Poor air quality inflicts short-term toll on heart

Exposure to elevated concentrations of small particulate matter appears to confer an immediate increase in the risk of out-of-hospital cardiac arrest (OHCA), which subsequently decreases over a few days after exposure, according to data from the Pan-Asian Resuscitation Outcomes Study (PAROS) conducted in Singapore.

For every 10-μg/m³ increase in PM_2.5, OHCA risk rose by about 2 percent (relative risk [RR], 1.022, 95 percent confidence interval [CI], 1.002–1.043), a trend that persisted over the first 2 days. However, this risk subsequently waned during the next 3 days (days 3–5; RR, 0.976, 95 percent CI, 0.955–0.998). [Lancet Public Health 2022;7:e932-e941]

Notably, the association between increasing PM_2.5 concentration and OHCA 0–2 days after exposure was modified by cardiac arrest rhythm (nonshockable: RR, 1.027, 95 percent CI, 1.004–1.050 vs shockable: RR, 1.002, 95 percent CI, 0.956–1.051) and location of OHCA (at home: RR, 1.033, 95 percent CI, 1.008–1.057 vs not at home: RR, 0.955, 95 percent CI, 0.957–1.035).

“One possible explanation for the short-term risk increase is a harvesting effect, such that an increase in PM_2.5 concentration triggered earlier OHCA in those who had compromised health and who would probably have had a cardiac arrest subsequently,” according to PAROS investigators from the Duke-NUS Medical School, Singapore.

“After this initial harvesting effect within the first few days of exposure, the number of cases of OHCA might decrease because the population who are susceptible has decreased,” they added.

In hypothetical scenarios, the investigators found that the number of OHCA events associated with PM_2.5 could be brought down by 8 percent and 30 percent for every 1- and 3-μg/m³ reduction in PM_2.5 concentrations, respectively.

“Public health strategies to reduce PM_2·5 concentrations might lead to a decrease in the population burden of cardiac arrests that occur out of hospital and reduce the demand for PM_2.5-attributable emergency health services,” they said.

PAROS

The analysis included 18,131 individuals who had experienced OHCA over a period of 8 years (2010–2018). The median age of the cohort was 65 years, and 11,647 (64.2 percent) were men. In terms of ethnicity, 12,270 (67.7 percent) were Chinese, 2,873 (15.8 percent) were Malay, and 2,010 (11.1 percent) were Indian.

Exposures to PM₁₀, ozone (O₃), nitrogen dioxide (NO₂), and sulphur dioxide (SO₂) at any of the time points had a null effect on the risk of OHCA. Meanwhile, carbon monoxide (CO) was linked to a cumulative decreased risk of OHCA across 0–5 days after exposure (RR, 0.876, 95 percent CI, 0.770–0.997) and at days 3–5 after exposure (RR, 0.810, 95 percent CI, 0.690–0.949).

The findings are in line with those in another study conducted in Nanjing, China, wherein the association between PM_2.5 concentration and overall or cardiovascular mortality was initially positive at 0–1 day after exposure but turned negative 2 days after exposure. Furthermore, in a separate study that looked at seven major cities in South Korea, the incidence of cardiovascular death associated with PM₁₀ increased 0–1 day after exposure, decreased within 28 days of exposure, and increased again over 0–45 days after exposure. [Chemosphere 2021;265:129035; Int J Epidemiol 2021;49:1802-1812]

“Taken together, PM might lead to an acute increase in OHCA in the first few days of exposure due to a harvesting effect, but in the medium and longer term might lead to a genuine increase in the incidence of OHCA. Further research is needed with longer lag durations to confirm this hypothesis,” the investigators said.

Underlying mechanisms

The investigators cited several mechanisms for the association between PM and OHCA. First was that PM might promote systemic inflammation, which subsequently leads to increased coagulation, platelet aggregation, and thrombus formation in the coronary arteries. Additionally, PM could cause autonomic imbalance, which has been implicated in cardiac events, sustained ventricular tachycardia, and mortality. [Transl Res 2007;149:324-332; Circulation 2000;101:1267-1273]

“In particular, PM_2.5 is more strongly associated with ST-elevation myocardial infarction (STEMI) than non-STEMI… PM_2.5 might trigger STEMI through increased oxidative stress and inflammatory reactions, elevation of blood pressure due to endothelial dysfunction and autonomic dysfunction, and thrombosis caused by the hypercoagulable state,” they said. [Int J Environ Res Public Health 2016;13:748]

“Singapore has variations in air quality that are contributed by both local and nonlocal sources of emissions, including regional land fires. The resultant variation in air quality, in addition to Singapore's robust surveillance, provide optimal real-world data for assessing its effect on population health,” according to the investigators. [Int J Cardiol 2018;271:352-358]

Environmental surveillance data

In an accompanying editorial, an expert who was not involved in the study pointed out that PAROS made several key contributions to the evidence informing air pollution and cardiovascular disease onset. First was that increases in PM concentrations even at low levels of air pollution exposure could up the risk of OHCA. [Lancet Public Health 2022;7:e890-e891]

“Second, this research provided real-world evidence on the different types and locations of cardiac arrest events. PM_2.5 concentrations affected non-shockable OHCA events and had less of an effect on shockable OHCA events, the cause of which is still to be explored. Finally, the investigators found the effects of increasing PM_2·5 concentrations were the largest in the immediate 2 days after exposure, indicating an acute manifestation of OHCA due to air pollution,” wrote Prof John Ji from Tsinghua University, Beijing, China.

Nevertheless, Ji acknowledged the presence of some issues that were not addressed by PAROS, as follows: “Is the peak exposure or the cumulative average exposure most predictive of health outcomes? Particularly in the case of cardiovascular events, is the strongest risk within the first hour of exposure, over the course of the day, or within a few days? Second, how do single pollutants or mixtures of pollutants affect outcomes?”

Ji pointed to an opportunity to use new health surveillance and sensing technologies to further the understanding of air pollution’s link to OHCA. He explained that these technologies could help provide environmental surveillance data on duration of exposure, severity of exposure, timing of exposure, coexposures, and location of exposure that could be useful in forecasting cardiac arrest onset in low time-lapse intervals.

“Future clinical guidelines should include air pollution screening and ways to alert patients and providers ahead of a pollution event, thereby preventing medical emergencies,” he said.