We examined the chemical composition and biological response associated with particulate emissions from the two largest cities in New Zealand, Auckland and Christchurch. The organic and water-soluble fractions were isolated from the particulate matter (PM). The organic fraction was examined for PAH content, direct mutagenicity, CYP1A1 induction, and cytotoxicity and TNF-alpha release in RAW264.7 macrophages. The water-soluble fraction was examined for metal content, and cytotoxicity and TNF-alpha release in RAW264.7 macrophages. Particulate, PAH and water-soluble metal concentrations were all higher in PM collected from Christchurch, being highest in May-July when woodburners for home heating are widely in use. In contrast, PM from Auckland showed the highest concentrations in March, but PAH and metal concentrations were highest in July. We found marked differences in the biological response elicited by ambient air PM: the organic extracts of Christchurch PM(2.5) and PM(10) showed higher mutagenicity and CYP1A1 induction compared with PM(10) from Auckland. In contrast, water-soluble extracts of Auckland PM were more cytotoxic and resulted in greater TNF-alpha release than those from Christchurch PM, although they had a lower metal content. The organic fraction of PM from both cities did not induce any cytokine release, and the organic extract from Auckland samples showed no cytotoxicity; smaller PM mass was available for testing for these samples. Biological responses typically occurred at lower doses of the organic extract, indicating that organic components may be more important in eliciting effects than water-soluble components. Preliminary apportionment of the biological responses to the dominant sources of PM in both cities-woodburners and vehicles-was undertaken. This indicated that for both cities, vehicles have a greater contribution to the direct mutagenic activity of ambient PM than woodsmoke, despite a lower contribution to ambient PM. In contrast, woodsmoke is estimated to have a greater contribution to CYP1A1 induction of ambient PM. The calculated activity forms only a small proportion of the activity observed in extracts of ambient PM from Christchurch, particularly for mutagenicity, and may indicate a significant influence of atmospheric transformation processes on biological response. Only data for mutagenicity and CYP1A1 activity could be used for apportionment as low and/or variable cytotoxicity or TNF-alpha release response were obtained for either the individual source or ambient PM at the doses tested. Further, in the case of the water-soluble extracts from Auckland, additional components are suggested to have a role in the observed activity.