Other environmental factors have attracted the interest of epidemiologists and experimental researchers. Although they do not serve as allergens, these factors are capable of up-regulating existing IgE responses or leading to disease manifestation or aggravation of symptoms. Guinea pig and mouse experiments suggested an increase of allergic sensitization to ovalbumin after experimental exposure to trafficor industry-related pollutants. A strong association between allergic rhinitis caused by cedar pollen allergy and exposure to heavy traffic was reported in Japan.
Important sociodemographic confounders turned out to be problems in interpreting study results. Other investigators were unable to describe any relationship between traffic exposure and the prevalence of hay fever or asthma. The role of tobacco smoke, a complex mixture of various particles and organic compounds, was extensively studied.
Recent review studies consistently demonstrate that the risk of lower airway diseases such as bronchitis, recurrent wheezing in infants, and pneumonia is increased. Whether passive tobacco smoke exposure is causally related to the development of asthma is still disputed.
Until recently, data about the risk of sensitization have been lacking. The prospective birth cohort MAS in Germany suggests that an increased risk of sensitization is found only in children whose mothers smoked up to the end of their pregnancies and continued to smoke after childbirth. In this subgroup of the cohort, a significantly increased sensitization rate of IgE antibodies to food proteins, particularly to hen’s egg and cow’s milk, was observed during infancy.
The effect of environmental tobacco smoke exposure is particularly strong in families with susceptibility for atopy
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