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Relations between exposure to arsenic, skin
lesions, and glucosuria
Mahfuzar Rahman, Martin Tondel, Ireen Akhter Chowdhury, Olav Axelson
Abstract
Objectives—Exposure to arsenic causes
keratosis, hyperpigmentation, and hypo-
pigmentation and seemingly also diabetes
mellitus, at least in subjects with skin
lesions. Here we evaluate the relations of
arsenical skin lesions and glucosuria as a
proxy for diabetes mellitus.
Methods—Through existing measure-
ments of arsenic in drinking water in
Bangladesh, wells with and without ar-
senic contamination were identified.
Based on a questionnaire, 1595 subjects
>30 years of age were interviewed; 1481
had a history of drinking water contami-
nated with arsenic whereas 114 had not.
Time weighted mean arsenic concentra-
tions and mg-years/l of exposure to ar-
senic were estimated based on the history
of consumption of well water and current
arsenic concentrations. Urine samples
from the study subjects were tested by
means of a glucometric strip. People with
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 prevalence
ratios for glucosuria, as adjusted for age
and sex, were 0.8, 1.4, and 1.4 for those
without skin lesions, and 1.1, 2.2, and 2.6
for those with skin lesions. Taking expo-
sure as <1.0, 1.0–5.0, >5.0–10.0 and >10.0
mg-years/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 those with skin
lesions. All series of risk estimates were
significant for trend, (p<0.01).
Conclusions—The results suggest that
skin lesions and diabetes mellitus, as here
indicated by glucosuria, are largely inde-
pendent eVects of exposure to arsenic
although glucosuria had some tendency to
be associated with skin lesions. Impor-
tantly, however, glucosuria (diabetes mel-
litus) may occur independently of skin
lesions.
(Occup Environ Med 1999;56:277–281)
Keywords: drinking water; glucosuria; keratosis
In Bangladesh, a large part of the population
has been drinking water contaminated with
arsenic at concentrations >0.05 mg/l,1–4 the
permissible limit by the World Health Organis-
ation. Some 30–70 million people are thought
to be exposed—that is, the populations of 41
districts out of the 64 in this country.5
Exposure to arsenic is known to cause skin dis-
orders such as keratosis, hyperpigmentation,
and hypopigmentation.6Recently, epidemio-
logical studies have also indicated an excess
risk of diabetes mellitus among subjects
exposed to arsenic, either at work or through
drinking water.7–10 In a previous study from
Bangladesh an increased risk of diabetes melli-
tus was assessed among subjects with skin
lesions only,10 whereas another study did not
consider the question of how the occurrence of
diabetes mellitus might relate to skin lesions.7
Diabetes mellitus has also been associated with
occupational exposure to arsenic in mortality
based studies but without any reported associ-
ation with skin lesions.89 Considering a rural
population in Bangladesh, we here evaluate the
relation of skin lesions and diabetes mellitus
taking glucosuria as a proxy for this disease. A
clear relation would obviously be of interest for
screening purposes in a developing country.
The arsenic contamination of the tubewell
water in Bangladesh is probably derived from
the fine aluvial sediments of the Ganges delta.4
The duration of the exposure to arsenic is
uncertain, but it is thought to have started in
the late 1960s when drilling of tubewells began
as part of a wide irrigation plan. The tubewells
have a depth of 20–100 m and the arsenic con-
centrations may vary widely even between
adjacent wells. There has not been any regula-
tion on withdrawal of ground water in Bangla-
desh and as a result, ground water exploration
goes on unchecked, and pumping causes
seasonal fluctuations in the water table. These
fluctuations could perhaps explain the chemi-
cal changes such as oxidation of arsenic
containing minerals—such as iron pyrites—
and subsequent release of arsenic into the
groundwater.
