In the present study, we found that joint higher prenatal exposure to fine particulate matter and postnatal ETS doubled the risk of eczema symptoms occurring at any point in the first year life. From the other perspective, our findings have shown that a higher maternal fish intake in pregnancy had a protective effect on the risk and frequency of infantile eczema. The adjusted preventive effect of fish consumed in pregnancy could only be demonstrated at the higher level of fish intake (>205 g/week), which may suggest a threshold below which the preventive effect is irrelevant. To our knowledge, there have been no other studies that have considered the effects of prenatal exposure to fine particles and postnatal ETS on infantile eczema in the context of the preventive effect of maternal fish intake.
Fish intake during pregnancy may have potential benefits for healthy fetal development as it is a rich source of long-chain polyunsaturated fatty acids (PUFAs), including eicosapentaenoic and docosahexaenoic acids, which are necessary for the healthy development of fetal tissues. PUFAs are important constituents of cells, where they play a role in membrane protein function, maintenance of membrane fluidity and regulating gene expression and cellular function [31
]. In addition, there is evidence that PUFAs can modulate immune responses affecting the production of key inflammatory cytokines and the Th1 versus Th2 balance, thereby exerting beneficial effects in a variety of inflammatory diseases such as allergic diseases, asthma, atherosclerosis-related cardiovascular diseases or psoriasis. A number of molecular mechanisms have been postulated to explain how PUFAs could interfere with immune cell function [33
]. Alternatively, fish intake may be a marker of some other maternal or infantile characteristics not considered in our study that are associated with the healthy development of babies (for instance quality of maternal care, other nutritional factors or housing).
The biological mechanisms whereby prenatal PM2.5
might cause infantile eczema are still unclear. Ambient fine particulate matter contains a whole complex of toxic agents that could adversely affect fetal development. Typically, the PM2.5
fraction contains constituents of soot including polycyclic aromatic hydrocarbons (PAHs), tobacco and wood smoke, traffic exhaust containing organic compounds, sulfates and metals [40
]. Transplacental exposure to PAHs from maternal inhalation can produce cytotoxic reactive oxygen species that ultimately induce inflammatory and oxidant stress responses [41
], cause disruptions to the endocrine system and lead to disturbances of the pituitary-adrenocortico-placental system [42
]. Formation of PAH adducts may induce the activation of apoptosis [43
] or the binding to receptors of placental growth factors [44
], resulting in the decreased exchange of oxygen and nutrients and possibly enhancing the production of IgE antibodies and Th2 cytokines. It may be hypothesized that postnatal exposure of infants to environmental pollutants may strengthen the effect of the prenatal exposure to fine particulate matter, possibly by damaging the infantile skin barrier function and the postnatal development of new skin cells.
Some weakness in our study could have resulted from the possible maternal reporting bias of the medical diagnosis of skin disorders in the children under study; however, a differential bias in reporting a medical diagnosis of eczema between the exposed and nonexposed infants is not likely to occur since the children being compared did not differ in terms of maternal education and access to medical care. Our data on fish consumption were based on the FFQ method, which is useful for ranking individuals but does not necessarily permit confident assessments of absolute intake. The FFQ method can be subject to systematic errors in reporting, and therefore our results must be interpreted cautiously. Moreover, the portion sizes were not weighed but approximated, and information on the type of fish consumed by the study participants was not collected.
On the other hand, the major strength of our study is the fact that the study sample of infants belonged to a low-risk group recruited from an urban community. However, the birth cohort differed from the broader population in several respects as the study excluded women with conditions that could have affected the health of the babies, such as active maternal cigarette smoking, multiple pregnancy or preexisting chronic diseases. One strength of our study is the careful prospective monitoring of eczema symptoms by regular interviews performed at 3-month intervals, as well as the accurate personal prenatal exposure assessments of fine particulate matter and ETS exposure in the perinatal period, which had not been taken into account in previous studies on infantile eczema. Our assessment of total personal individual exposure to fine particulate pollutants included all potential sources of exposure during pregnancy, both indoors and outdoors.
In conclusion, our findings indicate that high prenatal exposure to fine particulate matter combined with postnatal exposure to ETS may increase the risk of infantile eczema, while maternal fish intake in pregnancy may reduce the risk of infantile eczema. If replicated, the results of this study may have important preventive implications for the health of babies and older children as well.