In our study, passive smoking and exposure to traffic-related air pollution, both in utero life and in the first year of life, and dampness were found to be risk factors for various asthma phenotypes in the first year of life, while contact with cats and domestic wood heating were found to be protective against asthma in the first year of life. Some studies had observed the effects of air pollutants and related sources that we considered in our study. Results of the SIDIRA-2 study (Italian Studies on Respiratory Disorders in Children and the Environment-2nd phase) had showed that passive smoking, high traffic and dampness were risk factors for asthma in children aged 6–7 years . Our data further support the associations in the first year of life.
Evidence for the association between asthma and prenatal and postnatal parental smoking is fairly consistent [10, 28–30]. Recently, a systematic review of prospective studies published between 1997 and February 2011 indicated that both prenatal maternal smoking and postnatal maternal smoking were associated with wheezing in the first 2 years of life (OR = 1.41 (95% CI: 1.19-1.67) and OR = 1.70 (95% CI: 1.24-2.35), respectively) . In our study, prenatal maternal smoking had a greater impact on childhood asthma than postnatal heavy parental smoking. This could be explained by the fact that the proportion of prenatal maternal smoking (25%) is higher than that of heavy parental smoking in the last 12 months (13%) in our population. Notably, results of a recent French national prenatal survey showed that 24% of women smoked during pregnancy , which is in agreement with our data. Furthermore, compared to postnatal passive smoking, prenatal maternal smoking is more likely to reduce respiratory function after birth , which would consequently have a greater impact on the development of asthma.
The association between asthma and traffic-related air pollution has been well documented in the literature [21, 27, 33–37], but few studies have investigated the association between traffic-related air pollution and asthma in the first year of life. In a previous case–control study in 5 French metropolitan areas, results indicated that traffic related pollutants might be associated with the incidence of asthma in children aged 0–3 years old . In our study, results showed that there were robust associations between in utero and first year of life exposure to traffic-related air pollution and asthma phenotypes in the first year of life. Furthermore, the impact of traffic-related air pollution on asthma phenotypes in the first year of life was greater than that of other risk factors even after adjustment for potential confounders, which is consistent with the results of the SIDIRA-2 study previously described . One asset of our study is that we used Google Earth® and traffic volume provided by local authorities at mothers’ address to check the validity of the subjectively measured exposure to traffic and thus minimise the exposure misclassification. The subjectively measured variable of traffic-related air pollution showed high concordance with the Google Earth®-derived variable, with up to 92% of children were well classified. Only 5% of the children whose mother reported traffic-related air pollution were not exposed according to the Google Earth®-derived variable, whereas 3% of the children that did not declare to be exposed were exposed according to this objectively assessed variable. Some studies have compared the subjectively measured exposure to traffic with objectively assessed exposures, implying that both have their own advantages and no method could be per se considered as the gold standard . In the USA, Gauderman et al. reported that the simple and widely available indicator of the distance between living house and freeway was as strongly and precisely associated with childhood asthma as were more complex objective estimates based on dispersion models .
Interestingly, our data further confirmed the findings from previous studies having related bronchiolitis to passive smoking  and air pollution [40, 41]. This is important in terms of public health because bronchiolitis is an important phenotype of asthma in early life .
More consistently, several investigations showed a positive association between dampness and asthma, although very few have considered it in the first year of life. In the DRIAS study (Respiratory Symptoms in children and the Environment in Sardegna, Italy), results showed that exposure to dampness during the first year of life was associated with increased prevalence of current wheeze for primary school children (OR = 1.96; 95% CI: 1.34-2.88) . Similarly, a more recent review implied that dampness was the risk factor for respiratory and allergic health in birth cohorts . However, because of recall bias in the case of questionnaire investigation, the relationship between dampness in the last 12 months and asthma phenotypes in the first year of life needs to be further confirmed. Contrarily to other investigations , we did not find any relationship between exposure to house dust mite and the prevalences of asthma phenotypes, probably because the sources (carpets, or glazing, or curtains) we considered were not sufficient.
Our data showed that contact with cats in the last 12 months may be protective against asthma in the first year of life. This is in agreement with previous studies . A potential mechanism was proposed by Platts-Mills et al. who indicated that contact with cats could induce IgG and IgG4 antibody responses, which is protective against the development of asthma .
In our study, domestic wood heating in the last 12 months was found to be negatively associated with asthma phenotypes in the first year of life. Among other authors, Kilpeläinen et al. investigated the association between early life exposure to wood stove heating and subsequent asthma development, results showed that a farm environment was the main confounding factor for the association between wood stove heating and asthma . However, in the present study, the associations between domestic wood heating and asthma phenotypes were not confounded by the rural environment. This is in agreement with the fact that in France wood begins to be widely used for heating even in the urban and peri-urban settings because of its low cost. In addition, it is publicly supported in terms of tax reductions.
The major limitation of our study is that exposures and health outcomes were assessed by questionnaires, without objective assessments. However, our data collection was prospective and the mothers replied for well-standardised questionnaires that were previously validated. In addition, our findings are consistent with those of other studies conducted in other Western European countries and based on questionnaire investigation [14, 36, 37]. Another limitation of our study is that the exposure to risk factors was assessed simultaneously with asthma outcomes except for prenatal maternal smoking and in utero exposure to traffic-related air pollution. Therefore, the causal link implied by our study should be interpreted with caution. Lastly, the questions for assessing in utero and first year of life exposure to traffic-related air pollution were different (as showed in Table 1). This is because, after the survey time point of at birth, in order to take results from recent studies into account [46, 47], we modified the questionnaire and assessed distances of the dwellings to major road, and in particular the 200 m circular buffer with which a risk of asthma had been associated. As a consequence, responses for in utero and first year of life exposure to traffic were not exactly comparable. In addition, the response rates varied from one survey to the other. Indeed, for some mothers, it was difficult to figure out the exact circular buffer and there were more missing values for the variable of first year of life exposure to traffic-related air pollution than for the variable of in utero exposure to traffic-related air pollution. Notably, some mother-child pairs changed their residences after the birth of the child. However, in spite of these differences, the associations between asthma phenotypes and the exposure to traffic-related air pollution in utero life and in the first year of life are consistent.
The strength of our investigation lies in the fact that the sample is large and drawn from the general population and that we use standardised instruments for the assessment of both exposure and asthma phenotypes. The fact that our investigation focuses on the first year of life which is crucial for the development of asthma using the data of a birth cohort constitutes an added value. In addition, we used different models to analyse the relationships between asthma outcomes and in utero and first year of life exposures respectively, taking into account the temporal sequence in relation to asthma outcomes. We also considered the potential confounders and effect modifiers in the models to show the independent effects of exposures in utero life and in the first year of life. Lastly, several asthma phenotypes covering a large spectrum of asthma outcomes in early childhood were included thus reducing misclassification of asthmatic cases.