Our study included a group of local women of childbearing age in northern China; multiple follow-ups were conducted to explore the potential involvement of serum metal(loid)s in the relationship between PM2.5 and blood pressure. Overall, systolic and diastolic blood pressures were positively associated with ambient PM2.5 exposure after adjustments for important confounders. In addition, serum concentrations of the metal(loid)s Mn, Ni, Sn, Cr, and As were associated with PM2.5 exposure. However, with the exception of Mo, no significant associations were observed between serum concentrations of the other metal(loid)s and blood pressure. In general, our results indicate that PM2.5 pollution may have adverse effects on blood pressure in adult women; these effects may be mediated by the intake of various metal(loid)s.
Our study mainly focused on women of childbearing age and demonstrated the potential adverse effects of PM2.5 on blood pressure in this population. The study area experiences relatively high PM2.5 pollution. The average outdoor PM2.5 concentration over the five visits was > 100 µg/m3, which is significantly higher than the national annual standard of 75 µg/m3 in China. Furthermore, this concentration is higher than concentrations observed in other provinces in China, as well as concentrations observed in the USA, Brazil, and the Netherlands [27, 28, 29, 30, 31, 32]. We found that PM2.5 was positively associated with both systolic and diastolic blood pressures after adjustments for the main confounders, with or without including ambient temperature. Similar results were also obtained in a cross-sectional study of 39 million adults of childbearing age in China [33]. To the best of our knowledge, there have been few other studies regarding the effects of PM2.5 on blood pressure in women of childbearing age. The associations between PM2.5 exposure and systolic and diastolic blood pressures have been widely reported for other populations, but the results of these studies have been inconsistent. Some studies indicated that ambient PM2.5 exposure was positively associated with both systolic and diastolic blood pressures [6, 34], whereas others reported that PM2.5 exposure was only positively associated with systolic blood pressure [35, 36, 37, 38]. A number of studies have also found that PM2.5 exposure was not significantly associated with either systolic or diastolic blood pressures [27, 30, 39]. This inconsistency could have multiple sources, such as study design, PM2.5 exposure level, sample size, and participant characteristics. Our study had a repeated-measurement design, which involved five visits. In most other repeated-measurement studies, the participants received two to four visits [36, 40, 41]. Likewise, in previous studies, the intervals between surveys were shorter than 2 weeks [42, 43]; in our study, the intervals between surveys were several months in length. PM2.5 concentrations fluctuated greatly between any two consecutive visits. Hence, we were able to investigate the effects of PM2.5 exposure on blood pressure in the study population, as well as any lag effects related to PM2.5 exposure. For example, the difference in PM2.5 concentrations between the first and third surveys was > 100 µg/m3, which is much larger than the changes reported in other repeated-measurement studies [40, 43]. However, our study included only 35 women; thus, the study had fewer participants than other similar studies. This may have affected the reliability of the dose-response analysis.
Both organic and inorganic components of PM2.5 may contribute to the adverse effects of PM2.5 on blood pressure. Polycyclic aromatic hydrocarbons, organic constituents of PM2.5, are reportedly not significantly associated with the risk of hypertension [44, 45]. Thus, our study focused mainly on inorganic metal(loid) components, because their associations with blood pressure are well-known [19, 20]. In northern China, metal elements comprise a large proportion of PM2.5 [9, 10, 11]. Inhalable particulate matter may be an important exposure route by which many metals enter the body [46]. Therefore, it is important to investigate how the inorganic components of PM2.5 affect blood pressure stability. Here, we found that PM2.5 concentration was significantly correlated with some serum metal(loid)sࣧpositively with serum Mn and As, and negatively with serum Ni, Sn, and Cr. Our previous study revealed that indoor air pollution level was associated with hair metal(loid) concentrations (positively with As and Pb, and negatively with Ni, Sn, Cr, and Co) in women in Shanxi Province, China [12]. However, a study conducted in Wuhan did not find any significant associations between urinary metal contents and PM2.5 exposure [25]. The relationships between PM2.5 exposure and internal metal(loid) concentrations can vary with location, PM2.5 concentration, lifestyle, exposure biomarkers, and other factors. Compared with other biomarkers, serum metal(loid)s can indicate recent exposure (days) in a population and have been used as exposure biomarkers in previous studies [47, 48]. Although diet is the main intake route for various metal(loid)s [46], it was not considered in our study. Hence, additional in-depth studies are needed to confirm our findings.
Toxicity patterns associated with nutrients and toxic metals vary. For essential trace metals, toxic effects usually occur when their exposure levels are above or below their acceptable ranges. For toxic metals, toxic effects on blood pressure usually increase linearly with their exposure concentrations, especially when the exposure levels are above threshold levels [16, 19]. Our study findings indicate that PM2.5 may interfere with the balance of trace elements in the body by enhancing the levels of toxic metals and reducing the levels of nutrient elements. However, we did not find a strong relationship between serum metal(loid)s and blood pressure. Possible explanations are that the serum concentrations of various metal(loid)s do not represent long-term exposure levels, or that they are subject to lag effects, which were not investigated in our study. Another explanation is that PM2.5 may induce blood vessel injuries via other pathways, such that the effects of internal metal(loid) intake are negligible. To the best of our knowledge, there is little evidence that internal metal(loid) intake contributes to the association between PM2.5 and blood pressure. Further research is needed to clarify the results obtained in this study.
Our study had two important limitations. First, the metal(loid) contents in outdoor PM2.5 were not measured, and the quantities inhaled by the participants could not be determined. Second, the effects of dietary foods were not considered. However, we were able to reveal the impact of PM2.5 on blood pressure and the potential involvement of metal(loid)s. PM2.5 concentrations during our study period were relatively high and varied greatly over the five visits; thus, we could investigate the effects of high levels of PM2.5 exposure on blood pressure. Because we adopted a repeated-measurement design, we effectively reduced the influences of some confounding factors. Furthermore, by collecting serum samples, we were able to characterize population internal exposure to PM2.5.