Improving local air quality in cities: to tree or not to tree?

Vegetation is often quoted as an effective measure to mitigate urban air quality problems. In this work we demonstrate by the use of computer models that the air quality effect of urban vegetation is more complex than implied by such general assumptions. By modelling a variety of real-life examples we show that roadside urban vegetation rather leads to increased pollutant concentrations than it improves the air quality, at least locally. This can be explained by the fact that trees and other types of vegetation reduce the ventilation that is responsible for diluting the traffic emitted pollutants. This aerodynamic effect is shown to be much stronger than the pollutant removal capacity of vegetation. Although the modelling results may be subject to a certain level of uncertainty, our results strongly indicate that the use of urban vegetation for alleviating a local air pollution hotspot is not expected to be a viable solution.

Studies on the adaptive response in mouse female germ cells X-irradiated in vitro at two different stages of maturation.

BACKGROUND: Radioadaptation is a phenomenon whereby cells exposed to a low dose of ionizing radiation are more resistant to a much higher dose delivered some time thereafter. This phenomenon could result from the activation of damage repair and/or antioxidant defense systems by the low dose. MATERIALS AND METHODS: The existence of a cytogenetic adaptive response in female germ cells was investigated using a recently developed in vitro system. Mouse ovarian follicles were cultured from an early preantral stage up to ovulation. The follicles were X-irradiated with either 2 or 4 Gy ("challenge dose") preceded or not by 50 mGy ("conditioning dose", 5 h earlier), on days 0 or 12 of the culture. Ovulated oocytes were collected on day 13, fixed and analyzed for the presence of chromosome aberrations. RESULTS: Irradiation with 2 or 4 Gy on days 0 or 12 did not influence ovulation but had dose-dependent effects on the germinal vesicle breakdown of the oocytes. It also caused dose-dependent chromosome damage, with a greater sensitivity of oocytes to this effect when irradiation occurred on day 12 than on day 0. Prior irradiation of oocytes with the dose of 50 mGy led to a reduction in the yield of chromosome aberrations when irradiation occurred on day 12 but not on day 0. CONCLUSION: These results suggest that pre-irradiation of mouse pre-ovulatory oocytes with a low conditioning dose could confer on them some protection against radiation-induced chromosomal damage by a subsequent challenge dose of a few Gy.

Developmental abnormalities induced by X-irradiation in p53 deficient mice.

In order to assess the influence of p53 inactivation on radiation-induced developmental effects, male mice heterozygous for the wild-type p53 allele (mimicking the human Li-Fraumeni syndrome) were crossed with C57BL females, and their heterozygous p53+/- progeny were mated with each other to obtain p53+/-, p53-/- and p53+/+ embryos. Pregnant females were X-irradiated with 0.5 Gy on days 1 (pre-implantation period), 8 or 11 (organogenesis period) of gestation. Dissection of the pregnant females occurred on day 19 of gestation. The p53 genotype of the foetuses was determined by PCR from small pieces of soft tissues. Exencephaly was the only external malformation found in the control group. It affected essentially p53-/- female foetuses. A number of p53+/- and p53+/- control foetuses also showed dwarfism, or underdevelopment. In the group irradiated on day 1, the frequency of abnormal foetuses was, paradoxically, lower than that found in the control group. As in that group, exencephaly and dwarfism constituted the only anomalies that were found. Exencephaly affected only homozygous p53-/- females, while dwarfism concerned either p53-/- or p53+/- foetuses, with a majority of females. Irradiation on day 8 of gestation induced a significant increase in the frequency of abnormal foetuses, compared to the control group. Various malformations were observed in addition to exencephaly, including gastroschisis, polydactyly, cephalic oedema and cleft palate. All malformed foetuses were either homozygous p53-/- or heterozygous p53+/- while most affected foetuses were females, as was the case for dwarf individuals. Irradiation on day 11 did not cause an increase in the frequency of abnormal foetuses, in comparison with the controls. However, a large spectrum of external malformations was again noticed, as in the group irradiated on day 8. All affected foetuses were homozygous p53-/- and there were slightly more abnormal females than males (3 out of 5). No dwarfs were found in this group. Overall, these results confirm the importance of the p53 tumour-suppressor protein for normal embryonic development. They clearly show that homozygous p53-/- (or heterozygous p53+/- to a lesser extent) foetuses are more at risk for radiation-induction of external malformations during the organogenesis period, and that the risk of developing such malformations is much higher for females than for males. In contrast to results published very recently by others, we found that malformed foetuses resulting from an X-irradiation with a low-dose during the highly sensitive period of gastrulation are able to survive to birth.