Toxicology Reflections

EDC Properties of Cadmium


Author –

The topic I have chosen to explore is how the metal cadmium (Cd) may potentially result in endocrine disruption. Endocrine disrupting compound (EDC) are those that have the potential to alter hormone pathways that regulate reproduction (Arcand-Hoy and Benson 1998). They have investigated widely in the literature as have the release of metals through anthropogenic activities.  Cadmium is a naturally occurring metal but it is not essential in normal cellular processes so exposure and uptake of Cd can have adverse effects. Cadmium exposure can occur through ingestion of food or water containing Cd as well as inhalation. Inhalation exposure occurs most notably through cigarette smoke but also from coal burning. Cadmium can be food in food that is grown in soils containing either naturally higher Cd levels or in areas where the soil has been increased through anthropogenic uses (Silva et al. 2011).

Cadmium has been identified as a carcinogen by the WHO and is a pollutant considered to be of worldwide concern. It has also been linked to testicular and breast cancer (Pan et al. 2010). As well as having impacts on sperm quality and quantity in human males and implantation success and oocyte development in animal models (Thompson and Bannigan 2008; Pant et al. 2013). So ultimately my goal during these reflections is to gain a more through and clear understanding of the role Cd may play in endocrine disruption and more specifically on how it may affect estrogen pathways.


Arcand-Hoy LD, Benson WH. 1998. Fish reproducition: An ecologically relevant indicator of endocrine disruption. Environ Toxicol Chem 17: 49-57.

Pan J, Plant JA, Voulvoulis N, Oates CJ, Ihlenfeld. 2010. Cadmium levels in Europe: implcaitons for human health. Environ Geochem Health 32: 1-12.

Pant N. Pant AB, Chaturvedi PK, Shukla M, Mathur N. Gupta YK, Saxena DK. In Press. Semen quality of environmentally exposed human population: the toxicological consequence. Environ Sci Pollut Res

Silva N, Peiris-John R, Wickremasinghe R, Senanayake H, Sathiakumar N. 2012. J Appl Toxicol 32: 318-332.

Thompson J, Bannigan J. 2008. Cadmium: Toxic  effects on the reproductive system and the embryo. Reproductive Toxicology 25: 304-315.


15 thoughts on “EDC Properties of Cadmium

  1. Interestingly enough, a mechanism of cadmium toxicity related to endocrine disruption is the enhancement or inhibition of progesterone production1. At low levels cadmium has been found to enhance progesterone production in certain tissues1. Progesterone is an important hormone in the regulation of ovarian cycles and in maintaining pregnancy1. Alternately, high doses of cadmium can inhibit progesterone production1. This type of contradictory MOA based on dose is present for several pathways of cadmium toxicity and may make for an interesting discussion when determining the risk associated with low-level versus high-level exposure.

    Henson M.C., Chedrese P.J. (2004). Endocrine Disruption by Cadmium, a Common Environmental Toxicant with Paradoxical Effects on Reproduction. Experimental Biology and Medicine. 229: 383 – 392

  2. Endocrine disrupting compounds (EDCs) are an interesting topic since most of the studies focus on effects in males due to the more distinct abnormalities that appear. Melissa mentions some of the effects in men including impacts on sperm quality. However, there is growing literature regarding the effects of EDCs on female reproductive development, fertility, and onset of menopause (Fowler et al. 2012). Among these EDCs is Cadmium (Cd), which acts as a metallo-oestrogen (Fowler et al. 2012).

    Cd typically has a low rate of excretion from the body and can accumulate in the blood, kidney, liver and reproductive organs such as the placenta, testis, and ovaries (Henson et al. 2004). Melissa mentioned that “inhalation exposure occurs most notably through cigarette smoke”, which is a major source of gestational Cd that can accumulate in the human placenta up to 2 times higher in female smokers compared to non-smokers (Fowler et al. 2012). Stasenko et al. (2010) demonstrated that Cd can also disrupt the normal function of trophoblast cells, which play an important role in embryo implantations and interaction with the maternal uterus, by down-regulation of leptin. Leptin is involved with placental maintenance. Thus, disruption of these normal processes can affect normal placentation and placental function. This is supported by data on the negative effects of cigarette smoking on in vitro fertilization (IVF) outcomes in women (Neal et al. 2005).

