Could bronchial asthma be an endogenous, pulmonary expression of retinoid intoxication?
Asthma has become a major public health problem, affecting about 17 million people in the United States, including 4.8 million children. A striking increase in asthma and other forms of atopy has occurred in children in the U.S. and other western countries during the past 30 years. Several studies have reported an inverse association between childhood infectious illness and the development of atopy, suggesting that certain forms of infection protect against and even inhibit asthma. This may involve a shift in the balance of CD4 T lymphocyte helper cells from a Th2 to a Th1-type cytokine profile. However, the underlying mechanisms remain uncertain. Based on a review of the literature, it is conjectured that in the absence of certain types of childhood infection, retinoids (vitamin A and its congeners) accumulate in the lung. Later, upon exposure to known triggers for asthma, retinoid metabolites may be produced in such high concentration that they produce an acute, localized form of retinoid intoxication, recognized as status asthmaticus.