Date of Award

2015

Document Type

Thesis

Publisher

Edith Cowan University

Degree Name

Bachelor of Health Science Honours

School

School of Exercise and Health Sciences

Faculty

Faculty of Health, Engineering and Science

First Supervisor

Associate Professor Amanda Devine

Second Supervisor

Dr Anna Callan

Third Supervisor

Professor Richard Prince

Abstract

Introduction: Recent research suggests an association between environmental cadmium exposure and increased risk of, and death from, cardiovascular disease, the number one cause of mortality in Australia and worldwide. However, the research to date is neither comprehensive nor have there been any studies conducted on an Australian population. This study identified whether increasing concentrations of urinary cadmium in elderly West Australian women was associated with an increased odds of incidence of, and deaths from CVD, as well as all-cause mortality.

Method: Cadmium excretion was measured in urine samples collected at baseline (1998) from 1359 women from Perth who were at least 70 years old. Samples were analysed for cadmium concentrations using Inductively Coupled Plasma – Mass Spectrometer. Urine samples were also analysed for creatinine, and specific gravity. Morbidity and mortality data from the Western Australian Data Linkage System (WADLS) and the Western Australian Hospital Morbidity Data System (WAHMDS) for the follow-up period (1998-2013), which was collected by the Bone and Vascular Research Group were used for this study. Odds ratios (ORs) were calculated for CVD and all-cause mortality endpoints. Subsequent calculations of hazard ratios (HR) were completed for those endpoints, which were significantly associated with urinary cadmium in the logistic regressions. All analyses initially included the overall population, however, to identify the influence of smoking on risk, the models were repeated with stratification of the population by smoking history.

Results: The median (IQR) concentration of cadmium in urine for the sample population was 0.180 (0.09-0.32) μg/L. Logistic regression analyses identified statistically significant relationships between six of the outcome variables and increasing urinary cadmium concentrations. In the total population an increased urinary cadmium was associated with an increased odds of atherosclerotic vascular disease death (OR = 1.156, 95% CI = 1.015-1.315), multiple causes of death heart failure (HF) (OR = 1.414, 95% CI = 1.141-1.751), HF event (OR = 1.181, 95% CI = 1.002-1.391), and those with urinary cadmium concentrations > 0.255 μg/L had an OR of 2.769 (95% CI = 1.439-5.327) for multiple causes of death HF when compared to the participants in the lowest cadmium concentration tertile (≤ 0.155 μg/L). When stratified by smoking history, never smokers with increasing cadmium concentrations were at greater odds of multiple causes of death HF (OR = 1.304, 95% CI = 1.026-1.657) and peripheral arterial disease (PAD) event (OR = 2.260, 95% CI = 1.011-5.053), whilst participants with cadmium concentrations > 0.255 μg/L reported OR’s of 2.422 (95% CI = 1.149-5.327) and 2.26 (95% CI = 1.011-5.053) for multiple causes of death HF and PAD event, respectively, when compared to participants with concentrations ≤ 0.155 μg/L. In ever smokers, participants with increasing urinary cadmium concentrations were at increased odds of all-cause mortality (OR = 1.423, 95% CI = 1.153-1.756), HF event (OR = 1.627, 95% CI = 1.089-2.341) and PAD event (OR = 2.639, 95% CI = 1.101-6.327). Ever smokers with cadmium concentrations > 0.255 μg/L were at increased odds of allcause mortality (OR = 2.105, 95% CI = 1.190-3.411), HF event (OR 4.823, 95% CI = 1.295-17.966) and PAD event (OR = 2.639, 95% CI = 1.101-6.327) compared to those with concentrations ≤ 0.155 μg/L. In the survival analysis, ever smokers with cadmium concentrations > 0.255 μg/L reported a hazard ratio (HR) of 1.683 (95% CI = 1.155- 2.451) for time until death resulting in all-cause mortality, when compared to participants with the lowest cadmium concentrations (≤ 0.155 μg/L). All models were adjusted for demographic and cardiovascular risk factors.

Conclusion: Low-level environmental exposure to cadmium was associated with five CVD endpoints as well as all-cause mortality. When stratified by smoking history, those who had never smoked were at significantly greater odds of multiple causes of death heart failure and peripheral arterial disease event. In ever smokers, participants with higher cadmium concentrations were at greater odds of all-cause mortality, heart failure event and peripheral arterial disease event. This research indicates that low environmental exposure to cadmium may be a risk factor in mortality and CVD in Australian populations. More research in different Australian populations to confirm these findings is required.

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