    Additionally, Cd has been shown to interfere with ovarian steriodogenic pathways in rats (Godt et al. 2006), with production of progesterone and testosterone most affected (Piasek et al 1999). Henson et al. (2004) demonstrated hormesis effect, a topic discussed in class, with regard to Cd effects on rats. In this instance, low dosages of Cd were demonstrated to stimulate ovarian progesterone biosynthesis, which high doses inhibited it in rats (Henson et al. 2004). It is difficult to distinguish results from animal studies, as current literature supports the hypothesis that Cd is an EDCs while others report no effects. One study with rats reported that Cd precipitates enhanced mammary development and increased uterine weight (Johnson et al. 2003), while others report that maternal exposure to Cd is associated in low birth weight and in increase in spontaneous abortions (Frery et al. 1993; Shiverick and Salafia, 1999).

    Overall, the uncertainty associated with the EDC properties of Cd rest in our ability to quantify the effects and determine an acceptable exposure. Do you believe there is an acceptable exposure to Cd based on the effects presented in the literature, and is there a way to reduce our exposure to Cd if it is so ubiquitous in our environmental surroundings?


    Henson, M. C., & Chedrese, P. J. (2004). Endocrine disruption by cadmium, a common environmental toxicant with paradoxical effects on reproduction. Experimental Biology and Medicine, 229(5), 383-392.

    Godt, J., Scheidig, F., Grosse-Siestrup, C., Esche, V., Brandenburg, P., Reich, A., & Groneberg, D. A. (2006). The toxicity of cadmium and resulting hazards for human health. J Occup Med Toxicol, 1(22), 1-6.

    Fowler, P. A., Bellingham, M., Sinclair, K. D., Evans, N. P., Pocar, P., Fischer, B. & O’Shaughnessy, P. J. (2012). Impact of endocrine-disrupting compounds (EDCs) on female reproductive health. Molecular and cellular endocrinology, 355(2), 231-239.

    Frery, N., Nessmann, C., Girard, F., Lafond, J., Moreau, T., Blot, P. & Huel, G. (1993). Environmental exposure to cadmium and human birthweight. Toxicology, 79(2), 109-118.

    Johnson, M. D., Kenney, N., Stoica, A., Hilakivi-Clarke, L., Singh, B., Chepko, G., Clarke, R., Sholler, P.F., A Lirio, A., Foss, C. Reiter, R., Trock, B., Paik, S. & Martin, M. B. (2003). Cadmium mimics the in vivo effects of estrogen in the uterus and mammary gland. Nature medicine, 9(8), 1081-1084.

    Neal, M. S., Hughes, E. G., Holloway, A. C., & Foster, W. G. (2005). Sidestream smoking is equally as damaging as mainstream smoking on IVF outcomes. Human reproduction, 20(9), 2531-2535.

    Piasek, M., & Laskey, J. W. (1999). Effects of in vitro cadmium exposure on ovarian steroidogenesis in rats. Journal of Applied Toxicology, 19(3), 211-217.;2-4/abstract

    Shiverick, K. T., & Salafia, C. (1999). Cigarette smoking and pregnancy I: ovarian, uterine and placental effects. Placenta, 20(4), 265-272.

    Stasenko, S., Bradford, E. M., Piasek, M., Henson, M. C., Varnai, V. M., Jurasović, J., & Kušec, V. (2010). Metals in human placenta: focus on the effects of cadmium on steroid hormones and leptin. Journal of Applied Toxicology, 30(3), 242-253.

  3. Reblogged this on Chemistry and Life and commented:
    This post on the Toxcentre blog is a nice review of the endocrine disrupting properties of cadmium.

