Asthma and COPD are two chronic inflammatory disorders of the airway characterized by airflow limitation. While many similarities exist between these two diseases, they are pathologically distinct due to the involvement of different inflammatory cells; predominantly neutrophils, CD8 lymphocytes in COPD and eosinophils and CD4 lymphocytes in asthma.

Cigarette smoking is associated with accelerated decline of lung function, increased mortality, and worsening of symptoms in both asthma and COPD. Furthermore, exposure to cigarette smoke can alter the inflammatory mechanisms in asthma to become similar to that seen in COPD with increasing CD8 cells and neutrophils and may therefore alter the response to therapy.

Cigarette smoke exposure has been associated with a poor response to inhaled corticosteroids which are recommended as first line anti-inflammatory medications in asthma and as an add-on therapy in patients with severe COPD with history of exacerbations. While the main proposed mechanism for this altered response is the reduction of the histone deacetylase 2 (HDAC2) enzyme system, other possible mechanisms include the overexpression of GR-β, activation of p38 MAPK pathway and increased production of inflammatory cytokines such as IL-2, 4, 8, TNF-α and NF-Kß.

Few clinical trials suggest that leukotriene modifiers may be an alternative to corticosteroids in smokers with asthma but there are currently no drugs which effectively reduce the progression of inflammation in smokers with COPD. However, several HDAC2 enhancers including low dose theophylline and other potential anti-inflammatory therapies including PDE4 inhibitors and p38 MAPK inhibitors are being evaluated.

OBJECTIVE: Sandstorms frequently cause adverse health effects especially in patients with asthma. The aim of our research was to explore the mechanism of sandstorm-induced asthmatic exacerbation by administering dust aerosol through an environmentally controlled exposure chamber.

METHODS: Four samples of soil (Ganganagar clay, Bikaner sand, Jaipur sand, and Ganganagar sand) were collected from three sandstorm-prone areas of Rajasthan, the desert state of India. Twenty patients with asthma, who had stable disease with a forced expiratory volume in first second (FEV(1)) more than 70% of predicted, volunteered to participate in this randomized single-blind placebo-controlled crossover study. The four samples of dust and placebo were administered randomly on 5 study days. FEV(1) was measured for the next 60 minutes and the maximal decline in FEV(1) (ΔFEV(1)) from baseline was measured. The samples of dust were also analyzed for particle size and adhesiveness.

RESULTS: The maximal decline in FEV(1) was observed 15 minutes post-exposure with all dust samples. Mean ΔFEV(1) was 0.69 ± 0.08 liters for Ganganagar clay, 0.52 ± 0.06 liters for Bikaner sand, 0.39 ± 0.07 liters for Jaipur sand, and 0.32 ± 0.04 liters for Ganganagar sand dust aerosol samples. Decline in FEV(1) correlated with volume of dust particles with size <10 μm (PM(10)) and adhesiveness of the dust particles.

CONCLUSION: Smaller-size sandstorm dust particles with higher adhesive properties have a greater potential of aggravating asthma.