Background: Heavy metals, such as vanadium (V), chromium (Cr), cobalt (Co), cesium (Cs), and cadmium (Cd), constitute major environmental contaminants that aggravate both chronic obstructive pulmonary disease (COPD) and renal impairment. These stresses trigger oxidative stress, inflammation, and cellular damage, which are key factors in the progression of both conditions. Inhaled heavy metals damage the respiratory epithelium, reduce lung function, and worsen airway inflammation, worsening COPD symptoms and progression. At the same time, heavy metals build up in the kidneys because they help expel these toxins, leading to oxidative damage, inflammation, and kidney toxicity. Furthermore, previous research indicates that individuals experiencing acute exacerbations of chronic obstructive pulmonary disease (AECOPD) exhibit a significantly higher incidence and rate of acute kidney injury (AKI). Within our study cohort, patients diagnosed with COPD who encounter AKI during exacerbations tend to develop multiple comorbidities, thereby increasing the burden on health insurance resources and the capacity of the healthcare system. Furthermore, chronic kidney disease (CKD) is commonly observed among patients with COPD, with prevalence rates reaching as high as 43% in Taiwan. Methods: Our study, conducted in Kaohsiung, Taiwan, shows a unique global pattern of heavy metal pollution linked to PM2.5, steel production, and the petrochemical sector. A study involved 150 COPD patients from the area, with an average age of 66.8 years and a BMI of 25.5, reflecting a slightly overweight group. Exhaled Breath Condensate (EBC) offers a novel, noninvasive way to evaluate airway inflammation, which may also be associated with kidney impairment. By analyzing EBC and urine samples using advanced omics technologies, researchers assess biomarkers such as neopterin, IP-10, CRP, and KIM-1, a marker of kidney injury, and also profile metabolites. Results: Our data indicate that urinary concentrations of heavy metals differ significantly across groups categorized by heavy metal exposure levels (p < 0.05) in cases of renal dysfunction induced by chronic obstructive pulmonary disease (COPD). Specifically, cobalt (p=0.008), copper (p=0.038), and nickel (p=0.024) are markedly elevated in the urine samples of the cohort with COPD-related renal injury. In addition, our analysis stratified by zip code indicates that nickel (p=0.007) and manganese (p=0.005) also show significant increases in the COPD-renal injury group. Conclusion: Our study demonstrates that elevated urinary concentrations of heavy metals are significantly associated with pulmonary dysfunction and Increased symptom severity observed among patients with COPD. This underscores the critical role of heavy metal exposure in the progression of the disease and accentuates the necessity for targeted mitigation strategies. This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.
Kao et al. (Fri,) studied this question.
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