A new study is the first to report evidence that nonsteroidal anti-inflammatory drugs (NSAIDs) like aspirin may lessen the adverse effects of air pollution exposure on lung function.
The team of researchers from the Columbia Mailman School of Public Health, Harvard Chan School of Public Health, Boston University School of Medicine published their findings in the American Journal of Respiratory and Critical Care Medicine.
The researchers analyzed a subset of data collected from a cohort of 2,280 male veterans from the greater Boston area who were given tests to determine their lung function. The average age of participants was 73 years.
The researchers examined the relationship between test results, self-reported NSAID use, and ambient particulate matter (PM) and black carbon in the month preceding the test, while accounting for a variety of factors, including the health status of the subject and whether or not he was a smoker.
They found that the use of any NSAID nearly halved of the effect of PM on lung function, with the association consistent across all four weekly air pollution measurements from same-day to 28 days prior to the lung function test.
Because most of the people in the study cohort who took NSAIDs used aspirin, the researchers say the modifying effect they observed was mainly from aspirin, but add that effects of non-aspirin NSAIDs are worthy of further exploration.
While the mechanism is unknown, the researchers speculate that NSAIDs mitigate inflammation brought about by air pollution.
“Our findings suggest that aspirin and other NSAIDs may protect the lungs from short-term spikes in air pollution,” says first and corresponding author Xu Gao, Ph.D., a post-doctoral research scientist in the Department of Environmental Health Sciences at the Columbia Mailman School.
“Of course, it is still important to minimize our exposure to air pollution, which is linked to a host of adverse health effects, from cancer to cardiovascular disease.”
“While environmental policies have made considerable progress toward reducing our overall exposure to air pollution, even in places with low levels of air pollution, short-term spikes are still commonplace,” says senior author Andrea Baccarelli, MD, Ph.D., chair of the Department of Environmental Health Sciences at the Columbia Mailman School. “For this reason, it is important to identify means to minimize those harms.”
An earlier study by Baccarelli found that B vitamins may also play a role in reducing the health impact of air pollution.
Increased particulate air pollutant concentrations (PM) were previously associated with triggering of acute cardiovascular and cerebrovascular events including acute myocardial infarction and ischemic stroke in the previous few hr to days, in many but not all studies (Chen, et al., 2015; Chang, et al., 2015; D’Ippoliti, et al., 2003; Mustafic, et al., 2012; Gardner, et al., 2014; Nuvolone et al., 2011; Peters et al., 2001; 2005; Rich et al., 2010; Wellenius, et al., 2005, 2012; Zanobetti & Schwartz, 2005), with others reporting similar associations with long term exposures to PM (Beckerman et al 2012; Pope and Dockery, 2006; Hoek et al 2013).
Potential mechanisms that may explain triggering of these acute events, by particulate matter (PM) include vascular dysfunction, inflammation, and coagulation among others (Brook, 2004; Langrish et al., 2012; Simkhovich et al, 2008). Previous studies in humans linked higher levels of ambient PM pollution with increases in systemic inflammatory markers such as C–reactive protein, fibrinogen, and IL-6 levels in the previous day (Bind et al., 2012; Rückerl et al., 2007; Ghio et al., 2012), or genes involved in inflammation (Brocata et al., 2014.
Various investigators also reported increases in platelet activation markers (CD40L and p-selectin) associated with elevated ambient air pollution levels in the previous few days in healthy young subjects (Rich et al, 2012a; Strak et al., 2013; Wu et al., 2012) and patients with type II diabetes (Frampton et al., 2012; Stewart et al., 2010).
Aspirin has long been used clinically as an anti-platelet drug for patients at high risk of cardiovascular outcomes such as individuals with type 2 diabetes mellitus.. Aspirin reduces the production of thromboxane A2 by inhibiting acetylation of cyclooxygenase -1 (COX-1) and subsequent production of other pro-inflammatory and pro-thrombotic prostaglandins (Collaboration, 2002; Grundy, 2004; Gurbel et al., 2007).
However, Krasopoulos et al (2008) showed that 28% of individuals displayed biochemical aspirin resistance (i.e. “nonresponse”), which attenuated the anti-platelet function of aspirin especially in patients with diabetes mellitus. Omega-3 fatty acids (eicosapentaenoic acid [EPA] and docosahexaenoic acid [DHA]) were also found to exert potent cardioprotective effects by antagonizing metabolism of arachidonic acid via the COX-1 pathway into thromboxane A2 and pro inflammatory products, which are known to increase the risk of acute cardiovascular events (GISSI-Prevenzione Investigators, 1999; Iso et al., 2001; Kris-Etherton, 2002; Lemaitre et al., 2003). Recently Abdolahi et al (2014) reported that fish oil and aspirin + fish oil combined therapy may reduce cardiovascular risk in patients with type II diabetes mellitus by reducing plasma lypophospholipids and platelet aggregation.
Data exploring whether fish oil or aspirin therapy blunts adverse cardiovascular consequences of ambient air pollution are limited. One study in Mexico City noted decreased heart rate variability (a marker of autonomic dysfunction) associated with short term increases in PM, but no such association in subjects taking fish oil supplements (Romieu et al., 2008). Tong et al (2012) reported that fish oil supplementation attenuated fine and ultrafine concentrated ambient particles (CAP) induced changes in heart rate variability and repolarization parameters, and blunted CAP-induced elevation in plasma lipids in a controlled exposure study of type II diabetes patients.
To our knowledge, no study has examined whether fish oil, aspirin, or combined fish oil and aspirin therapy modifies the effect of PM pollution on markers of platelet function in patients with type II diabetes mellitus. Data from a sequential therapy trial in patients with type II diabetes mellitus, and continuous ambient air pollution data were coupled to weather data monitoring in Rochester, New York, as used in our previous studies (Evans et al, 2014; Rich et al., 2010; 2012b;; Wasserman et al., 2014) to examine two separate hypotheses. First, it was postulated that ambient PM air pollution levels in the previous few hr and days might be associated with increased platelet aggregation and thromboxane B2 production. Second, it was proposed that aspirin and fish oil, both independently and together, might lessen or mute this response.
More information: Xu Gao et al, Nonsteroidal Anti-Inflammatory Drugs Modify the Effect of Short-Term Air Pollution on Lung Function, American Journal of Respiratory and Critical Care Medicine (2019). DOI: 10.1164/rccm.201905-1003LE
Journal information: American Journal of Respiratory and Critical Care Medicine
Provided by Columbia University’s Mailman School of Public Health
