Baiqi Chen, Wenlou Zhang, Yahong Chen, Chen Zhao, Zhihong ZHANG, Shurun Li, Li Zhao, Liqiong Guo, Masayuki Shima, Yoshiko Yoda, S. Felix Wu, Xinbiao Guo, Furong Deng
Background About half of patients with chronic obstructive pulmonary disease (COPD) have hypertension, which significantly worsens prognosis. Yet its critical environmental drivers and vulnerable phenotypes remain unclear. Objectives To evaluate associations between size-fractionated particulate matter (PM) and blood pressure, assess differential effects by hypertension status and identify susceptible individuals by smoking and inflammatory phenotypes. Methods In this prospective panel study, 82 patients with COPD (42 with hypertension) completed 281 clinical visits. Personal exposure to ambient inhalable PM (PM 10 ), fine PM (PM 2.5 ) and ultrafine particles (UFPs) of 0–7 days was estimated using infiltration factors and time-activity patterns. Inflammatory phenotypes were defined by blood neutrophils and eosinophils. Linear mixed-effect models were applied to evaluate blood pressure changes associated with PM. Results UFPs and PM 2.5 , rather than PM 10 , were significantly associated with increased systolic blood pressure (SBP), whereas diastolic blood pressure (DBP) and pulse pressure showed non-significant changes. The effects appeared earlier after UFP exposure (lag 03d) than PM 2.5 exposure (lag 06d), with central responses exceeding brachial responses. Notably, hypertensive individuals exhibited stronger responses to UFPs and PM 2.5 exposure, in whom significant elevations were observed in both SBP and DBP. Stratification by smoking status revealed no evidence of effect modification. Comparatively, individuals with an eosinophilic, instead of neutrophilic, phenotype showed heightened susceptibility to PM 2.5 -related and UFP-related blood pressure increases, particularly in those with hypertension. Conclusions Small-sized PM is an important risk factor for blood pressure elevations in patients with COPD, especially among those with hypertension and an eosinophilic inflammatory phenotype. Trial registration number NCT05076630 .