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Studies report serious adverse effects of air pollution on CV health
Recent studies have illustrated various associations between fine particulate matter, vehicle emissions and a variety of gaseous pollutants and increased risk for CVD, cardiac arrest and diminished vascular function across the globe.
These studies highlight the potential CV health risks associated with fine particulate matter and cardiac arrest in Japan; particulate matter and CVD risk in China; and the effects of diesel exhaust on vascular function.
Fine particulate matter and cardiac arrest
As exposure to concentrations of fine particulate matter and gaseous pollutants increased above the Japanese daily median, the risk for same day out-of-hospital cardiac arrest rose as well, according to research published in Lancet: Planet Health.
Researchers found that for every 10 μg/m³ increase in concentration of fine particulate matter, defined as particulate matter with diameter 2.5 μm or smaller (PM2.5), above the median Japanese levels (11.98 μg/m³), the risk for all-cause out-of-hospital cardiac arrest increased on the same day (OR = 1.016; 95% CI, 1.009-1.023) and at lags of up to 3 days (OR at 1 day = 1.015; 95% CI, 1.008-1.022; OR at 0 to 3 days = 1.033; 95% CI, 1.023-1.043). Investigators observed similar results for cardiac out-of-hospital cardiac arrest (OR at 1 to 2 days = 1.016; 95% CI, 1.007-1.025]; OR at 0 to 3 days = 1.034; 95% CI, 1.021-1.047).
Moreover, patients aged older than 65 years were more susceptible to PM2.5 exposure than younger patients, but no sex differences were identified, according to the study.
“We could expect further health gains in the areas which satisfy the WHO air quality standard if we can improve our air quality more,” Kazuaki Negishi, MD, PhD, head of discipline of medicine at the Nepean Clinical School at the University of Sydney, told Healio. “We demonstrated independent associations between short-term exposure to PM2.5 and out-of-hospital cardiac arrest, even at relatively low concentrations, even lower than Australian and WHO standards (25 μg/m3), where inconsistency in the effects existed among previous reports, especially at lower concentrations,”
In other findings, carbon monoxide (CO), photochemical oxidants (Ox) and sulfur dioxide (SO2) were also associated with out-of-hospital cardiac arrest while nitrogen dioxide (NO2) was not. After analysis using two-pollutant models of PM2.5 and gaseous pollutant exposure however, only PM2.5 and NO2 were independently associated with increased risk for out-of-hospital cardiac arrest.
“This study has by far the largest sample size of 249,372 cases, approximately three times as many as the total number of out-of-hospital cardiac arrests reported in preceding articles, with world-standard quality data from Japan,” Negishi said in an interview. “The large sample size allowed us to identify a higher-risk population, ie, the elderly who are more than 65 years old.”
Researchers linked prospectively collected population-based registry data for out-of-hospital cardiac arrest in Japan from 2014 through 2015, to daily PM22.5, CO, NO2, Ox and SO2 exposure on the day of cardiac arrest (lag 0) or 1 to 3 days prior (lags 1 to 3), as well as average exposure across days 0 to1 and days 0 to3. Exposure was measured using monitoring stations in the same prefectures as the cardiac arrests.
“Several future research projects are planned to elucidate more precise mechanisms and insights between air pollution and cardiovascular disease in order to mitigate or prevent these effects,” Negishi told Healio. “Based on other groups and our data, it is fair to say there is no safe threshold. Thus, regulatory standards and targets need to incorporate the potential health gains from continual air quality improvement even in locations already meeting WHO standards.”
PM 1 and CVD risk
Researchers in China assessed the link between particulate matter of a diameter less than 1 μm (PM1) and found that each 10 μg/m3 increase in the PM1 above the mean 37 μg/m3 was associated with a 0.19% (95% CI, 0.09-0.28) increase in risk for non-accidental mortality, according to a study published in Environmental Science and Technology Letters.
Moreover, the risk for CVD increased to 0.29% (95% CI, 0.12-0.47) for every 10 μg/m3 above mean levels. According to the study, this increase in risk for CVD was significantly higher in PM1 compared with PM2.5 and PM10 exposure.
“To our knowledge, this is the first study to provide estimates of PM1 with related cause-specific mortality risk in nationwide scale in China,” Zhaomin Dong, of the school of space and environment and the Beijing Advanced Innovation Center for Big Data-Based Precision Medicine, Beihang University, Beijing, China, told Healio. “However, this pilot study is a population-based cross-sectional study, some mechanism supports are required from further cohort studies and animal studies.”
The study was performed from 2014 through 2017 and assessed PM1 levels in 65 cities across China.
“Two following studies are planned, including one to simulate how much PM deposit in the lung, bronchus and other organs in multiple cities and then to address the influence from various size-fractioned PM on cause-specify mortality,” Dong said in an interview. “Another will be done to conduct cohort or follow-up studies to support prior notions.”
Diesel emissions and vascular function
Compared with exposure to filtered air, exposure to diesel exhaust fumes for a 2-hour session conferred decreased flow-mediated dilation and increased pulse wave velocity and augmentation index for as long as 24 hours after exposure (P < .001 for all).
According to findings published in the European Journal of Preventive Cardiology, in the study of 40 healthy participants, diesel exhaust exposure also impaired the standard deviation of normal to normal R-R intervals compared with filtered air (P = .007).
“After 2 hours of breathing polluted air, study participants showed the first steps of cardiovascular disease and the effects lasted for 24 hours,” Dimitris Tousoulis, MD, PhD, FACC, FESC, of the National and Kapodistrian University of Athens, Greece, said in a press release. “To avoid permanent harm, we had to keep pollution levels in the study under safe limits, implying that even ‘safe’ levels may be devastating to health when frequently repeated, as occurs in city dwellers.”
In other findings, C-reactive protein and fibrinogen levels were significantly elevated following diesel exhaust exposure while levels of protein C and protein S activity decreased (P < .01 for all).
Moreover, researchers observed that exposure to diesel exhaust fumes also conferred significantly elevated C-reactive protein concentration, particularly in smokers compared with nonsmokers (P < .001).
“Our study provides insights into the mechanisms by which diesel exhaust fumes heighten cardiovascular risk,” Tousoulis said in the release. “The damaging effects shown in this research are likely to multiply with repeated, and for some people lifelong, exposure to high levels of diesel exhaust fumes in cities, heavy traffic, road tunnels, enclosed garages and on large highways. More efficient public health measures are needed to improve air quality in cities and prevent needless heart attacks and strokes.” – by Scott Buzby
References:
Tousoulis D, et al. Eur J Prev Cardiol. 2020;doi:10.1177/2047487319898020.
Yin P, et al. Environ Sci Technol Lett. 2020;doi:10.1021/acs.estlett.9b00735.
Zhao B, et al. Lancet Planet Health. 2020;doi:10.1016/S2542-5196(19)30262-1.
Disclosures: The authors report no relevant financial disclosures.
Editor's Note: This article was updated on Feb. 3, 2020, to correct instances of a missing micro- notation. The editors regret the error.
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Tousoulis D, et al. Eur J Prev Cardiol. 2020;doi:10.1177/2047487319898020.
Yin P, et al. Environ Sci Technol Lett. 2020;doi:10.1021/acs.estlett.9b00735.
Zhao B, et al. Lancet Planet Health. 2020;doi:10.1016/S2542-5196(19)30262-1.