  4. Author –

    Cadmium (Cd) is used in array of applications, most notably in batteries, pigments, stabilizers, coatings and in some alloys (Wood et al. 2012). Concentrations in water range from 1µg/L up to 400 µg/L Cd in exposed sites and a range of 1 – 10 µg/L Cd has been noted in drinking water (Tilton et al. 2003, Wood et al. 2012). The concerns surrounding Cd rest in it being toxic at very low concentrations but also its association with being a carcinogen, mutagen, immunotoxin and potential EDC (Kusch et al 2007, Pan et al. 2010). Again as mentioned when introducing this topic for the structured reflections, Pan et al. 2010 linked exposure to Cd via the diet in humans with incidences of breast and prostate cancer, and it has been classified as a human carcinogen (Das and Mukherjee 2013). The most severe manifestation of human chronic Cd2+ toxicity in people was in the Jinzu River basin in Japan and is referred to as Itai-Itai disease (Henson and Chedrese 2004).

    Cadmium is a highly toxic and persistent metal that humans are exposed to at higher levels due to anthropogenic activities. Therefore, before addressing specific endocrine disrupting possibilities, discussing the effects of Cd on humans in general is applicable. In acute exposure scenarios symptoms are severe abdominal pain, nausea, vomiting, diarrheas, headaches and vertigo. Death can occur within 24hrs or 1-2 weeks post exposure from liver and kidney damage (Pan et al. 2010). Chronic exposure is associated with respiratory problems, renal dysfunction, calcium (Ca) metabolism disorders, bones are often affected with the occurrence of osteoporosis and fractures (Pan et al. 2010).

    The term metalloestrogens has been used to categorize inorganic metal ion, such as Cd, that can bind to and activate estrogen receptors. Metalloestrogens can be both essential and nonessential metal ions and estrogen may not be the only hormone affected (Darbre 2006; Silva et al. 2011). From an in vitro perspective using human breast cancer cell lines, Cd has shown estrogenic effects. Silva et al. (2011) summarized these effects as follows:

    Binding to the estrogen receptor (ER)
    Activation of either endogenously or exogenously expressed ERs
    Interaction with estrogen related genes
    Alteration of transcription and mRNA formation of estrogen regulated genes
    Translation of and amount of protein product from estrogen regulated genes affected
    Activation of intracellular signaling similar to that of estrogen
    Proliferation of estrogen dependent cells
    However, contradictory in vitro findings have been noted. Le Guevel et al. (2000) found that rainbow trout and human ER transfected into yeast cells did exhibit inhibited ER-transcriptional activity of 17β-estradiol following Cd exposure. Yet exposure to Cd did not significantly induce activation of either the rainbow trout or human ER with lower activity seen in the human ER yeast cells. Which lead the author to believe there are some species-sensitivity differences. Another study by Silva et al. (2006) found that Cd across a range of concentrations did not induce cell proliferation as in prior studies but only toxic effects on the cells. As well only a slight activation of ER in the cells, lower than reported by other studies.

    Although, this does not detail all the work evaluating Cd as an EDC in in vitro studies it does begin to show that potential effects do exist. The next thing to consider will be moving from in vitro to in vivo studies where effects on the hypothalamic-pituitary-ovarian (HPO) axis can be considered. The majority of these studies are carried out with mice rather than human cancer cell lines but do provide useful insight into Cd as a metalloestrogen. This will lead right into some of the findings Sarah had mentioned as well.


    Darbre PD. 2006. Metalloestrogens: an emerging class of inorganic xenoestrogens with potential to add to the oestrogenic burden of the human breast. J Appl Toxicol 26: 191-197.

    Das S, Mukherjee D. 2013. Effects of cadmium chloride on secretion of 17β-estradiol by the ovarian follicles of common carp, Cyprinus carpio. Gen Comp Endocrin 181; 107-114.

    Henson MC, Chedrese PJ. 2004. Endocrine disruption by cadmium, a common environmental toxicant with paradoxical effects on reproduction. Experimental Bio Med 229: 383-3912.

