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Benzo(ghi)perylene and benzo(a)pyrene/show~'~he highest concentrations of all 7/PAH in
the air and in the dust collected from kitchens and living rooms (Tab. 2 and 3). The' ratio of
the PAHs ~hlghly constant for all homes regardless of emission source or situations, for
which air dust collection took place (Tab. 5).
Frying, boiling, and steaming of f~d~ncreas~'PAH levels in air and dust of kitchens ~ab.
6 to 8).
Water heaters operated in the kitchen for up to 90 mini24 h are claimed to almost half the
levels of PAH in dust (Tab.8), and kitchen window ventilating fans ~_~e claimed to reduce
PAH levels both in air and dust (Tab. 9).
Burning of religious incense increase,,,d" PAH levels in dust and air of living rooms and
kitchens (Tab.8 and 12).
• The claimed decrease in air or dust PAH with cigarette smoking may not be
The claimed decrease in kitchens refers to 4 out of 33 homes, where smoking
occured. In 3 cases 1 to 5 cigarettes, and in 1 case 6 cigarettes were reported to be
smoked within the 24-hour sample collection period. The decrease in air
concentration was approx. 15 %, that in dust concentration up to 40%. These
decreases are statistically insignificant.
The claimed tendency that with more ETS, PAH levels rise per cubic meter air but
decrease per mg dust refer to 8 living rooms, where smoking occured. The
concentration of the total PAH in air is reported to be increased up to 30% (claimed
to be stat. not significant) but that of airborne dust decreased a,~Eprox, by 10% with
smoking of 3 to 11 cigarettes during 24 hours (Tab. 1 ~).~,These data require
verification with a higher number of samples. Repetitive determinations in the same
homes would have improved the significance of the data.
The "compensation behaviour hypothesis" does not explain the observed
increase and decrease of PAH air and dust concetrations reported for rooms with
Behavioural responses such as increasing ventilation to perceived air pollution
(e.g. claimed distinct smell of ETS) are proposed by the authors to explain the
reported decrease of airborne PAH levels (p.414/415). It is difficult to imagine,
however, how such stimulated increased ventilation could result in an increase of
air PAH concentration with simultaneous decrease of dust PAH concentration as
claimed for the living rooms with smoking.
The absence of results of determinations of the airborne particle concentration
(e.g."RSP-conc~"),and of outdoor PAH levels are limitations of the study.
RSP data would strengthen the analytical results and facilitate the interpretation
of air vs. dust PAH concentrations.