Biomonitoring Summary


CAS No. 7440-43-9

General Information

Cadmium is a soft, malleable, bluish-white metal that is obtained chiefly as a by-product of processing zinc-containing ores (principally sphalerite, as zinc sulfide) and to a lesser extent, during refining of lead and copper from sulfide ore. The predominant commercial use of cadmium is in battery manufacturing. Other uses include pigment production, coatings and plating, plastic stabilizers, and nonferrous alloys. Since 2001, U.S. cadmium use has declined in response to environmental concerns ( icon). Important sources of airborne cadmium in the environment are burning fossil fuels such as coal or oil, and incineration of municipal waste materials. Cadmium also may be emitted into the air from zinc, lead, or copper smelters (U.S EPA 2000). Cadmium in soil is absorbed by plants, including many food crops such as cereal grains, wheat, rice, potatoes, and various seeds. To a lesser exten
t, drinking water is a source for cadmium intake.

Cadmium is absorbed via inhalation and ingestion. Inhalation of cigarette smoke is a predominant source of exposure in smokers, whose body burdens of cadmium can be approximately twice that of nonsmokers. For nonsmokers who are not exposed to cadmium in the workplace, ingestion through food is the largest source of exposure. The gastrointestinal absorption of dietary cadmium is about 5% in adult men and 10% or higher in women (Diamond et al., 2003; Horiguchi et al., 2004a; Kikuchi et al., 2003), however, individual values vary and are affected by factors such as dietary intake of essential nutrients (iron, calcium, zinc, copper) and protein. Cadmium absorption may be increased with iron deficiency (Berglund et al., 1994), a factor that may contribute to the higher absorption of cadmium by women (Diamond et al., 2003). With chronic exposure, cadmium accumulates in the liver and kidneys where it is bound to metallothionein, an inducible metal binding protein. About one-third to one half of the total body burden accumulates in the kidney tissues (Nordberg and Nordberg, 2001). The estimated half-life of cadmium in the kidney is from one to four decades (ATSDR 2008; Diamond et al., 2003).

The kidney is a critical target and shows the earliest sign of cadmium toxicity. Renal tubular and glomerular damage, manifested by irreversible proteinuria and progressive reduction in glomerular filtration rate, can result from high dose chronic exposure, most often a result of occupational exposure (Roels et al., 1999). Most studies of relatively low level environmental exposure to cadmium have demonstrated associations between higher urine or blood cadmium levels and an increased prevalence of various biomarkers of renal tubular effects (Alfven et al., 2002; Jarup et al., 2000; Noonan et al., 2002; Olsson et al., 2002; Staessen et al., 1996, 1999). However, two studies in Japan did not find an association between cadmium in urine and renal biomarkers (Ezaki et al., 2003; Horiguchi et al., 2004b). Whether the markers of renal tubular effects found in populations with low environmental exposure are likely to progress or predict an increased risk for developing clinically evident renal dysfunction
is unknown (Hotz et al., 1999).

Increased urinary excretion of calcium and phosphorus and decreased hydroxylation of vitamin D metabolites that accompany advanced renal tubular damage resulted in painful osteomalacia or osteoporosis. Known as “itai-itai” (“ouch-ouch”), this condition affected postmenopausal women living in a cadmium-polluted region of Japan, mainly during the 1950’s and 1960’s. Kidney dysfunction that led to osteoporosis was associated with very high urine cadmium levels in residents of an area of China where extensive environmental cadmium pollution occurred (Jin et al., 2004). At lower environmental exposures, older adults and postmenopausal women with greater urine cadmium levels may have an increased risk for bone fracture and diminished bone mineral density (Alfven et al., 2002; Staessen et al., 1999).

Acute and heavy exposure to airborne dusts and fumes, as may occur from welding cadmium-alloyed metals, has resulted in severe, potentially fatal pneumonitis (Fernandez et al., 1996). Chronic inhalation exposure to cadmium particulates was associated with changes in pulmonary function and chest radiographs that were consistent with emphysema (Davidson et al., 1988). Workplace exposure to airborne cadmium particulates was associated with decreases in olfactory function (Mascagni et al., 2003). Animal studies have demonstrated reproductive and teratogenic effects. Small epidemiologic studies have noted an inverse relationship between cadmium in cord blood, maternal blood or maternal urine and birth weight (Nishijo et al., 2002; Salpietro et al., 2002) and length at birth (Nishijo et al., 2004; Zhang et al, 2004).