    Le Guevel R, Petit FG, Le Goff P, Metivier R, Valotaire Y, Pakdel F. 2000. Inhibition of rainbow trout (Oncorhynchus mykiss) estrogen receptor activity by cadmium. Biol Reprod 63: 259-266.

    Pan J, Plant JA, Voulvoulis N, Oates CJ, Ihlenfeld C. 2010. Cadmium levels in Europe: implications for human health. Environ Geochem Health 32: 1-12.

    Silva N, Peiris-John R, Wickremasinghe R, Senanayake H, Sathiakumar N. 2012. J Appl Toxicol 32: 318-332.

    Silva E, Lepez-Espinosa MJ, Molina-Molina JM, Fernandez M, Olea N, Kortenkamp A. 2006. Lack of activity of Cd in in vitro estrogenic assays. Toxicol Appl Pharmacol 216: 20-28.

    Tilton SC, Foran Cm, Benson WH. 2003. Effects of cadmium on the reproductive axis of Japanese medaka (Oryzias latipesi). Comp Biochem Phys C 136: 265-276.

    Wood CM, Farrell AD, Brauner CJ. 2012. Homeostasis and toxicology of non- essential metals: Volume 31B. Academic Press/Elsevier, Waltham, Massachusetts, USA.

  5. Interesting topic – I don’t often think of metals as endocrine disruptors. Schantz and Widholm 2001 suggested that endocrine disruptors, including cadmium, can have cognitive effects in addition to reproductive effects due to the fact that many cognitive processes are mediated by hormones. Are cognitive effects generally considered when looking at endrocrine disruptors, especially something as toxic as cadmium and are endocrine disruptors recognized as neurotoxins? What implications might this have for developing brains of children and young adults?

  6. That is great suggestion and not one that I have come across so far in my research. I will definitely look into more for sure.

  7. Author –
    In the continued evaluation of Cd as a potential EDC, it would be to look at how Cd exposure may affect the hypothalamic-pituitary-gonad (HPO) axis. Briefly, the HPO axis is central in the regulation of mammalian reproduction function, interference with the components of the axis or the feedback mechanisms, which may result in effects on reproduction (Silva et al. 2012). The axis can be summarized as: gonadotropin releasing hormone (GnRH) from the hypothalamus acts on the anterior pituitary which will release follicle-stimulating hormone (FSH) and luteinizing hormone (LH), where FSH will interact with granulosa cells and LH with theca cells and ultimately release estrogen and progesterone. FSH is responsible for early maturation of ovarian follicles, FSH and LH together lead to final maturation and a LH surge is associated with ovulation. LH is also responsible for the formation of the corpus lutem which secretes estrogen and progesterone. The ovary stimulated by FSH will secrete estrogen, progesterone and androgens. All of this will occur in a feedback system where the resulting estrogen and progesterone levels will influence the release of GnRH and FSH or LH from the hypothalamus and anterior pituitary, respectively (Zhang et al. 2008; Silva et al. 2012)

    The in vivo work examining Cd on the HPO has had some interesting results. Han et al. (2006) found pigs fed a feed supplemented with 10 mg/kg Cd had significantly reduced FSH, estrogen and progesterone levels compared to control pigs. Work with golden hamsters found that Cd given at a dose of 5mg/kg resulted in a failure to ovulate and was associated with decreased plasma progesterone levels as well as hemorrhaging and necrosis of the ovary (Saksena and Salmonson 1983). A review by Henson and Chedrese (2004) summarized a collection of studies that found Cd decreased pituitary, GnRH, prolactin, ACTH, growth hormone, and thyroid-stimulating hormone in rats. Studies have also found inhibition of progesterone synthesis in human and rat granulosa cells and in pseduopregnant rats. Studies found that cultured human trophoblast cells showed inhibition of progesterone synthesis. Zhang et al. (2008) noted decreased progesterone and estrogen levels in ovary serum of rats. When Piasek et al. (2001) examined progesterone levels in pregnant women who did and did not smoke; a 2-fold increase in Cd levels was noted in smokers along with an almost 50% decrease in progesterone levels. While the review by Henson and Chedrese (2004) also highlighted that some studies have found the contrary that Cd exposure resulted in increased synthesis and serum levels of progesterone. Additionally, a look at multiple studies indicated that Cd may have stimulatory effects on progesterone synthesis at low doses and inhibitory at higher doses. Based on this the assumption that Cd does have affects on reproduction is supported but the doses for toxicity and actual mechanism(s) of action are not yet clearly defined.