Skin lesions—such as hyperpigmentation or
hypopigmentation and keratosis—are known as
a hallmark of high exposure to arsenic and have
been found in populations exposed to well
water contaminated with arsenic in
Argentina,11 Chile,12 13 India,14–17 Taiwan,18 19
and Thailand,20 but negative findings also have
been reported.21 Other manifestations resulting
from ingestion of drinking water contaminated
with arsenic include weakness, conjunctival
congestion, oedema, portal hypertension,
bronchitis, hepatomegaly, and malignant
neoplasm.14 15
Skin lesions pose a public health problem in
Bangladesh. Subjective symptoms are usually
mild, but patients with obvious palmoplantar
Occup Environ Med 1999;56:277–281 277
Division of
Occupational and
Environmental
Medicine, Department
of Health and
Environment, Faculty
of Health Sciences,
Linköping University,
581 85 Linköping,
Sweden
M Rahman
M Tondel
O Axelson
Radda-MCH FP
Centre, Mirpur, Dhaka
1216, Bangladesh
I A Chowdhury
Correspondence to:
Dr Mahfuzar Rahman,
Division of Occupational and
Environmental Medicine,
Department of Health and
Environment, Faculty of
Health Sciences, Linköping
University, 581 85
Linköping, Sweden.
Telephone 0046 13 221440;
fax 0046 13 145831.
Accepted 12 November 1998
group.bmj.com on July 16, 2011 - Published by oem.bmj.comDownloaded from
keratosis may have pain while walking or work-
ing and the disfigurement may lead to social
isolation.16 A question is how closely diabetes
mellitus might be associated with the skin
lesions and to what extent also subjects without
skin lesions can be aVected. In our previous
study of exposure to arsenic and diabetes mel-
litus, skin lesions were taken as an indicator of
definite exposure.10 In the present study,
arsenic concentrations ranged from non-
detectable to 2.04 mg/l.
Methods
STUDY AREA
Four villages located in four diVerent districts
in Bangladesh (Faridpur, Jessore, Narayon-
gong, and Nawabgong) were selected for the
study on the basis of a survey of arsenic in
drinking water. These study villages were suit-
able because of a proper contrast in exposure
within the villages. The exact number of wells
in each village was not known, but from the
existing measurements most of the wells in the
study area were known to have arsenic concen-
trations of >0.05 mg/l but a few had no
increase in concentrations.
SUBJECTS
All people who had lived in the study areas
throughout their lifetime and who had used the
same well as long as it had existed, were
considered eligible for the study. However, an
age restriction was applied because of our pre-
vious experience that glucosuria due to expo-
sure to arsenic is unlikely to occur before the
age of 30.10 Out of 1794 people, a total of 1595
were at home at the time of our visit to the vil-
lages and all of them could be interviewed and
medically examined, 1481 of whom were
exposed.
QUESTIONNAIRE INTERVIEW AND EXAMINATION
Data on the duration of water consumption
including the water source, a detailed residen-
tial history, personal and family history of
diabetes mellitus, and hypertension were ob-
tained at an interview with the interviewers fill-
ing in a questionnaire.
The interviews and the medical examina-
tions were performed at a door to door visit and
carried out by two experienced physicians from
the National Institute of Preventative and
Social Medicine (NIPSOM), who both had
considerable experience in diagnosing arseni-
cal skin lesions in Bangladesh.
Each participant in the study was examined
for skin lesions according to the description
givenbyYeh.
22 Arsenical skin lesions were
diagnosed in the presence of one or more of the
following signs: keratosis, hyperpigmentation,
or hypopigmentation. Hyperpigmentation oc-
curs anywhere on the body, often as a rain
drop-like pigmentation or a diVuse dappling of
dark brown, especially marked on the trunk,
buttock, and upper thigh. Hypopigmentation
follows the same distribution and depigmented
spots may be present even in the absence of
hyperpigmentation. Keratosis is characterised
by diVuse bilateral thickening of palms or soles
with or without nodules of various shapes and
sizes, most often on the thenar eminence and
the lateral borders of palms and fingers.
