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.

Highlights The killed oral ETEC vaccine ETVAX ± dmLT adjuvant was safe in Bangladeshi adults. All vaccinees responded to all 5 primary vaccine antigens in ALS specimens. A majority of vaccinees responded to ≥4 antigens in plasma specimens. A sensitive electrochemiluminescence assay was established for small sample volumes. ALS responses measured by electrochemiluminescence and ELISA assays correlated well.

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Since conflicting results have been reported on non-specific immune response in type 1 diabetes, this study evaluates polymorphonuclear neutrophil (PMN) functions in the infection free Long Evan diabetic rats (type 1) by using tests that include: polarization assay, phagocytosis of baker\'s yeasts (Saccharomyces cerevisiae) and nitroblue tetrazolium (NBT) dye reduction. Polarization assay showed that neutrophils from diabetic rats were significantly activated at the basal level compared to those from the controls (p < 0.001). After PMN activation with N-formylmethionyl-leucyl-phenylalanine (FMLP), control neutrophils were found to be more polarized than those of the diabetic neutrophils and the highest proportions of polarization were found to be 67 % and 57 % at 10(-7) M FMLP, respectively. In the resting state, neutrophils from the diabetic rats reduced significantly more NBT dye than that of the controls (p < 0.001). The percentages of phagocytosis of opsonized yeast cells by the neutrophils from control and diabetic rats were 87 % and 61 %, respectively and the difference was statistically significant (p < 0.001). Evaluation of the phagocytic efficiency of PMNs revealed that control neutrophils could phagocytose 381 +/- 17 whereas those from the diabetic rats phagocytosed 282 +/- 16 yeast cells, and the efficiency of phagocytosis varied significantly (p < 0.001). Further, both the percentages of phagocytosis and the efficiency of phagocytosis by the diabetic neutrophils were inversely related with the levels of their corresponding plasma glucose (p = 0.02; r = -0.498 and p < 0.05; r = -0.43, respectively), which indicated that increased plasma glucose reduced the phagocytic ability of neutrophils. Such relationship was not observed with the control neutrophils. These data clearly indicate that PMN functions are altered in the streptozotocin (STZ)-induced diabetic rats, and hyperglycemia may be the cause for the impairment of their functions leading to many infectious episodes.

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This study conducted in Bangladesh reports the relationship of clinical complications with nutritional status and the prevalence of leukopenia among arsenic exposed patients living in the rural villages. A total of 115 exposed individuals diagnosed as arsenicosis patients were randomly selected from four known arsenic endemic villages, and age-matched 120 unexposed subjects were enrolled in the study program. The duration of arsenic exposure in about 37% of the patients was at least 10 yrs, while the population mean and range were 7.6 ± 5.2 yrs, and 1 -25 yrs, respectively. The mean arsenic concentrations in the drinking water for the exposed and unexposed (control) population were 218.1 µg/L and 11.3 µg/L, respectively. The spot urine sample of the arsenicosis patients contained an average of 234.6 µg/L arsenic. Although very few patients showed elevated WBC count, 16% had leukopenia (below normal count), and the whole population had significantly low WBC count than the control subjects. Prevalences of neutropenia and lymphocytosis were observed in patients with chronic exposure to high levels of arsenic in water. The body mass index was found to be lower than 18.5, the cut-off point for malnutrition (underweight), in about 28% of the arsenicosis cases compared to 15% of the controls. The monthly income and total calorie consumption per day showed the patients were underprivileged than the controls. Arsenical symptoms and complications were more severe in the nutritionally vulnerable (underweight) patients than the overweight ones. Also, the incidences of leukopenia and anaemia were more common in the female patients who were underweight. The findings of this research demonstrate that the poor nutritional status of patients increases the complications of chronic arsenic toxicity; suggest the possibility of other sources of arsenic contamination different from drinking water in the study area; and establish a higher prevalence of leukopenia and lymphocytosis in arsenicosis patients.

An estimated 40 million people in Bangladesh have been suffering from arsenic toxicity-related diseases because of drinking water contamination with high levels of naturally occurring arsenic. To evaluate the biochemical changes in chronic arsenic exposure, a total of 115 exposed subjects diagnosed as arsenicosis patients were examined and interviewed, and 120 unexposed volunteers were enrolled in this study. Drinking water, urine and peripheral blood samples were collected from all participants and analyzed. The average levels of arsenic in the drinking water and spot urine samples of the arsenicosis patients were 218.18g/L and 234.68g/L, respectively, and duration of exposure was 7.6 ± 5.2 yrs that ranged from 1-25 yrs. Prevalence of diabetes mellitus among chronic arsenic-exposed subjects was about 2.8 times higher than the unexposed subjects. The activities of alkaline phosphatase were significantly elevated in the patients, 197 U/L compared to 149 U/L in the controls, but alanine transaminase and aspartate transaminase were mostly normal. The patients had significantly lower levels of serum creatinine, 0.97 mg/dL compared to 1.15 mg/dL in the controls; but had significantly elevated levels of total protein, 84 g/L and 77 g/L respectively. The mean level of inorganic phosphate in the serum of arsenicosis patients was 6.4 mg/dL compared to 4.6 mg/dL in the unexposed subjects and the level was significantly higher, indicating substitution of the pentavalent arsenate for the phosphate ion causing underutilization of the latter. Evaluation of the lipid profiles showed while the levels of triacylglycerol were not much different, the patients had significantly lower levels of cholesterol, HDL-cholesterol and LDL-cholesterol compared to the unexposed subjects. These findings suggest significant changes in biochemical parameters in human arsenic toxicity.