    Further examination into the mechanism by Zhang and Jai (2007), found that Cd decreased the expression of steriodogenic acute regulatory protein (StAR) and cytochrome P450 side chain cleavage (P450scc). Where StAR delivers cholesterol to inner mitochondrial membrane and P450scc conveys cholesterol to pregnenolone which are both steps in progesterone synthesis. However, there are a number of factors involved and multiple sites along the HPO axis that may be affected. Though reproductive affects associated with Cd appear to be via direct interactions with the biosynthetic pathway and not inhibition by morphological changes (Henson and Chedrese 2004).


    Han XY, Xu ZR, Wang YZ, Du WL. 2006. Effects of cadmium on serum sex hormone levels in pigs. Jrl Animal Phys Animal Nutrition 90: 380-384.

    Henson MC, Chedrese PJ. 2004. Endocrine disruption by cadmium, a common environmental toxicant with paradoxical effects on reproduction. Experimental Bio Med 229: 383-3912.

    Piasek M, Blanusa M, Kostial K, Laskey JW. 2001. Placental cadmium and progesterone concentrations in cigarette smoke. Repro Toxicol 15: 673-681.

    Sakensa SK, Salmonson R. 1983. Effects of cadmium chloride on ovulation and on induction of sterility in the female golden hamster. Biol Reprod 29: 249-256.

    Silva N, Peiris-John R, Wickremasinghe R, Senanayake H, Sathiakumar N. 2012. Cadmium a metalloestrogen: are we convinced. J Appl Toxicol 32: 318-332.

    Zhang W, Jai H. 2007. Effect of mechanism of cadmium on the progesterone synthesis of ovaries. Toxicol 239: 204-212.

    Zhang W, Pang F, Huang Y, Yan P, Lin W. 2008. Cadmium exerts toxic effects on ovarian hormone release in rats. Toxicol Letters 182: 18-23.

  8. As I read up a little on Cd, I was surprised to find that quite a few countries have concerns regarding the concentration of Cd in soils, food and water (e.g. China, India, Australia and New Zealand).

    What caught my attention was a study conducted on children ages 6-15 in the USA found an association between Cd exposures and an increased incidence of learning disabilities requiring special education (Bellinger et al. 2012). The associations they discovered may not be unusual; however, Bellinger et al. (2012) claim these associations were found at Cd exposure concentrations that were previously thought to have no effects. On the other hand, the authors caveat their study by suggesting that their methods for diagnosis of learning disabilities and special education requirements could have been improved. I think this uncertainty with regard to study conclusions is similar to much of the research we have found for our respective chemicals. It brings home the point we discussed in class that increased uncertainty gives us an ambiguity in risk assessment that needs to be dealt with or at least acknowledged.

    Bellinger, D.C., T. Ciesielski, B. Lanphear, J. Schwartz, J. Weuve and R. O. Wright. 2012. Cadmium exposure and neurodevelopmental outcomes in U.S. children. Environmental Health Perspectives. 120(5):759p

  9. Author –
    In this reflection I wanted to touch on two things that were brought up in comments. One was why do we use cadmium and how may Cd be related to cognitive issues as mentioned last week.