Standing height and body weight were
measured with the subjects having light clothes
and not wearing shoes. Individual body mass
index (BMI) was calculated as weight (kg)
divided by height (m) squared.
EXPOSURE ASSESSMENT
The available data for exposure assessment
came from various sources, including our pre-
Table 1 Distribution of exposed subjects with and without skin lesions and cases of glucosuria along with cr ude prevalence
ratios and Mantel-Haenszel prevalence ratios (MH-PR) adjusted by age,sex, and BMI
Age BMI Skin lesions yes or no
Glucosuria
Men Women
Non-cases Cases Non-cases Cases
30–44 <19 Yes 36 11 42 8
No 124 15 89 8
19–22 Yes 57 10 14 5
No 116 17 71 19
>22 Yes 45 11 13 13
No 100 10 63 13
45–60 <19 Yes 18 9 19 5
No 60 8 53 8
19–22 Yes 19 8 5 5
No 54 10 30 9
>22 Yes 31 6 9 4
No 50 10 42 4
>60 <19 Yes 3 2 2 1
No 15 6 6 2
19–22 Yes 7 2 1 2
No 11 2 2 0
>22 Yes 3 1 1 2
No 16 0 5 3
Total Yes 219 60 106 45
No 546 78 361 66
Crude prevalence ratio 1.7 1.9
95% CI 1.2to2.4 1.3to2.7
MH-PR 1.7 2.1
95% CI 1.2to2.4 1.4to2.9
Crude prevalence ratio,
men and women 1.8
95% CI 1.4to2.3
MH-PR 1.9
95% CI 1.5to2.4
278 Rahman, Tondel, Chowdhury, et al
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vious study,10 an oYcial report,23 and an
unpublished report of water analyses per-
formed by the National Institute of Preventive
and Social Medicine. As shown elsewhere,2
there is considerable variation in arsenic
concentrations even between adjacent wells
and probably also over time. Details of this are
still lacking. The concentrations of total arsenic
in drinking water were all measured by flow
injection hydride generation atomic absorption
spectrometry.
Individual exposure was calculated in two
ways. Firstly, we assessed the mean exposure to
arsenic for each subject, in principle a time
weighted average. Because the subjects had
lived all their lives in the same place, the time
weighted mean exposure was equal to the
measured concentration, assuming that the
present concentrations were representative also
of the past. The resulting estimates were then
categorised as I, II, or III, corresponding to
arsenic concentrations of <0.5 mg/l, 0.5–1.0
mg/l, and >1.0 mg/l, respectively.
Secondly, mg-years/l of exposure to arsenic
were calculated for each subject, multiplying
the arsenic concentration in the well by the
number of years that it had been used by the
person, assuming that the current concentra-
tions of arsenic in the well water were
representative of the past. The resulting
estimates were then categorised as <1.0
mg-years/l, 1.0–5.0 mg-years/l, >5.0–10.0 mg-
years/l, and >10.0 mg-years/l.
GLUCOSE STATE
Urine samples were obtained from all subjects
at the time of the health examination. The
samples were analysed by means of a glucomet-
ric strip (BM-Test Glucose, Boehringer Mann-
heim GmbH, Mannheim, Germany). People
with positive tests were classified as cases.
DATA ANALYSIS
Subjects were stratified by age (30–44, 45–60,
and >60), sex, and body mass index (BMI);
BMI had categories of <19, 19–22, and >22.
Mantel-Haenszel weighted prevalence ratios
(MH-PRs) with 95% confidence intervals
(95% CIs) and a test of the trend were
calculated by means of the Epi-Info package.24
Results
Out of the 1481 exposed adults who partici-
pated in this study (903 men and 578 women),
29 % (430/1481) showed at least one of the
cutaneous signs of chronic arsenic poisoning.
As shown in table 1, the crude overall
prevalence ratio (or risk) for glucosuria in
exposed subjects with skin lesions amounted to
1.8. After adjusting for age, sex, and BMI, the
prevalence ratio was increased (MH-PR 1.9)
Although keratosis was more common in
exposed men (31% for men, 26% for women),
the risk for glucosuria was slightly greater in
women (MH-PR 1.7 for men v2.1 for
women).
