Objectives-Exposure to arsenic causes keratosis, hyperpigmentation, and hyp
opigmentation and seemingly also diabetes mellitus, at least in subjects wi
th skin lesions. Here we evaluate the relations of arsenical skin lesions a
nd glucosuria as a proxy for diabetes mellitus.
Methods-Through existing measurements of arsenic in drinking water in Bangl
adesh, wells with and without arsenic contamination were identified. Based
on a questionnaire, 1595 subjects greater than or equal to 30 years of age
were interviewed; 1481 had a history of drinking water contaminated with ar
senic whereas 114 had not. Time weighted mean arsenic concentrations and mg
-years/l of exposure to arsenic were estimated based on the history of cons
umption of well water and current arsenic concentrations. Urine samples fro
m the study subjects were tested by means of a glucometric strip. People wi
th positive tests were considered to be cases of glucosuria.
Results-A total of 430 (29%) of the exposed people were found to have skin
lesions. Corresponding to drinking water with <0.5, 0.5-1.0, and >1.0 mg/l
of arsenic, and with the 114 unexposed subjects as the reference, the preva
lence ratios for glucosuria, as adjusted for age and sex, were 0.8, 1.4, an
d 1.4 for those without skin lesions, and 1.1, 2.2, and 2.6 for those with
skin lesions. Taking exposure as <1.0, 1.0-5.0, >5.0-10.0 and >10.0 mg-year
s/l of exposure to arsenic the prevalence ratios, similarly adjusted, were
0.4, 0.9, 1.2, and 1.7 for those without and 0.8, 1.7, 2.1, and 2.9 for tho
se with skin lesions. All series of risk estimates were significant for tre
nd, (p<0.01).
Conclusions-The results suggest that skin lesions and diabetes mellitus, as
here indicated by glucosuria, are largely independent effects of exposure
to arsenic although glucosuria had some tendency to be associated with skin
lesions. Importantly, however, glucosuria (diabetes mellitus) may occur in
dependently of skin lesions.