    Cadmium exists naturally in the environment and is released by volcanic activity, weathering/erosion, and river transport. However, more than 90% of Cd in surface environments is from anthropogenic sources. These sources can be rock phosphate fertilizers, ash from fossil fuel combustion, cement manufacturing, metal works, municipal waste and sewage and atmospheric deposition (Pan et al. 2010; WHO 2010). Exposure to Cd through these pathways is mainly due to Cd being an impurity in the compounds (Wood et al. 2012). The actual uses of Cd include pigments (yellow and red), stabilizers (reduce degradation of PVCs), coatings, constituents in alloys and mainly in battery production which accounts for 83%. It also used in electroplating in the aircraft industry for example as it resist corrosion when applied to steel products. Though its use in products has been declining in recent years due to the health concerns surrounding Cd (WHO 2010; Wood et al. 2012). It is through these production processes that emissions of Cd are released into the atmosphere it can contribute to the long range transport of Cd into soils and water through atmospheric deposition. Thus contributing to elevated levels of Cd in water and soils which can enter into foodstuff such as leafy greens, root crops, cereals and grains. Another significant source of Cd exposure is through cigarette smoke (ASTDR 2008; Pan et al. 2010).

    So jumping ahead we have been discussing Cd as an EDC and as a metalloestrogen in the prior reflections because of its association with endocrine disruption. Since Cd, along with other chemicals such as dioxins, PCBs, and OPs for example, have been linked to hormone disruption some studies have looks at these disruptions in relation to cognitive effects. This linkage is that some of the central nervous system (CNS) development and functions are hormonally mediated (Schantz and Widholm, 2001). Which has led to speculation that environmental exposure to these compounds may result in cognitive deficits. As well as the interconnection between these hormonal systems may combine to result in cognitive defecits.

    Schantz and Widholm (2001) summarized that effects on brain development and cognition may occur by interference with sex steroid hormones, thyroid hormones and glucocorticoids. Where alteration in the timing of exposure to the sex steroid hormones, estrogen or testosterone may affect patterns of male and female development. Hypothyroidism during development may result in delayed myelinogenesis, alterations in cell migration, delayed or impaired neuronal differentiation and synaptogenesis, and alteration in neurotransmitter function. These alterations may result in permanent impairments in reflex development, motor activity, emotionality, and learning/memory deficits. Elevated levels of glucocorticoids can result in early ceasation of cell proliferation and affect axonal outgrowth, myelination, dendritic spines formation and synapotgensis.

    Ciesielski et al. (2013) summarized that Cd has been linked to reading difficulties, behavioral problems, reduced visual-motor performance, reduced attention and memory, and lower cognitive scores. However, many of these studies were with elderly adults and potential contributing factor were poorly assessed or not included. In their own study they found that a study of US adults aged 20-59 higher urinary Cd levels were associated with poorer performance on the four neurological tests given, when adjusted for only urinary creatine. However, these relationships were not significant after adjustments for confounding variables were made. Some of variables were age, sex, race-ethnicity, smoking status, education (in yrs), poverty income, blood lead, serum cotinie, and language exam was given. Where the authors concluded that higher cumulative cadmium exposure may be subtly related to decreased performance in attetion and perception requiring tasks. Another factor to consider when evaluating Cd based effects using cigarette smoke as a pathway of exposure is that cigarettes also contains other compounds, for example ammonia, acetaldehyde, benzene, styrene and chloroform. The industry has sacknowkleged that 599 different additives are included in cigarettes (Rabinoff et al. 2007; Jackson et al. 2011). Where a review of studies by Durazzo et al. (2010), indicates that chronic cigarette smoking was associated with deficines in neurocognition.

    From this I would suggest that Cd may have a role to play in cognitive effects but the scope of the studies need to be expanded so that confounding factors, (i.e. cigarette smoke) are better understood. So as to reduce overestimation of risk as will as to avoid under estimation of risk.


    ASTDR. Cadmium Toxicity Cover Page. 2008.

    Ciesielski T, Bellinger DC, Schawrtz J, Hauser R, Wright RO. 2013. Assocaitions between cadmium exposure and neurocognitive test scores in a cross-sectional study of US adults. Environ Health 12.

    Durazzo TC, Meyerhoff DJ, Nixon SJ. 2010. Chronic cigarette smoking: implications for neurocognition and brain neurobiology. Int J Environ Res Public Health 7: 3760-3791.

