Associations between particle physicochemical characteristics and oxidative capacity:: An indoor PM10 study in Beijing, China

A study was undertaken to determine the use of a plasmid DNA scission assay to evaluate the causal relationships between particle oxidative capacity and physico-chemistry. Field emission scanning electron microscopy (FESEM), image analysis (IA) and inductively coupled plasma-mass spectrometry (ICP-MS) were employed to investigate the physicochemical characteristics of indoor PM10 (particulate matter with an aerodynamic diameter of 10 mu m or less) in Beijing, China. Six PM10 samples (indoor smoker's living room; indoor non-smoker's living room and kitchen; and outdoor Beijing city; winter versus summer) were selected to represent typical indoor Beijing PM10 environments that contain high particle mass. The PM10 collected from a kitchen and two smoker's homes had the lowest TD50 (toxic dosage of PM10 causing 50% plasmid DNA damage), being as low as 45 mu g ml(-1) (kitchen) and 100 mu g ml(-1) (living room), which suggests a high oxidative capacity, with the PM10 generated in kitchens appearing to be the most toxic. The indoor PM10 from the non-smoker's home and outdoor PM10 samples demonstrated high TD50 values and were deemed less bioreactive (i.e. caused limited DNA damage). FESEM observations revealed that four types of particle species were prevalent in Beijing indoor PM10; soot aggregates, minerals, coal fly ash and unknown tine particles. IA showed that higher percentages of soot and unknown fine particles were associated with the lower TD50 values, suggesting that soot and the unknown fine particles may be important components responsible for the observed plasmid DNA damage. The water-soluble trace elements were negatively correlated with the TD50 values, implying that the DNA damage may be attributed to the water-soluble fraction of the PM10. Water-soluble zinc revealed the best relationship with the TD50 values than other analyzed elements, signifying it may play a role in driving the oxidative damage. (C) 2007 Published by Elsevier Ltd.