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HomeEnvironmental HealthAir pollution's tiny particles may trigger non-fatal heart attacks

Air pollution's tiny particles may trigger non-fatal heart attacks

Transient exposure to air pollution's ultrafine particles may trigger the onset of nonfatal myocardial infraction, found a German study.

Myocardial infarction is a major form of cardiovascular disease worldwide. Ultrafine particles (UFP) are 100 nanometers or smaller in size. In urban areas, automobile emissions are the primary source of UFP.

The study is believed to be the first epidemiological investigation of the effects of UFP exposure and heart attacks using the number of particles and the particle length and surface area concentrations at hourly intervals of exposure.

"This study confirms something that has long been suspected – air pollution's tiny particles can play a role in serious heart disease. This is particularly true within the first few hours of exposure," said Dr Kai Chen, assistant professor at Yale School of Public Health and the study's first author. "Elevated levels of UFP are a serious public health concern."

UFP constitute a health risk due to their small size, large surface areas per unit of mass, and their ability to penetrate the cells and get into the blood system. "We were the first to demonstrate the effects of UFP on the health of asthmatics in an epidemiological study in the 1990s," said Annette Peters, director of the Institute of Epidemiology at Helmholtz Centre Munich and a co-author of this paper. "Since then approximately 200 additional studies have been published. However, epidemiological evidence remains inconsistent and insufficient to infer a causal relationship."

The lack of consistent findings across epidemiological studies may be in part because of the different size ranges and exposure metrics examined to characterize ambient UFP exposure. Chen and his co-authors were interested in whether transient UFP exposure could trigger heart attacks and whether alternative metrics such as particle length and surface area concentrations could improve the investigation of UFP-related health effects.

With colleagues from Helmholtz Centre Munich, Augsburg University Hospital and Nördlingen Hospital, Chen examined data from a registry of all nonfatal MI cases in Augsburg, Germany. The study looked at more than 5, 898 nonfatal heart attack patients between 2005 and 2015.

The individual heart attacks were compared against air pollution UFP data on the hour of the heart attack and adjusted for a range of additional factors, such as the day of the week, long-term time trend and socioeconomic status.

"This represents an important step toward understanding the appropriate indicator of ultrafine particles exposure in determining the short-term health effects, as the effects of particle length and surface concentrations were stronger than the ones of particle number concentration and remained similar after adjustment for other air pollutants," said Chen. "Our future analyses will examine the combined hourly exposures to both air pollution and extreme temperature. We will also identify vulnerable subpopulations regarding pre-existing diseases and medication intake."

Background: Epidemiological evidence on the health effects of ultrafine particles (UFP) remains insufficient to infer a causal relationship that is largely due to different size ranges and exposure metrics examined across studies. Moreover, evidence regarding the association between UFP and cardiovascular disease at a sub-daily timescale is lacking.
Objective: We investigated the relationship between different particle metrics, including particle number (PNC), length (PLC), and surface area (PSC) concentrations, and myocardial infarction (MI) at an hourly timescale.

Methods: We collected hourly air pollution and meteorological data from fixed urban background monitoring sites and hourly nonfatal MI cases from a MI registry in Augsburg, Germany, during 2005–2015. We conducted a time-stratified case-crossover analysis with conditional logistic regression to estimate the association between hourly particle metrics and MI cases, adjusted for air temperature and relative humidity. We also examined the independent effects of a certain particle metric in two-pollutant models by adjusting for copollutants, including particulate matter (PM) with an aerodynamic diameter of ≤10μm or 2.5μm (PM10 and PM2.5, respectively), nitrogen dioxide, ozone, and black carbon.
Results: Overall, a total of 5,898 cases of nonfatal MI cases were recorded. Exploratory analyses showed similar associations across particle metrics in the first 6–12 h. For example, interquartile range increases in PNC within the size range of 10–100 nm, PLC, and PSC were associated with an increase of MI 6 h later by 3.27% [95% confidence interval (CI): 0.27, 6.37], 5.71% (95% CI: 1.79, 9.77), and 5.84% (95% CI: 1.04, 10.87), respectively. Positive, albeit imprecise, associations were observed for PNC within the size range of 10–30 nm and 100–500 nm. Effect estimates for PLC and PSC remained similar after adjustment for PM and gaseous pollutants.
Conclusions: Transient exposure to particle number, length, and surface area concentrations or other potentially related exposures may trigger the onset of nonfatal myocardial infraction.

Kai Chen, Alexandra Schneider, Josef Cyrys, Kathrin Wolf, Christa Meisinger, Margit Heier, Wolfgang von Scheidt, Bernhard Kuch, Mike Pitz, Annette Peters, Susanne Breitner

[link url=""]Yale School of Public Health material[/link]

[link url=""]Environmental Health Perspectives abstract[/link]

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