Int. J. Environ. Res. Public Health 2012, 9 282 prevalence of air conditioning reduces O3 exposure) and differences in the pollution mix (e.g., negative correlation with primary combustion components). There could be two explanations to the overall effect of early and mid-gestation NO2 concentrations. One explanation is that there is no effect; the other is that we fail to catch important variability in exhaust exposure during the first and second trimester as we were unable to take into account spatial variation in exposure. However, in the Californian studies there was spatial resolution in the exposure data, still they found no or weak indications of an adverse effect of early gestation exposure to higher ambient NO2 levels [3,5]. The observation of an adverse association of exposure to higher NO2 levels during the last period of gestation has been observed in several studies [3-5,9,13]. There have also been observations of a effect of exposure to higher NO2 levels during the last part of pregnancy [10]. The correlations between NO2 and other pollutants, such as particles, may differ between the different study locations. All season-specific estimates of exposure to higher O3 levels during the first trimester were associated with an elevated risk of preterm delivery and a shorter duration of gestation, although the association with preterm birth was slightly weaker for conceptions in autumn than for conceptions during any other season. This strengthens our belief that there seems to be a negative effect of early gestation exposure to O3 on the duration of the gestational period. The season-specific findings are not in accordance with the findings of Jalaludin et al., who found statistically significant positive associations with O3 levels during the first trimester for women who conceived during spring or summer [10]. The association with O3 levels we found is robust in that we observe the effect regardless of whether we study duration of gestation or preterm delivery. The pathway by which we believe O3 may cause preterm delivery is through oxidative stress. Oxidative stress caused by exposure to air pollution may lead to inflammatory response in the respiratory system [30]. Expression of proinflammatory cytokines could disrupt trophoblast invasion during the formation of the placenta [13,31]. This could lead to preeclampsia, which is an important predictor of preterm birth. Alternatively systemic oxidative stress may affect the embryo at the earliest phase of development, which may cause intra-uterine growth retardation or preterm birth [32]. Exposure to air pollution in a later stage of gestation may cause disturbances in cord blood flow or increased susceptibility for maternal infections, which may cause premature rupture of membranes leading to an earlier birth [5]. We have shown that although the air pollution level is moderate in Sweden there is an association between exposure to air pollution during pregnancy and reduction of gestational age. Our results support the observation that there is some seasonality in the association with air pollution. Further studies are needed to find out more about these associations and possible mechanisms. How important are these effects of moderate air pollution from a public health point of view? A comparison with smoking shows that the impact of air pollution must be taken seriously. 6.5% of the mothers (7,520) were heavy smokers with a prevalence of preterm birth of 6.76% compared to 4.84% preterm among non-smoking mothers. This corresponds to 144 preterm births attributed to heavy smoking. The estimated attributable fraction preterm births associated with heavy smoking was 2.1%. 10.6% of the mothers were moderate smokers with a prevalence of preterm birth of 5.36%, and 64 preterm births attributed to moderate smoking. The adjusted ORs (heavy smoking 1.37, moderate smoking 1.12) would give similar numbers. The upper quartile of first trimester O3 exposure has a mean value of 27.7 μg/m3 over the lowest quartile, which corresponds to an OR of 1.18. The fraction