Cadmium exposure and cardiovascular end-points: differences by gender in the U.S. National Health and Nutrition Examination Survey
- Autores: María Téllez Plaza
- Directores de la Tesis: Ana Navas Acien (dir. tes.), Eliseo Guallar (dir. tes.), Miquel Porta (tut. tes.)
- Lectura: En la Universitat Autònoma de Barcelona ( España ) en 2010
- Idioma: español
- Tribunal Calificador de la Tesis: Ginés Sanz Romero (presid.), Teresa Puig (secret.), Jordi Sunyer i Deu (voc.)
- Materias:
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- Resumen
Environmental cadmium exposure is widespread in the general population. Cadmium induces hypertension in animal models. Epidemiologic studies of cadmium exposure and hypertension, however, have been inconsistent. At high-levels of exposure cadmium is a well-known nephrotoxic metal. Consequently, it is also possible that cadmium induces hypertension and cardiovascular disease by producing injury to the kidney, a key organ in blood pressure regulation. Finally, experimental and epidemiological evidence suggests that in addition to vasopressor and nephrotoxic roles, cadmium could also directly favor atherosclerosis initiation and progression. In summary, mounting evidence provide plausibility for cadmium as a cardiovascular risk factor. Nonetheless, few studies have evaluated the associations between low-level concentrations of cadmium and cardiovascular end-points. Additionally, several lines of evidence suggest that the effects of cadmium may be different in men and women. However, gender differences have seldom been explored.
The main objective of this dissertation was to investigate the association of cadmium exposure with the following cardiovascular-related end points in the general population: 1) hypertension, 2) kidney disease, and 3) peripheral arterial disease, with a special attention to gender differences. To achieve this goal we used data from the US population participating in the National Health and Nutrition Examination Survey (NHANES) from 1999 to 2006. Blood and urine cadmium were measured by atomic absorption spectrometry (AAS) and inductively coupled plasma-mass spectrometry (ICPMS), respectively. Serum creatinine concetrations were measured by using a kinetic rate Jaffé method and were calibrated to account for laboratory differences across time and to standardize to creatinine measures at the Cleveland Clinic Research Laboratory (Cleveland, Ohio). The estimated glomerular filtration rate (GFR) was calculated using the abbreviated Modification of Diet in Renal Disease (MDRD) Study formula. Urinary albumin was measured in spot urine samples by solid-phase fluorescence immunoassay. Brachial systolic and diastolic blood pressure levels and ankle-brachial blood pressure index (ABPI) were measured using standardized protocols. Peripheral arterial disease was defined as an ABPI < 0.9 in at least one leg.
After multivariable adjustment, the average differences in systolic and diastolic blood pressure comparing participants in the highest and lowest quartiles of the blood cadmium distribution were 1.93 mmHg (95% confidence interval (CI) 0.40, 3.46) and 1.17 mmHg (95% CI 0.21, 2.13), respectively. No association was found for urine cadmium. There was no association either between cadmium exposures and the prevalence of hypertension. After multivariable adjustment, the average differences in creatinine-corrected albuminuria and estimated GFR comparing participants in the highest and lowest quartiles of the blood cadmium distribution were 18.01 mg/g creatinine (95% CI 3.68, 32.34) and -0.61 mL/min/1.73m2 (-1.74 to 0.51), respectively. After multivariable adjustment, the odds ratio for albuminuria > or = 30mg/g and estimated glomerular filtration rate < or = 60 mL/min/1.73m2 were 1.48 (95% CI 1.24, 1.78) and 1.31 (95% CI 1.10, 1.56), respectively, comparing the 80th vs the 20th percentiles of the blood cadmium distribution. No gender-differences were observed in the association between hypertension or kidney disease and cadmium concentrations.
We found gender-differences in the association between cadmium exposures and peripheral arterial disease. In men, the adjusted odds ratio (95% CI) for PAD comparing the 80th vs the 20th percentiles of blood and urine cadmium distributions were 1.95 (1.28, 2.96) and 3.28 (1.82, 5.91), respectively, with a progressive dose-response relationship and no difference by smoking status. In women, the corresponding odds ratios were 1.47 (0.82, 2.66) and 0.65 (0.35, 1.21), and there was evidence of effect modification by smoking: in ever smoking women there was a positive, progressive dose-response relationship, while in never smoking women there was an U-shaped dose-response relationship. Cardiovascular-related cadmium associations should always be explored in gender and smoking specific strata.
In our study sample, cadmium exposure was associated to several cardiovascular end-points. Overall, this dissertation adds to current concerns on cadmium exposure as a cardiovascular risk factor at concentrations of exposure that are relevant to risk assessment in most human populations.
