Study adds to evidence linking ambient air quality with CV risk

Short-term exposure to ambient air pollution increased risk for myocardial infarction (MI) death, an observational case-crossover study in China found.

The study looked at air levels of particulate matter less than 2.5 microns in diameter (PM2.5), particulate matter less than 10 microns in diameter (PM10), nitrogen dioxide (NO2), and other pollutants.

“In this large case-crossover study in China from 2013 to 2018, we found consistent evidence that short-term exposure to PM2.5, PM10, and NO2 was associated with increased risk of MI mortality,” wrote Yuewei Liu, MD, PhD, of Sun Yat-sen University in Guangzhou, and co-authors in the Journal of the American College of Cardiology.

“For PM2.5 and PM10, the exposure response association was nonlinear, with risk increasing steeply at relatively low exposures and flattening out at higher exposures, while the association for NO2 exposure was linear,” they said.

The researchers examined 151,608 MI deaths in China’s Hubei province. Pollution levels were based on home address and data from the closest air monitoring station. For mean exposure on the day of death and 1 day prior, the group found:

  • MI mortality odds associated with PM2.5 and PM10 increased sharply before a breakpoint and were flatter at higher exposure levels: for PM2.5, the breakpoint was 33.3 micrograms/m310, it was 57.3 micrograms/m3.
  • MI mortality risk for PM2.5 increased by 4.14% (95% CI 1.25%-7.12%) per 10 microgram/m3 increase below the breakpoint.
  • MI mortality risk for PM10 increased by 2.67% (95% CI 0.80%-4.57%) per 10 microgram/m3 increase below the breakpoint.
  • Each 10-microgram/m3 increase in NO2 exposure was associated with a 1.46% increase in MI mortality odds (95% CI 0.76%-2.17%), which was greater in older adults.

No consistent associations were seen for carbon monoxide, ozone, or sulfur dioxide in adjusted analyses.

“More than 50% of deaths attributable to air pollution are secondary to cardiovascular (CV) disease, with a continuous relationship from very low levels, even below current World Health Organization guidelines and national standards,” noted Sanjay Rajagopalan, MD, of Case Western Reserve University in Cleveland, Ohio, and Jagat Narula, MD, of the Icahn School of Medicine in New York City, in an accompanying editorial.

The strong association between NO2 and CV mortality in this study “and the observation that the estimates for PM2.5 and CV mortality were strengthened with NO2 in the model, is suggestive of an important influence of vehicular exhaust,” they noted.

“Experimental studies in animal models, controlled exposure, and prospective studies in humans with robust biomarkers such as coronary calcium have provided the necessary certainty to propose air pollution as a modifiable risk factor for CV disease,” they added.

The 2020 update of the American Heart Association scientific statement on air pollution and cardiovascular disease noted that since 2010, “unequivocal evidence” of the causal role of PM2.5 in cardiovascular disease has emerged.

“Despite the intrinsic complexity of air pollution, a mixture of gaseous and particulate components, the mass of PM2.5 has been a simple measure of enduring value that has helped explain most of the health effects of air pollution including cardiovascular events,” the editorialists noted. “Co-pollutants such as sulfur oxides and nitrogen oxides comprise a substantial portion of the mass of PM2.5 as sulfates and nitrates and serve as excellent surrogates for air pollution from sources such as vehicular exhaust and coal plant emissions.”

A 2020 review summarized evidence for a strong link between PM2.5 and risk for cardiovascular events and all-cause mortality across a range of concentrations. Proposed mechanisms for links between air pollution and MI include oxidative stress, inflammation, abnormal regulation of the cardiac autonomic system, thrombosis, and endothelial dysfunction.

In their study, Liu and colleagues analyzed data from the national mortality surveillance system in Hubei province for persons who died from MI between January 2013 and December 2018. More than half the people in the study (54%) were male, and mean age at death was 75.2 years. Using a case-control design in which each case serves as its own control, they assigned the day of death as the case day and determined 3-4 non-death control days with exposures estimated for all case and control days.

Pollutant exposures were determined with inverse distance weighting of 24-hour average for 109 air monitoring stations in the province.

Stratified analysis showed that higher odds of MI mortality was associated with NO2 exposure for people 75 years or older (percent change in odds 2.24%, 95% CI 1.39%-3.10%) compared with people under age 75 (percent change in odds 0.36%, 95% CI –0.64% to 1.38%; P for effect modification = 0.006).

Limitations of the study include the lack of personal measurement of air pollution exposures. This may have led to inaccurate estimates given indoor exposure and activity patterns, which were not considered. Exposures to some pollutants were highly correlated, making it difficult to distinguish their respective effects on MI mortality.

  1. Short-term exposure to ambient air pollution increased risk for myocardial infarction death, an observational case-crossover study in China found.

  2. The study adds to the growing literature suggesting air pollution is a modifiable risk factor for cardiovascular disease.

Paul Smyth, MD, Contributing Writer, BreakingMED™

This work was supported by the Hubei Provincial Health Commission in China, the Fundamental Research Funds for the Central Universities, the National Natural Science Foundation of China, and the Jiangsu Social Development Project.

The researchers reported no conflicts.

The editorialists reported no conflicts.

Cat ID: 358

Topic ID: 74,358,730,358,192,149,925