As shown in tables 2 and 3, the risk for glu-
cosuria was analysed separately for subjects
with and without skin lesions. Considering
time weighted mean exposure to arsenic, and
taking unexposed people as the reference (table
2), the adjusted prevalence ratios for glucosuria
among the subjects without skin lesions were
0.8, 1.4, and 1.4 in exposure categories I, II,
and III. With the same reference, subjects with
skin lesions had adjusted prevalence ratios of
1.1, 2.2, and 2.6, respectively. The dose-
response was significant (for subjects without
skin lesions p<0.01, and with skin lesions
p<0.001). Considering mg-years/l of exposure
Table 2 Distribution of subjects with and without skin lesions into exposure categories of
arsenic concentrations and cases of glucosuria along with Mantel-Haenszel prevalence
ratios (MH-PR) adjusted by age and sex and 95% CI (unexposed is the reference)
Unexposed
Exposure category*
I II III
No skin lesions:
Cases 14 47 63 34
Non-cases 100 434 306 167
Total 114 481 369 201
MH-PR (1.0) 0.8 1.4 1.4
95%CI 0.4to1.3 0.8to2.3 0.7to2.4
÷
2For dose-response trend among 8.9
the exposed categories p<0.01
Skin lesions:
Cases 19 58 28
Non-cases 123 149 53
Total 142 207 81
MH-PR 1.1 2.2 2.6
95%CI 0.5to2.0 1.3to3.8 1.5to4.6
÷
2For dose-response trend among
the exposed categories
14.4
p<0.001
*Category I <0.5 mg/l; category II 0.5–1.0 mg/l; category III >1.0 mg/l.
Table 3 Distribution of subjects with and without skin lesions into exposure categories of mg-years/l and cases of
glucosuria along with Mantel-Haenszel prevalence ratios (MH-PR) (95% CIs) adjusted by age and sex (unexposed is the
reference)
Unexposed
Category of mg-years/l of arsenic exposure
<1.0 1.0–5.0 >5.0–10.0 >10.0
No skin lesions:
Cases 14 10 61 29 44
Non-cases 100 159 416 170 162
Total 114 169 477 199 206
MH-PR (1.0) 0.4 0.9 1.2 1.7
95%CI 0.1to1.0 0.5to1.7 0.6to2.2 1.0to2.9
÷
2For dose-response trend among
the exposed categories
18.11
p<0.001
Skin lesions:
Cases 7 52 22 24
Non-cases 62 164 58 41
Total 69 216 80 65
MH-PR 0.8 1.7 2.1 2.9
95%CI 0.3to1.9 0.9to2.9 1.0to4.0 1.6to5.2
÷
2For dose-response trend among
the exposed categories
12.16
p<0.001
Relations between exposure to arsenic, skin lesions, and glucosuria 279
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to arsenic with the same unexposed people as
the reference (table 3), the adjusted risks in
subjects without skin lesions showed a clearer
dose-response (0.4, 0.9, 1.2, and 1.7). For sub-
jects with skin lesions, the risk estimates were
even higher (0.8, 1.7, 2.1, and 2.9, respec-
tively). Both trends were highly significant
regardless of skin lesions, p<0.001.
Taking the lowest exposure category as the
reference, the risk estimates became higher
both for time weighted mean arsenic concen-
trations and arsenic-years/l, but the overall pat-
tern remained almost the same, with significant
trends.
Discussion
The presence of a stable population in rural
villages with diVerent degrees of exposure to
arsenic enabled us to study the chronic arsenic
poisoning and the relation of skin lesions and
glucosuria. There was a dose-response relation
between exposure to arsenic and glucosuria for
subjects both with and without skin lesions.
