Cardiac autonomic dysfunction from occupational exposure to polycyclic aromatic hydrocarbons

Abstract

Objectives Polycyclic aromatic hydrocarbons (PAHs) exposures have been associated with cardiopulmonary mortality and cardiovascular events. This study investigated the association between a biological marker of PAHs exposure, assessed by urinary 1-hydroxypyrene (1-OHP), and heart rate variability (HRV) in an occupational cohort of boilermakers. Methods Continuous 24-hour monitoring of the ambulatory electrocardiogram (ECG) and pre and post shift urinary 1-OHP were repeated over extended periods of the work week. Mixed effects models were fit for the 5-minute standard deviation of normal-to-normal intervals (SDNN) in relation to urinary 1-OHP levels pre and post workshift on the day they wore the monitor, controlling for potential confounders. Results We found a significant decrease in 5-min SDNN during work of −13.6% (95% confidence interval, −17.2% to −9.8%) for every standard deviation (0.53 microgram/gram [μg/g] creatinine) increase in the next-morning pre-shift 1-OHP levels. The magnitude of reduction in 5-min SDNN were largest during the late night period after work and increased with every standard deviation (0.46 μg/g creatinine) increase in post-shift 1-OHP levels. Conclusion This is the first report providing evidence that occupational exposure to PAHs is associated with altered cardiac autonomic function. Acute exposure to PAHs may be an important predictor of cardiovascular disease risk in the work environment.

A community study of the effect of polycyclic aromatic hydrocarbon metabolites on heart rate variability based on the Framingham risk score

“…Our results agree with epidemiological evidence from previous occupational studies, which found that occupational PAH exposure was linked to a significant dose-dependent decrease in HRV indices 5 6. However, our findings showing a significantly stronger and consistent pattern for SDNN, LF and LF/HF relative to PAH metabolites suggested that the three HRV indices might be a better indicator to capture the cardiac effects of PAH metabolites in the general population.…”

“…Xu et al 1 36 found that the metabolites of fluorene and phenanthrene were more likely associated with self-reported cardiovascular diseases and peripheral arterial disease using NHANES, but it is far from clear what role ΣOHFlu and ΣOHPh play in contributing to reduction in HRV. The direct neurocardiac toxicity of PAH on cardiac ion channels, blood and lung receptors, and indirect effects mediated through oxidative stress or inflammation may be other potential mechanisms 5 37 38…”

“…Due to the short half-lives of PAH, information provided by biomonitoring of urinary OH-PAH is limited to recent exposure 3 4. Recent studies, including those from our lab,5 6 found that occupational exposure to PAH is associated with decreased cardiac autonomic function, as assessed by heart rate variability (HRV), which is one of the major mechanistic pathways for adverse cardiac events. However, very little is known about adverse effects of background, enduring environmental exposure to PAH on HRV in the general population.…”

Oxidative stress and systemic inflammation as modifiers of cardiac autonomic responses to particulate air pollution

“…Nighttime may be a better time to investigate the cardiovascular effects of environmental pollutants because HRV is less influenced by potential confounders such as physical activity and mental stress. Several epidemiological studies have observed larger effects of environmental toxic pollutants including PM 2.5 and polycyclic aromatic hydrocarbons (PAHs) on HRV, especially during the night [4, 5]. Increased risk of stroke is associated with nighttime HRV, but not with 24-hr HRV in healthy individuals [6].…”

Urinary 1-hydroxypyrene in occupationally-exposed and non-exposed individuals in Silesia, Poland

“…Among those mentioned on the IARC ( [a,h]anthracene are the most prominent [3]. Direct harmful health effects of PAHs, such as PAHs-DNA adducts, chromosomal aberrations, cardiac dysfunction, neurotoxic effects or cancers are well documented [2,4,5]. Intake of PAHs happens through inhalation or dermal and gastrointestinal routes [2].…”