    Jackson LW, Howards PP, Wactawski-Wende J, Schisterman EF. 2011. The associations between cadmium, lead and mercury blood levels and reproducitve hormones among healthy, premenopausal women. Human Repro 26: 2887-2895.

    Pan J, Plant JA, Voulvoulis N, Oates CJ, Ihlenfeld. 2010. Cadmium levels in Europe: implcaitons for human health. Environ Geochem Health 32: 1-12.

    Rabinoff M, Caskey N, Rissling A, Park C. 2007. Pharmacological and chemical effects of cigarette additives. American Jrl Public Health 97:1981-1991.

    Schantz SL, Widholm JJ. 2001. Cognitive effects of endocrine-disrupting chemicals in animals. Environ Health Perspectives 109: 1197-1206.

    WHO. Cadmium. 2010. World Health Organization.

    Wood CM, Farrell AD, Brauner CJ. 2012. Homeostasis and toxicology of non- essential metals: Volume 31B. Academic Press/Elsevier, Waltham, Massachusetts, USA.

  10. I find the uptake of Cd into plants interesting. I was wondering if the Canadian government monitors Cd levels in produce? Are there certain species of crop that have a greater capacity to accumulate Cd relative to others that we should be concerned about? A quick scan of the literature revealed that cadmium has been found to hyperaccumulate (>100 mg/kg in tissue) in plants from the genus Thalspi and accumulation in rice grain and tobacco leaves are the greatest concern to humans (Kirkham 2006).

    Kirkham MB. 2006. Cadmium in plants on polluted soils: effects of soil factors, hyperaccumulation, and amendments. Geoderma, 137:19-32.

  11. That is an interesting route of exposure to investigate. I found an Aboriginal Affairs and Northern Development Canada Report (2010) investigating Cd as a metal of concern in Yukon and concluded that Willow (Salix artica) is known as a cadmium-accumulating plant. There are also established consumption guidelines for Cd in organ meats in Yukon game with caribou and moose which are continuously monitored.

    Breda has brought up this important consideration in discussion – that of differences in sensitive or more susceptible populations. After discussion in classes regarding northern populations that may rely more on game meat and other “delicacies”, it may be important in quantifying these differences in exposure to certain population in Cd assessments. With regard to this, diets that are low in calcium, iron and protein and that are high in fat, allow for higher absorption of Cd, which may be important when considering exposure to humans. Great discussion Melissa! It will be interesting to see what happens with the EDC effects of Cd in mixture with other metals/EDC compounds in your PhD research!

  12. Just a quick clarifying question about the HPO axis. If progesterone synthesis is being inhibited does that mean that the pathway is being over stimulated as there is no negative feedback? Or is the axis sufficiently inhibited by the synthesized estrogens?

  13. There is so much research on endocrine disrupters. It would be interesting to compare how cadmium compares to other endocrine disrupters in both exposure and toxicity. Is cadmium a major endocrine disruptor of concern or are there other endocrine disrupters that are much more potent and/or abundant? Furthermore, is there potential for cadmium to interact with other endocrine disrupters or are its effects additive?

  14. Author
    Many chemicals and metals have been linked to endocrine disruption. Some very strongly and others through weak associations. I am actually working on some of those comparisons in my PhD project. I can post that table on here as well once I have finished my literature review. To sort of answer your additive question there are likely be such interactions. Again, part of my project is to evaluate how Cd interacts with other metals on fish reproduction. So yes Cd could be additive with other EDC or the opposite where for example Zn seems to be protective of Cd exposure.

  15. Author –
    Exposure to Cd mainly occurs through occupational exposure or smoking. Though exposure can occur through ingestion of food and water containing Cd and inhalation of Cd in the atmosphere. Pan et al (2010) summarized estimated exposure concentrations (Tables 1 and 2) from a variety of studies and WHO data. Guideline values of maximum allowable Cd in drinking water are 2.5 ug/l for the US, 5.0 ug/l for Canada and 3.0 ug/L for WHO in industrial areas.

