 |
 |
 |
 |
 |
 |
 |
 |
||
| Brief Communication | ||
| Increased urinary cadmium excretion in never-smoking young hypertensive adults in south India – a cross-sectional study | ||
| Justin Vijay Gnanou*, Brinnell Annette Caszo*, Vinod George Thykadavil**
* Faculty of Medicine, Universiti Teknologi Mara (UiTM), Shah Alam, Malaysia.
Introduction In humans, cadmium is known to be toxic. It is absent from the human body at birth and accumulates over the years. A safe intake level has been set at 7 μg/kg body weight. Chronic exposure is associated with various carcinomas, increased risk of diabetes, atherosclerosis and most importantly hypertension. Two studies conducted in the United States indicated a positive correlation between cadmium in drinking water and blood pressure levels [1]. In another study, mortality from hypertension was moderately increased in a village with high cadmium soil levels [2]. Contrastingly, Shigematsu et al showed the prevalence of hypertension in areas of Japan where drinking water and rice were heavily contaminated with cadmium was not greater than in control areas [3]. In two other studies, the levels of cadmium in blood, hair, and renal tissue in normotensive and hypertensive subjects were not different [4,5]. The objective of this study was to determine urinary excretion of cadmium in young individuals with hypertension. Exposure to cadmium occurs mainly through
occupation (mining, battery industries), smoking
and dietary intake. High cadmium levels in
agricultural soil is attributed to the use of cadmium
containing fertilisers [6]. Thus, cadmium enters the
food chain and is present in most human food stuffs
albeit in varying quantities [7]. Thus our second
objective was to establish that dietary sources of
cadmium may be an important cause of cadmium Methods A total of 35 male hypertensive subjects volunteered to participate in this cross-sectional study. Of these subjects only 15 were between 20-35 years of age, were non-smokers with no occupational exposure to cadmium. These subjects were screened and found negative for pheochromocytoma using 24 hour urinary VMA. Hypertension was defined as systolic pressure ≥ 140 mmHg and/or diastolic pressure ≥ 90 mmHg. Blood pressure was measured using conventional sphygmomanometry. Urinary cadmium was measured using a tomic absorption spectrophotometry. Cadmium level of 0.00 – 4.0 μg/day was considered as the reference range for adults in this study and levels greater than 4.0 μg/day were considered toxic [8]. Ethical approval was obtained from the Institutional Ethical Review Board of St. John’s Medical College, Bangalore and all subjects gave informed consent. Cadmium in urine was estimated using a flameless
atomic absorption spectrophotometer (AAS). Urine
samples were diluted 4 times with 0.5% highly Linear regression analysis was performed using SPSS 16.0 to analyse the relationship between urinary cadmium excretion and blood pressure measurements. Results The mean age of the study group was 29.7 ± 5.4 years. The mean systolic and diastolic blood pressure in these subjects were 147.3 ± 11.0 mmHg and 97.8 ± 7.7 mmHg respectively. The subjects were screened to rule out pheochromocytoma using 24 hour urinary VMA. The mean 24 hour VMA in these subjects was 4.9 ± 2.2 mg/day. 24 hour urinary VMA of less than 7 mg/day ruled out the presence of pheochromocytoma. Cadmium toxicity was explored using 24 hour urinary cadmium levels. The mean cadmium content of the urine in these subjects was 12.2 μg / day and ranged from 4.2 to 30.4 μg/day. Linear regression analysis showed no correlation between 24 hour urinary cadmium levels and systolic (r=0.1) and diastolic blood pressure (r=0.3). Discussion Urinary cadmium excretion is considered to be a reliable indicator of cumulative lifetime or long term exposure of cadmium [9]. Our subjects were young, between the ages of 20-35 years and were diagnosed with hypertension. All the subjects in the present study had elevated urinary cadmium levels. Since these patients were non-smokers and had no occupational exposure to cadmium, the source of cadmium was from either water or food. Chronic low-dose cadmium exposure and its role in
the aetiology of hypertension have not been fully
elucidated. ‘Oxidative stress’ has been proposed for
the development of nephropathy with chronic low
dose cadmium exposure. Cadmium was found to
induce ‘oxidative stress’ by the generation of hydroxyl radicals and resulted in damage to
mitochondria. In addition, cadmium also caused
disruption of mitochondrial membrane potential
and mitochondrial swelling with the release of
cytochrome c and apoptosis [10]. However the
mechanism by which cadmium induces a
hypertensive phenotype is unknown. In chronic
feeding studies in rats, hypertension developed in
cadmium exposed rats. These rats also showed
increased mortality and marked renal vascular
changes [11]. Contrasting results are obtained from
human studies. Hypertension was never found
among the Japanese Itai itai disease patients who
ingested high amounts of cadmium from diet [12]. A
study of non-smoking Thai subjects found an In the present study, no correlation was found
between urinary cadmium excretion and systolic or
diastolic blood pressure, which may have been due
to a small sample size. However, the findings of this
study do indicate the presence of cadmium toxicity
in subjects with hypertension, but more importantly
this study stresses the importance of the nonoccupational
source of cadmium in these subjects.
This may be attributed to the continuing To conclude, young hypertensive non-smoking subjects with no occupational exposure have high cadmium excretion. Future studies based on differing genetic variants of hypertension in larger samplesizes are needed to study the role of chronic cadmium exposure in the aetiopathogenesis of hypertension.
References
|
||