RESUMO
We assessed the relationship between chronic arsenic exposure through drinking water with respiratory complications and humoral immune response by measuring serum immunoglobulin profiles in the affected subjects (arsenicosis patients) living in the arsenic endemic rural villages of Bangladesh. The duration of exposure was determined through detailed history of the patients (n=125) and the levels of arsenic in the drinking water and urine samples were determined. The mean duration of exposure in the patients was 7.4+/-5.3 y, and the levels of arsenic in the drinking water and urine samples were 216+/-211 and 223+/-302 micro g/L, respectively, compared to 11+/-20 and 29+/-19 microg/L, respectively, in the unexposed subjects. There was high prevalence of respiratory complications like breathing problems including chest sound, asthma, bronchitis and cough associated with drinking water arsenic toxicity. Arsenicosis patients had significantly elevated levels of IgG (P<0.001) and IgE (P<0.001) while the levels of IgA were also significantly higher (P<0.005) but IgM were similar to that of the control subjects. Analysis of the clinical symptoms based on skin manifestations showed the levels of both IgG and IgE were significantly elevated during the initial stages while IgE were further elevated with the duration of arsenic exposure. Arsenicosis patients with respiratory complications had mean serum IgE levels of 706+/-211 IU/mL compared to 542+/-241 IU/mL in patients without apparent involvement with the respiratory system (P<0.01). The eosinophil counts in the patients did not differ significantly from the unexposed subjects indicating that elevated levels of serum IgE might not be due to allergic diseases, rather it could be due to direct effects of arsenic. We found significant linear relationships between the levels of serum IgE and inorganic phosphorus (P<0.05), and serum IgA levels with urinary excretion of arsenic (P<0.001). These observations suggested that arsenic toxicity caused respiratory complications, induced changes in the humoral as well as mucosal immune responses.
