Theoretical equilibration time is supported by measurement study of residence time at dilution sampling on fine particulate matter emissions from household biofuel burning

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Kaiqiang Yang ◽  
Zihao Wang ◽  
Yan Xie ◽  
Philip K. Hopke ◽  
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Abstract Background The effects of ambient fine particulate matter (PM 2.5 ) exposure on blood pressure have been widely reported. However, there remains uncertainty regarding the underlying roles of particulate matter components. We aimed to investigate the association between ambient PM 2.5 exposure and blood pressure, as well as the potential mediating effects of trace metal(loid)s, in a repeated-measurement study that enrolled women of childbearing age. Methods Our study included 35 participants from Hebei Province, China, each of whom was visited five times. During each visit, questionnaire surveys were conducted, blood pressure was measured, and blood was collected. The daily PM 2.5 exposure for all participants was estimated according to their residential addresses using a spatiotemporal model that combined monitoring data with satellite measurements and chemical-transport model simulations. This model was used to calculate average PM 2.5 concentrations 1, 3, 7, 15, 30, and 60 days prior to each visit. Serum concentrations of various trace metal(loid)s were measured using an inductively coupled plasma-mass spectrometer. A linear mixed-effects model was used to investigate associations among study variables. Results PM 2.5 concentration was positively associated with both systolic and diastolic blood pressures, with or without adjustments for potential confounders. Likewise, PM 2.5 concentration was positively associated with serum concentrations of manganese and arsenic, and negatively associated with serum concentrations of nickel, tin, and chromium. Only the serum concentration of molybdenum was negatively associated with systolic blood pressure. Conclusion Ambient PM 2.5 exposure may contribute to elevated blood pressure, potentially by interfering with internal metal(loid) intake in the human body.


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