Feb 23, 2012

Pollutants and Tobacco Smoke

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

Allergen Exposure

Exposure to environmental allergens is the most extensively studied potential risk factor for sensitization and manifestation of atopy and asthma. From a number of cross-sectional studies performed in children and adults, it has become obvious that there is a close association between allergen exposure, particularly in the domestic environment, and sensitization to that specific allergen. Longitudinal studies such as the MAS (Multicenter Allergy Study) study in Germany have clearly demonstrated that during the first years of life there is a dose–response relationship between indoor allergen exposure to dust mite and cat allergens and the risk of
sensitization to cat and mites, respectively.

As far as the manifestation of atopic dermatitis and asthma are concerned, the situation is much less clear. Early studies performed by Sporik suggested that exposure of sensitized children to dust mite allergens determines not only the risk of asthma but also the time of the onset of the disease. More recent investigations by the same group, however, suggest that other factors besides allergen exposure are important in determining which children develop asthma.
In a comprehensive meta-analysis, evaluated several environmental factors said to be responsible for the incidence and severity of atopic diseases, particularly asthma. After comparing the strengths of the various effects, she concluded that on the basis of the literature, indoor allergen exposure is the environmental component with by far the strongest impact on the manifestation of asthma. In recent years, however, the paradigm that exposure induces asthma with airway inflammation via sensitization has been challenged. In several countries, the prevalence of asthma in children has been increasing independent of allergen exposure.

Data sets obtained from the MAS birth cohort suggest that while domestic allergen exposure is a strong determinant for early sensitization in childhood, it cannot be The Allergy Epidemic: A Look into the Future considered as a primary cause of airway hyper-responsiveness or asthmatic symptoms, since during the first 3 years of life the manifestation of wheeze is not related to elevated serum IgE levels or specific sensitization. Studies following up birth cohorts to adolescence have recently indicated that 90% of children with wheeze but without atopy lose their symptoms at school age and retain normal lung function in puberty. By contrast, sensitization to perennial allergens (house dust mites, cats, and dogs) developing in the first 3 years of life was associated with a loss of lung function at school age. Concomitant exposure to high levels of perennial allergens early in life aggravates this process. Such exposure also enhances the development of airway hyper-responsiveness in sensitized children with wheeze.
From these data, it can be concluded that impairment of lung function during school age is determined by continuing allergic airway inflammation beginning in the first 3 years of life.

A number of intervention studies to examine the effects of indoor allergen elimination on the incidence of asthma are currently being performed in cohorts followed prospectively from birth. The results will have a strong impact on public health policies because they will determine whether considering indoor allergen elimination as an important element of primary prevention of various atopic manifestations is meaningful. Even if the result is that other factors play major parts in determining whether an atopic child will develop asthma, so that allergen elimination as a measure of primary prevention is inefficient, reduction of allergen exposure will still remain as a very important element in secondary prevention.