The prevalence of asthma has increased constantly in recent decades 1 2 3 and different factors have been implicated in its aetiology. Although genetic factors are important determinants of asthma 4 , exposures to certain environmental factors play an essential role in the phenotypic expression of this condition 5 6 thus contributing substantially to the risk of its development 7 .

The strength of evidence for the associations between exposures to various air pollutants and the development of childhood asthma is diverse 8 . Robust data casually related asthma to allergens including aero-allergens such as house dust mite 9 . Studies consistently demonstrated that Environmental Tobacco Smoke (ETS) increases the risk of asthma in children 10 11 12 . Other investigations showed an independent effect of dampness and moulds on the development of childhood asthma 13 14 , although some investigations argued that the relationship may be partly explained by reporting bias 15 . Reversely, a protective effect was suggested for early life exposure to pets 16 17 , exposure to domestic wood heating and rural living 18 . In contrast with initial findings 19 , recent investigations, including birth cohort studies, have indicated a link between exposure to outdoor air pollution and subsequent asthma development 20 21 22 . Indoor air pollutants have also been related to asthma 23 , but there is a lack of longitudinal data in this respect.

The aim of our study is to investigate the impacts of exposures to passive smoking, traffic-related air pollution, dampness, visible moulds, bleaching agents, house dust mites, pets and domestic heating on the development of asthma in the first year of life, which is a period of life when the lung is still developing. For passive smoking and traffic-related air pollution, in utero exposures were taken into account to better understand the development of childhood asthma. The health outcomes we considered in this study included both single and multi-dimensional asthma phenotypes at 0–4 months, 4–8 months, and 8–12 months respectively as well as their evolution during the first year of life. To this extent, we used data from a birth cohort to study the impacts of the in utero and first year of life exposures on asthma phenotypes in the first year of life.

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 27 . 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 29 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) 30 . 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 31 , 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 32 , 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 34 35 36 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 37 . 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 27 . 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 38 . 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 34 .

Interestingly, our data further confirmed the findings from previous studies having related bronchiolitis to passive smoking 39 and air pollution 40 41 . This is important in terms of public health because bronchiolitis is an important phenotype of asthma in early life 42 .

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) 14 . Similarly, a more recent review implied that dampness was the risk factor for respiratory and allergic health in birth cohorts 43 . 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 9 , 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 17 . 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 44 .

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 45 . 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.

In our study, asthma outcomes in the first year of life were found to be positively related to maternal smoking, traffic-related air pollution and dampness, but negatively associated with contact with cats and domestic wood heating. Furthermore, in utero exposures to passive smoking and traffic-related air pollution were both related to the development of asthma phenotypes in the first year of life. After adjusting for potential confounders, traffic-related air pollution had a greater impact on the development of asthma phenotypes compared to other factors. Interventional studies need to be implemented to evaluate the consequences of the avoidance or the promotion of these factors.

Written informed consent was obtained from all participating women for publication of this report and any accompanying images.

OR: Odds ratio; aOR: Adjusted odds ratio; aPAR: Adjusted Population Attributable Risk; BMI: Body mass index; SD: Standard deviation; NO2: Nitrogen dioxide; PM10: Particulate matter with an aerodynamic diameter below 10 μm.

The authors declare that they have no competing interests.

IAM conceived the study. NB and IAM participated in the data collection. CZ performed statistical analysis and data interpretation with the assistance of NB and SB. CZ wrote the manuscript with the co-supervision of IAM and TZ. All authors read and approved the final manuscript.