Cadmium Intake and Systemic Exposure in Postmenopausal Women and Age-Matched Men Who Smoke Cigarettes

Abstract

Mean blood cadmium (B-Cd) concentrations are two- to threefold higher in smokers than in nonsmokers. The basis for this phenomenon is not well understood. We conducted a detailed, multifaceted study of cadmium exposure in smokers. Groups were older smokers (62±4 years, n = 25, 20% male) and nonsmokers (62±3 years, n = 16, 31% male). Each subject's cigarettes were machine smoked, generating individually paired measures of inhaled cadmium (I-Cd) versus B-Cd; I-Cd and B-Cd were each evaluated three times, at monthly intervals. Urine cadmium (U-Cd) was analyzed for comparison. In four smokers, a duplicate-diet study was conducted, along with a kinetic study of plasma cadmium versus B-Cd. Female smokers had a mean B-Cd of 1.21ng Cd/ml, with a nearly 10-fold range (0.29-2.74ng Cd/ml); nonsmokers had a lower mean B-Cd, 0.35ng Cd/ml (p < 0.05), and narrower range (0.20-0.61ng Cd/ml). Means and ranges for males were similar. Estimates of cadmium amounts inhaled daily for our subjects smoking ≥ 20 cigarettes/day were far less than the 15 µg Cd reported to be ingested daily via diet. This I-Cd amount was too low to alone explain the 3.5-fold elevation of B-Cd in our smokers, even assuming greater cadmium absorption via lungs than gastrointestinal tract; cadmium accumulated in smokers' lungs may provide the added cadmium. Finally, B-Cd appeared to be linearly related to I-Cd values in 75% of smokers, whereas 25% had far higher B-Cd, implying a possible heterogeneity among smokers regarding circulating cadmium concentrations and potentially cadmium toxicity.

Exploring the Association Between Demographics, SLC30A8 Genotype, and Human Islet Content of Zinc, Cadmium, Copper, Iron, Manganese and Nickel

“…Apart from cigarette smoke, the main sources of human exposure in non-smokers are dietary Cd contamination and occupational exposure 41–44 . The positive correlation between age and islet Cd content is consistent with prior reports of a long biological half-life of Cd in toxicokinetic population studies using kinetic models that rely on blood Cd level and urinary excretion 43, 45–47 .…”

Melatonin Improves Mitochondrial Function by Promoting MT1/SIRT1/PGC-1 Alpha-Dependent Mitochondrial Biogenesis in Cadmium-Induced Hepatotoxicity In Vitro

“…It is well known that cadmium induces hepatotoxicity in humans, as well as in farm and laboratory animals (Ebert-McNeill et al. , 2012; Wu et al. , 2012).…”

Association between urinary cadmium levels and prediabetes in the NHANES 2005–2010 population

“…Aside from cigarette smoke, the main sources of human exposure in non-smokers is dietary Cd contamination, occupational exposure, and Cd containing house dust inhalation (Afridi et al, 2008; Benemann et al, 2003; Benoff et al, 2009; Bulat et al, 2009; Dakeshita et al, 2009; Ebert-McNeill et al, 2012; Hoffmann et al, 1999; Hogervorst et al, 2007; Jarup et al, 1983; Link et al, 2007; Olsson et al, 2002; Ruiz et al, 2010). Reports of serum or blood Cd concentrations in the population range from 0.0009 to 0.087 μmol/L (Afridi et al, 2008; Benoff et al, 2009; Bulat et al, 2009; Dakeshita et al, 2009; Ebert-McNeill et al, 2012; Jarup et al, 1983; Link et al, 2007; Olsson et al, 2002; Ruiz et al, 2010). These exposure levels are traditionally considered to be mostly below the toxic exposure levels as defined based on the threshold for nephrotoxic effects of Cd (Maret and Moulis, 2013; Schulz et al, 2011).…”