    Production of Cd in the US began in 1907, peaked in 1969 and has been declining worldwide due primarily to health concerns and its association with cancer. In 2003 the EU prohibited incorporation of Cd and other heavy metals in most electrical and electronic concerns which helped further drop levels (Huff et al. 2007). These concerns arose from epidemiological and animal studies linking Cd exposure through various routes to the formation of benign and malignant tumors. More recently Cd has been linked with hormone dependant cancers such as breast cancer and prostate cancer due to its association with being an EDC (Huff et al. 2007, Pan et al. 2010). Silva et al (2012) summarized that studies have found increased blood or urine Cd levels leads to increased risk of breast cancer. Cantor et al. (1995), found in a study examining 33,000 death certificates attributed to cancer and 117 000 non cancer, there was association with occupational Cd exposure. McElroy et al. (2006) found in a study of women aged 20-69 with breast cancer, age matched with control women that higher urine Cd levels had a 2.9 increased risk of breast cancer. Åkesson et al. 2008 found a 2.9 increased risk in endometrial cancer in post menopausal women after long term dietary exposure. There are also studies that found no significant increase in risk and Cd exposure. One such study was carried out by Itoh et al. (2008) and found no association between urine Cd and endometriosis. When looking at prostate cancer recently Julin et al. (2012), carried out a study that found dietary exposure was associated with a slight increase in prostate cancer risk.

    As a quick wrap-up to Cd as an EDC, there is evidence that Cd can interact with estrogen receptors and progesterone levels. These associations have gone on to be associated with low birth weights, increased incidences of spontaneous abortion and premature delivery in females. In males sperm motility and mobility can be impaired by Cd exposure. As well as now being associated with hormone-dependant cancers. So what does this mean in regards to Cd? Well Cd is a metal that our exposure is mainly due to our activities and the effects of that exposure can have impacts on kidneys, liver, bone, reproductive organs, possibly cognition and incidences of cancer. Those at greatest risk are those exposed occupationally but also those who are smokers. Inhalation of cigarettes either actively or passively can change what is generally a fairly low exposure to much higher. Either way Cd is a highly toxic carcinogen and even at low levels can have detrimental effects in an array of potential outcomes.

    Åkesson A, Julin B, Wolk A. 2008. Long-term dietary cadmium intake and postmenopausal endometrial cancer incidence: a population-based prospective cohort study. Cancer Research 68: 6435-6441.

    Cantor KP, Stewart PA, Brinton LA, Dosemeci M. 1995. Occupational and female breast cancer mortality in the United States. JOEM 37: 339-348. PDF

    Huff J, Lunn RM, Waalkes Mp, Tomatis L, Infante PF. Cadmium-induced cancers in animals and humans. Int Jrl Occup Environ Health 13: 202-212. PDF

    Itoh K, Iwasaki M, Nakajima Y, Endo Y, Hanaoka T, Sasaki H, Tanaka T, Tsugane S. 2008. A case-control study of the association between urinary cadmium concentration and endometriosis in infertile Japanese women. Sci Total Environ 402: 171-175.

    Julin B, Wolk A, Johansson JE, Andersson SO, Andren O, Åkesson A. 2012. Dietary cadmium exposure and prostate cancer indicence: a population-based prospective cohort study. British Jrl Cancer 107: 895-900.

    McElroy JA, Shafer MM, Trenham-Dietz A, Hampton JM, Newcomb PA. 2006. Cadmium exposure and breast cancer risk. Jrl Natl Cancer Inst 98: 869-873.

    Pan J, Plant JA, Voulvoulis N, Oates CJ, Ihlenfeld. 2010. Cadmium levels in Europe: implications for human health. Environ Geochem Health 32: 1-12.

    Silva N, Peiris-John R, Wickremasinghe R, Senanayake H, Sathiakumar N. 2012. Cadmium a metalloestrogen: are we convinced. J Appl Toxicol 32: 318-332.

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