Eksponering for ultrafine partikler fra trafikken i København

Summary and conclusions

The purpose of this study is to assess person's exposure to ultrafine particles (UFP) during activities in Copenhagen as pedestrians, cyclists or as car drivers (driving in different street configurations) and to estimate the occurrence of DNA damage as a measure of biological effect related to the exposure.

The concentration of UFP is measured by breathing zone sampling with portable particle counters carried by the subjects. The breathing zone concentration is referred to as exposure and cumulated exposure (dose) is defined as exposure multiplied by time. In addition, the PM2.5 concentration (fraction of particles with diameters less than 2.5μm) is measured during car driving in different street configurations. These measurements are compared to air pollution and metrological measurements from stationary stations situated in street level and at 20 meters height (referred to as urban background).

Due to large inter- and intra-person variations in DNA damage level each of the 15 subjects is acting as her or his own control on experimental days with expected high exposure to traffic generated UFP during bicycling compared to days with low exposure. Since physical work, like bicycling, influences the DNA-damage level, the effect of bicycling has to be controlled. Consequently the study design for bicyclist's exposure to traffic generated UFP is chosen as:

Bicycling in traffic and exposure to traffic generated UFP (5 experimental days),

Bicycling on an ergometer bicycle in the laboratory and no (low) UFP exposure (one experimental day),

No bicycling and no (low) UFP exposure (2 experimental days).

The pulmonary ventilation is increased during physical work and then also the number of inhaled and deposited UFP. This increased deposition is estimated from the increased ventilation during bicycling compared to the pulmonary ventilation during rest or low activity.

The average personal UFP exposure, as geometric mean concentration, during rush hour bicycling in Copenhagen is 32.4•103 particles per cubic centimetre compared to an average indoor concentration of 14.1•103 particles per cubic centimetre.

The Comet method is applied to quantify the occurrence of DNA damage in lymphocytes from a blood sample delivered from each subject the morning after each experimental day.

The subjects DNA damage level is significantly elevated on traffic bicycling days compared to laboratory bicycling days. A linear model of DNA damage level by adjusted cumulated UFP exposure contains significant contributions from both outdoor and indoor exposure. The DNA damage level associated with outdoor cumulated exposure to UFP is almost 3 times higher than the level associated with the same indoor cumulated exposure.

Besides exposure measurements during bicycling in Central Copenhagen, exposure has been measured during travelling in 3 different street configurations:

  • High population density districts in Copenhagen (high traffic intensity, high buildings),
  • Radial roads (high traffic intensity, low buildings),
  • Residential neighbourhood (low traffic intensity, low buildings).

For convenience travelling by car was used in this part of the study.

The UFP concentrations is of order 50•103 particles per cubic centimetre during rush hour car driving at workdays in radial roads and in high population density districts in Copenhagen. The UFP concentrations changes follow the expected changes in traffic intensity, because lower concentrations have been measured at weekend days and in residential neighbourhood.

The PM2.5 concentration variations are not connected to traffic intensity changes, but are probably influence by metrological conditions. This is in agreement with the fact that the PM2.5 fraction mainly consist of long range transported particles.

In conclusion the association between exposure to traffic generated UFP and low level DNA damage as effect is described in a simple linear model. One further result of the study is the developed new method for assessment of personal UFP exposure based on breathing zone sampling. As part of the method, the influence of physical activity on UFP pulmonary deposition is accounted for by estimation of a pulmonary deposition proxy. Presently the proxy is based on the individual relation between physical work and measured heart rate.

 



Version 1.0 Maj 2005, © Miljøstyrelsen.