Cadmium can produce lung, pituitary gland and kidney tumors in animals and has been associated with lung cancer in humans in occupational epidemiologic studies. Both IARC and NTP consider cadmium a human carcinogen. Waalkes (2003) provides an overview and summarizes potential mechanisms for carcinogenicity. Workplace standards and guidelines for air exposure to cadmium have been established by OSHA and ACGIH, respectively, and drinking water and environmental standards have been established by U.S. EPA. Information about external exposure (i.e., environmental levels) and health effects is available from ATSDR at

Biomonitoring Information

Blood cadmium reflects both recent and cumulative exposures. In the typical environmental exposure, urinary cadmium reflects both cumulative exposure and the concentration of cadmium in the kidney.

Surveys of populations not known to have increased cadmium exposure have reported similar urine and blood levels (Becker et al., 2002; Becker et al., 2003; CDC, 2012; Friedman et al., 2006; Komaromy-Hiller et al., 2000; Wennberg et al., 2006; Wilhelm et al., 2006). Women had higher blood and urine cadmium levels compared to men of similar ages, with peak values observed in the fifth to sixth decades (CDC, 2012; Horiguchi et al., 2004b; Olsson et al., 2002; Wennberg et al., 2006). For NHANES 1999-2000, blood cadmium was also slightly higher in Mexican Americans and participants 20 years and older (CDC, 2012). Blood and urine cadmium levels are typically higher in cigarette smokers, intermediate in former smokers and lower in never-smokers (Becker et al., 2003; Becker et al., 2002; Mannino et al., 2004; Mortensen et al., 2011; Olsson et al., 2002). Blood cadmium levels are about twice as high in smokers compared to never-smokers (Becker et al., 2003; Becker et al, 2002; Olsson et al., 2002). Several studies of populations residing in areas with higher cadmium soil concentrations or with frank cadmium pollution have reported mean blood and urine cadmium levels considerably higher (as much as 10 times higher) than control groups or representative U.S. data (CDC, 2012; Ezaki et al., 2003; Jarup et al., 2000; Jin et al., 2004; Staessen et al., 1999; Staessen et al., 1996; Suwazono et al., 2000). Creatinine-corrected urine cadmium values in U.S. study subjects living near a former zinc smelter were similar to those from an unexposed community and to those in the U. S. population (CDC, 2012; Noonan et al., 2002).

People who are occupationally exposed may have blood and urine cadmium levels that are higher than those of the general population. The 95th percentiles for cadmium levels in the U.S. population were less than the OSHA standards for both blood cadmium (5 ?g/L) and urine cadmium (3 ?g/gram of creatinine) (CDC, 2012). Occupational standards are provided here for comparison only, not to imply a safety level for general population exposure.

Subtle increases in markers of renal tubular effects have been associated with urine cadmium levels as low as approximately 1 ?g/gram of creatinine (Akesson et al., 2005; Ezaki et al., 2003; Jarup et al., 2000; Moriguchi et al., 2004; Noonan et al., 2002). However, two studies of women in Japan with lower exposures found no correlation between renal tubular effect markers and blood or urine cadmium levels (geometric means were 1.26 and 3.46 ?g/gram of creatinine) (Ezaki et al., 2003; Horiguchi et al., 2004b). In postmenopausal women, decreased bone density was correlated with mean urinary cadmium levels of approximately 1 ?g/gram of creatinine (Staessen et al., 1999). In adults aged 60 years and older, the risk of low bone mineral density increased by nearly three-fold when the blood cadmium exceeded 1.1 ?g/L (Alfven et al., 2002). In the U.S. population, adult urinary and blood cadmium levels at the 95th and 90th percentiles, respectively, approached these values associated with subclinical changes in renal function and bone mineral density (CDC, 2012), and self-reported cigarette smoking in adults was associated with an increased risk for exceeding a cut-point of 1.0 ?g Cd/g creatinine (Mortensen et al., 2011) . Further research is needed to address the public health consequences of such exposure in the United States.

Finding a measurable amount of cadmium in blood or urine does not imply that the levels of cadmium cause an adverse health effect. Biomonitoring studies on levels of cadmium provide physicians and public health officials with reference values so they can determine whether people have been exposed to higher levels of cadmium than are found in the general population. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.


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