Emission of polycyclic aromatic hydrocarbons, toxicity, and mutagenicity from domestic cooking using sawdust briquettes, wood, and kerosene.

Abstract

Smoke samples, in both gas and particulate matter (PM) phases, of the three domestic stoves were collected using U.S. EPA modified method 5 and were analyzed for 17 PAH (HPLC-UV), acute toxicity (Microtox test), and mutagenicity (Amestest). The gas phase of smoke contributed > or = 95% of 17 PAH, > or = 96% of toxicity, and > or = 60% of mutagenicity. The highest emission factor of 17 PAH was from sawdust briquettes (260 mg/kg), but the highest emission of 11 genotoxic PAH was from kerosene (28 mg/kg). PM samples of kerosene smoke were not toxic. The total toxicity emission factor was the highest from sawdust, followed by kerosene and wood fuel. Smoke samples from the kerosene stove were not mutagenic. TA98 indicated the presence of both direct and indirect mutagenic activities in PM samples of sawdust and wood fuel but only direct mutagenic activities in the gas phase. TA100 detected only direct mutagenic activities in both PM and gas-phase samples. The higher mutagenicity emission factor was from wood fuel, 12 x 10(6) revertants/kg (TA100-S9) and 3.5 x 10(6) (TA98-S9), and lower from sawdust, 2.9 x 10(6) (TA100-S9) and 2.8 x 10(6) (TA98-S9). The low burning rate and high efficiency of a kerosene stove have resulted in the lowest PAH, toxicity, and mutagenicity emissions from daily cooking activities. The bioassays produced toxicity and mutagenicity results in correspondence with the PAH content of samples. The tests could be used for a quick assessment of potential health risks.