Short-term effects of ambient air pollution and outdoor temperature on biomarkers of myocardial damage, inflammation and oxidative stress in healthy adults

Abstract

The mechanisms whereby ambient air pollution and temperature changes promote cardiac events remain incompletely described. Seventy-three nonsmoking healthy adults (mean age 23.3, SD 5.4 years) were followed with up to four repeated visits across 15 months in Beijing in 2014-2016. Biomarkers relevant to myocardial damage (high-sensitivity cardiac troponin I [hs-cTnI]), inflammation (growth differentiation factor-15 [GDF-15]), and oxidative stress (8-hydroxy-2'-deoxyguanosine [8-OHdG]) were measured at each visit, while ambient air pollution and temperature were monitored throughout the study. Linear mixed-effects models coupled with distributed lag nonlinear models were used to assess the impacts of each exposure measure on study outcomes. During follow-up, average daily concentrations of fine particulate matter and outdoor temperature were 62.9 µg/m³ (8.1-331.0 µg/m³) and 10.1 °C (-6.5°C to 29.5°C). Serum hs-cTnI levels were detectable in 18.2% of blood samples, with 27.4% of individuals having ≥1 detectable values. Higher levels of ambient particulates and gaseous pollutants (per interquartile range) up to 14 days before clinical visits were associated with significant alterations in hs-cTnI levels of 22.9% (95% CI, 6.4, 39.4) to 154.7% (95% CI, 94.4, 215.1). These changes were accompanied by elevations of circulating GDF-15 and urinary 8-OHdG levels. Both low (5th percentile, -2.5 °C) and high (95th percentile, 24.8°C) outdoor temperatures, with breakpoint at ~13.0°C as the reference level, were also associated with elevations of hs-cTnI levels. Short-term exposure to ambient air pollution and temperature was associated with cardiac troponin, a biomarker of myocardial damage, along with increased inflammation and oxidative stress responses. These findings extend our understanding of the biological mechanisms linking pervasive environmental exposure to adverse cardiac events.

Keywords: Air pollution; Cardiac troponin; Myocardial damage; Temperature.

Figure 1.

Percent changes in circulating hs-cTnI levels associated with IQR increases in exposure to ambient air pollutants over cumulative lags of 0–13 days. Error bars indicate 95% confidence intervals. Significant associations (P-value < 0.05) are shown in red. The lagged association estimates were derived from linear mixed-effects models coupled with distributed lag non-linear models, with adjustments for body mass index, urinary cortisol, low-density lipoprotein cholesterol, season, ambient temperature, and RH. lag 0, averaged pollutant concentrations over the last 24 hours before each participant’s clinic visit; lag 0–1, 1 to 2 days; lag 0–2, 1 to 3 days and so on up to lag 0–13; PM_2.5, fine particulate matter; PNCx, particulate number concentrations in given size ranges (nm).

Figure 2.

Percent changes in circulating GDF-15 levels associated with IQR increases in exposure to ambient air pollutants over cumulative lags of 0–13 days. Error bars indicate 95% confidence intervals. Significant associations (P-value < 0.05) are shown in red. The lagged association estimates were derived from linear mixed-effects models coupled with distributed lag non-linear models, with adjustments for body mass index, urinary cotinine, season, ambient temperature, and RH. lag 0, averaged pollutant concentrations over the last 24 hours before each participant’s clinic visit; lag 0–1, 1 to 2 days; lag 0–2, 1 to 3 days and so on up to lag 0–13; PM_2.5, fine particulate matter; PNCx, particulate number concentrations in given size ranges (nm).

Figure 3.

Percent changes in urinary 8-OHdG levels associated with IQR increases in exposure to ambient air pollutants over cumulative lags of 0–13 days. Error bars indicate 95% confidence intervals. Significant associations (P-value < 0.05) are shown in red. The lagged association estimates were derived from linear mixed-effects models coupled with distributed lag non-linear models, with adjustments for sex, high-density lipoprotein cholesterol, day of week of clinical visits, season, ambient temperature, and RH. 8-OHdG, 8-hydroxy-2′-deoxyguanosine; lag 0, averaged pollutant concentrations over the last 24 hours before each participant’s clinic visit; lag 0–1, 1 to 2 days; lag 0–2, 1 to 3 days and so on up to lag 0–13; PM_2.5, fine particulate matter; PNCx, particulate number concentrations in given size ranges (nm).

Figure 4.

Exposure–response relationship curves (A–G) and the lag structures in the relative risks of hs-cTnI in low (5th percentile) and high (95th percentile) Temp exposures (H) over cumulative lags of 0–6 days. The black lines indicate mean effect estimates, and red regions are 95% confidence intervals. Blue reference line indicates the Temp breakpoints. The lagged association estimates of Temp are presented as relative risks (a 1°C change) of 5th percentile (−2.5°C) or 95th percentile (24.8°C) relative to the referent level (Temp breakpoint at lag 0–6, 13.0°C). Error bars indicate 95% confidence intervals. Significant associations (P-value < 0.05) are shown in red. All models were ran controlling the same covariates as the pollutant models but additional adjustments for corresponding exposure periods of fine particulate matter and O₃. lag 0, averaged levels of Temp over the last 24 hours before each participant’s clinic visit; lag 0–1, 1 to 2 days; lag 0–2, 1 to 3 days and so on up to lag 0–6.

Figure 5.

Exposure–response relationship curves (A–G) and the lag structures in the relative risks of 8-OHdG in low (5th percentile) and high (95th percentile) Temp exposures (H) over cumulative lags of 0–6 days. The black lines indicate mean effect estimates, and red regions are 95% confidence intervals. Blue reference line indicates the Temp breakpoints. The lagged association estimates of Temp are presented as relative risks (a 1°C change) of 5th percentile (−2.5°C) or 95th percentile (24.8°C) relative to the referent level (Temp breakpoint at lag 0–6, 3.0°C). Error bars indicate 95% confidence intervals. Significant associations (P-value < 0.05) are shown in red. All models were ran controlling the same covariates as the pollutant models but additional adjustments for corresponding exposure periods of fine particulate matter and O₃. 8-OHdG, 8-hydroxy-2′-deoxyguanosine; lag 0, averaged levels of Temp over the last 24 hours before each participant’s clinic visit; lag 0–1, 1 to 2 days; lag 0–2, 1 to 3 days and so on up to lag 0–6.