Illness resulting from acute exposure is usually not fatal although some exposure may cause bronchiolitis obliterans, pulmonary edema as well as rapid asphyxiation. If the concentration of exposure is excessively high, the gas may displace oxygen resulting in fatal asphyxiation.Generally, patients and workers should be educated by medical personnel on how to identify the signs and symptoms of Nitrogen dioxide poisoning. Farmers and other farm workers should be educated on the proper way of food grain storage to prevent silo fillers disease. Biochemical effects
Chronic exposure to high level of nitrogen dioxide results in the allosteric inhibition of glutathione peroxidase and glutathione S-transferase, both of which are important enzymes found in the mucous membrane antioxidant defense system, that catalyse nucleophilic attack by reduced glutathione (GSH) on non-polar compounds that contain an electrophilic carbon and nitrogen. These inhibition mechanisms generates free radicals that causes peroxidation from the lipids in the mucous membrane leading to increased peroxidized erythrocyte lipids, a reaction that proceeds by a free radical chain reaction mechanism that result in oxidative stress. The oxidative stress on the mucous membrane causes the dissociation of the GSTp-JNK complex, oligomerization of GSTP  and induction of the JNK pathway, resulting in apoptosis or inflammation of the bronchioles and pulmonary alveolus in mild cases. On migrating to the bloodstream, nitrogen dioxide poisoning results in an irreversible inhibition of the erythrocyte membrane acetylcholinesterase which may lead to muscular paralysis, convulsions, bronchoconstriction, the narrowing of the airways in the lungs (bronchi and bronchioles) and death by asphyxiation.
In harmony with the mycelium life cycle, incidence increases with periods of dryness after a rainy season; this phenomenon, termed "grow and blow", refers to growth of the fungus in wet weather, producing spores which are spread by the wind during succeeding dry weather. While the majority of cases are observed in the endemic region, cases reported outside the area are generally visitors, who contact the infection and return to their native areas before becoming symptomatic. North America
In the United States, C. immitis is endemic to southern and central California with the highest presence in the San Joaquin Valley. C. posadassi is most prevalent in Arizona, although it can be found in a wider region spanning from Utah, New Mexico, Texas, and Nevada. An estimated 150,000 infections occur annually, with 25,000 new infections occurring every year. The incidence of coccidioidomycosis in the United States in 2011 (42.6 per 100,000) was almost ten times higher than the incidence reported in 1998 (5.3 per 100,000). In area where it is most prevalent, the infection rate is 2-4%.Incidence varies widely across the west and southwest. In Arizona, for instance, in 2007, there were 3,450 cases in Maricopa County, which in 2007 had an estimated population of 3,880,181 for an incidence of approximately 1 in 1,125. In contrast, though southern New Mexico is considered an endemic region, there were 35 cases in the entire state in 2008 and 23 in 2007, in a region that had an estimated 2008 population of 1,984,356, for an incidence of approximately 1 in 56,695.