The Etiologies, Pathophysiology, and Alternative/Complementary Treatment of Asthma

Alternative Medicine Review, Feb, 2001 by Alan L. Miller

Indoor and Outdoor Air Pollution

An increase in inhaled particulate matter, whether from cigarette smoking, environmental tobacco smoke, fossil fuels, or wood burning stoves can exacerbate asthma symptoms. Recent animal research reveals secondhand smoke up-regulates the Th2 immune response. This mechanism might partially explain epidemiological evidence linking second-hand smoke with asthma prevalence.[71] Use of gas appliances in the home can increase the concentration of nitrogen dioxide in inspired air, correspondingly reducing lung function. Volatile organic compounds and formaldehyde in the indoor environment, from off-gassing of paints, adhesives, furnishings, and building materials can also increase the risk of asthma attacks. An excellent review of the subject of asthma and the home environment can be found in Jones' recent article in the Journal of Asthma.[31]

Does Heavy Metal Toxicity Promote Inflammation in Asthma?

Lead and mercury toxicity has been shown in animal studies to inhibit Th1 cells and stimulate a Th2 immune response and, in some animals, promote autoimmune diseases.[11,72] In humans, if heavy metals were proven to cause an imbalance in the normal Th1:Th2 ratio, it would explain practitioner reports of improvements in asthma symptoms after heavy metal detoxification.

Gastroesophageal Reflux: a Possible Connection

Another possible contributor to the etiology of asthma is gastroesophageal reflux (GER). An increased incidence of GER has been noted in asthma patients;[73,74] however, it is not fully understood if these conditions simply overlap, if GER causes or exacerbates asthma, or if asthma causes GER. In his 2000 review, Sontag[74] estimates that approximately 75 percent of asthmatic patients experience GER symptoms, 80 percent have abnormal acid reflux, 60 percent have a hiatal hernia, and 40 percent have esophageal damage (erosions or ulcerations). Two mechanisms have been proposed to explain how GER might cause asthma symptoms: (1) a vagal-mediated reflex from the irritated esophagus to the lung, causing reflex bronchoconstriction, or (2) microaspiration of gastric acid, causing pulmonary irritation, injury, and subsequent overproduction of mucus.

Proponents of the vagal reflex theory note that the esophagus and lungs share the same embryonic tissue and innervation. An irritated esophagus could, therefore, initiate a vagal reflex, resulting in increased bronchial reactivity.[74-79] Animal and human studies have shown increased pulmonary airway resistance with esophageal acid infusion. This bronchoconstriction was reversed with antacid therapy[80] or surgical interruption of the vagus nerves.[74] In a small study of pediatric asthma (n=9), acid was infused into the esophagus during sleep, causing bronchoconstriction only in the four children with previously diagnosed esophagitis (positive Bernstein test). These results led the researchers to comment that reflux, an irritated esophagus, and a low nocturnal threshold to bronchoconstrictive stimuli were all necessary for reflux to cause bronchoconstriction. It is interesting to note that, in this study, acid did not cause bronchoconstriction during a midnight infusion, but did in the 4-5 a.m. infusion.[78] In a study of 47 adults (20 asthmatics with reflux, 7 without, 10 participants with GER, and 10 controls) esophageal acid infusion caused a significant decrease in PEF in all participants; however, the group of asthma patients with reflux had a greater decrease in PEF, as well as further deterioration after the acid was cleared with normal saline. The authors stated that since there was no microaspiration of acid, a vagally mediated reflex must be involved.[77] Subsequent studies found increased vagal responsiveness in patients with asthma and GER; this was blocked by atropine, which inhibits vagal stimulation.[81,82]