The influence of long-range transported Saharan dust on the inflammatory potency of ambient PM_2.5 and PM₁₀

Although desert dust promotes morbidity and mortality, it is exempt from regulations. Its health effects have been related to its inflammatory properties, which can vary between source regions. It remains unclear which constituents cause this variability. Moreover, whether long-range transported desert dust potentiates the hazardousness of local particulate matter (PM) is still unresolved. We aimed to assess the influence of long-range transported desert dust on the inflammatory potency of PM_2.5 and PM₁₀ collected in Cape Verde and to examine associated constituents. During a reference period and two Saharan dust events, 63 PM_2.5 and PM₁₀ samples were collected at four sampling stations. The content of water-soluble ions, elements, and organic and elemental carbon was measured in all samples and endotoxins in PM₁₀ samples. The PM-induced release of inflammatory cytokines from differentiated THP-1 macrophages was evaluated. The association of interleukin (IL)-1β release with PM composition was assessed using principal component (PC) regressions. PM_2.5 from both dust events and PM₁₀ from one event caused higher IL-1β release than PM from the reference period. PC regressions indicated an inverse relation of IL-1β release with sea spray ions in both size fractions and organic and elemental carbon in PM_2.5. The PC with the higher regression coefficient suggested that iron and manganese may contribute to PM_2.5-induced IL-1β release. Only during the reference period, endotoxin content strongly differed between sampling stations and correlated with inflammatory potency. Our results demonstrate that long-range transported desert dust amplifies the hazardousness of local air pollution and suggest that, in PM_2.5, iron and manganese may be important. Our data indicate that endotoxins are contained in local and long-range transported PM₁₀ but only explain the variability in inflammatory potency of local PM₁₀. The increasing inflammatory potency of respirable and inhalable PM from desert dust events warrants regulatory measures and risk mitigation strategies.