matter air pollution during the Beijing Olympics: a panel study. Environ Res 133:4-11
Mu, Lina; Liu, Li; Niu, Rungui et al. (2013) Indoor air pollution and risk of lung cancer among Chinese female non-smokers. Cancer Causes Control 24:439-50
Li, Yanli; Chang, Shen-Chih; Niu, Rungui et al. (2013) TP53 genetic polymorphisms, interactions with lifestyle factors and lung cancer risk: a case control study in a Chinese population. BMC Cancer 13:607
Myneni, Ajay A; Chang, Shen-Chih; Niu, Rungui et al. (2013) Genetic polymorphisms of TERT and CLPTM1L and risk of lung cancer--a case-control study in a Chinese population. Lung Cancer 80:131-7
Li, Yanli; Rittenhouse-Olson, Kate; Scheider, William L et al. (2012) Effect of particulate matter air pollution on C-reactive protein: a review of epidemiologic studies. Rev Environ Health 27:133-49