The mg-years/l of exposure to arsenic may bet-
ter reflect the total exposure to arsenic than the
time weighted average concentrations, for
which the dose-response relation also was less
clear. The results obtained indicate that skin
lesions and glucosuria are largely independent
eVects of exposure to arsenic although higher
risk estimates were obtained for the subjects
with skin lesions.
A limitation of the study is the cross sectional
design and a lack of systematic sampling of
water supplies in the study area. Furthermore,
although glucosuria is a primary indicator of
diabetes mellitus, it would nevertheless have
been desirable to identify the hyperglycaemic
patients among those with glucosuria; this was
not economically possible, however.
In our study, each person had only one main
source of drinking water, with a known arsenic
concentration. Arsenic concentrations might
vary considerably from well to well in the same
area and even in the same well.218 The
calculated, approximate time weighted expo-
sure to arsenic can obviously not take into
account any occasional but unknown use of
other wells, nor any time trends in past
exposure, or likely fluctuations in the exposure
depending on precipitation and other circum-
stances. Another limitation is the lack of infor-
mation on the amount of water consumed by
each study subject during diVerent periods of
his or her lifetime, hampering any more exact
calculation of the cumulative exposure to
arsenic.
It is not known whether other trace elements
could be of importance as present in water
together with arsenic. However, there is no
definite evidence of the presence of other toxic
trace elements in the study area, nor is it clear
whether any other elements would have an
influence on the occurrence of glucosuria.
This study also has some other limitations to
be discussed. Not all primarily identified
subjects were finally available at the time of the
door to door visit. As all study subjects were
recruited from rural villages, occupation, socio-
economic status, and lifestyle variables should
be reasonably similar between exposed and
unexposed people and should therefore be
unlikely to influence glucosuria either in the
presence or absence of skin lesions. There was
an indication of some slight negative confound-
ing for women for age and BMI, for which
adjustments were made (table 1). Also when
applying a linear regression model, BMI
exerted weak negative confounding and was
therefore not taken into account in further
analyses.
Inorganic arsenic is known to induce black-
foot disease and seemingly also ischaemic heart
disease through a direct eVect on the athero-
sclerotic process involving endothelial cells,
smooth muscle cells, platelets, and macro-
phages.25 Diabetes mellitus is another impor-
tant determinant for peripheral vascular dis-
ease and ischaemic heart disease. Thus,
cardiovascular diseases might also be caused
indirectly through arsenic induced diabetes
mellitus. A transient hyperglycaemia and struc-
tural â-cell changes were found in mice treated
with arsenite plus hydroxylamine.26 Besides a
potentially toxic eVect on the â-cells, arsenic
might act on the peripheral insulin receptor in
the tissue, causing diabetes mellitus. There is
also an indication that trivalent arsenic may
induce hyperglycaemia acting on the central
nervous system.27 Arsenic has been reported to
induce renal insuYciency after cortical necro-
sis with haematuria, leukocyturia, and glucos-
uria.28 Whether the glucosuria is caused by any
or several of these mechanisms needs further
exploration. There is also a need for further
evaluating how well glucosuria serves as a
proxy for diabetes mellitus in subjects exposed
to arsenic.
This is the first population based study con-
sidering the relation of skin lesions and risk for
glucosuria and thereby also diabetes mellitus.
On the basis of our findings, we conclude that
the appearance of dermatological signs of
chronic arsenic toxicity is a poor marker for a
risk of glucosuria and diabetes mellitus, as
these conditions may well occur also in the
absence of skin lesions.
We thank Drs Sk Akhtar Ahmad and MH Faruquee,
Department of Occupational and Environmental Health, NIP-
SOM, Dhaka, Bangladesh, for their support, especially in the
field survey, and for providing existing water measurements by
NIPSOM. The study was approved by the ethics committee of
Bangladesh Medical Research Council, and participation was
voluntary.
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doi: 10.1136/oem.56.4.277
1999 56: 277-281Occup Environ Med
M Rahman, M Tondel, I A Chowdhury, et al.
lesions, and glucosuria.
Relations between exposure to arsenic, skin
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