Abstract
Inhalation of fine particulate matter PM(2.5)-bound arsenic (PM(2.5)-As) may cause significant cardiovascular damage, due to its high concentration, long transmission range, and good absorption efficiency in organisms. However, both the contribution and the effect of the arsenic exposure pathway, with PM(2.5) as the medium, on cardiovascular system damage in nonferrous smelting sites remain to be studied. In this work, a one-year site sample collection and analysis work showed that the annual concentration of PM(2.5)-As reached 0.74 μg/m(3), which was 120 times the national standard. The predominant species in the PM(2.5) samples were As (V) and As (III). A panel study among workers revealed that PM(2.5)-As exposure dominantly contributed to human absorption of As. After exposure of mice to PM(2.5)-As for 8 weeks, the accumulation of As in the high exposure group reached equilibrium, and its bioavailability was 24.5%. A series of animal experiments revealed that PM(2.5)-As exposure induced cardiac injury and dysfunction at the environmental relevant concentration and speciation. By integrating environmental and animal exposure assessments, more accurate health risk assessment models exposed to PM(2.5)-As were established for metal smelting areas. Therefore, our research provides an important scientific basis for relevant departments to formulate industry supervision, prevention and control policies.