Background information on cadmium poisoning in support of a "fact sheet" for lay adjudicators

Prepared for the Occupational Disease Panel (Industrial Disease Standards Panel)
Ministry of Labour
Ontario, Canada
Jennifer Penney
July 1993

The following report "Background information on cadmium poisoning in support of a "fact sheet" for "lay adjudicators" was commissioned by the Occupational Disease Panel. The Panel has not entered into deliberations on this subject and takes no official position on the findings of this researcher.

      Part 1. Sources of Cadmium Exposure
    Occupational exposures
    Non-occupational exposures
      Part 2. Health Outcomes of Cadmium Exposure
    Acute effects
    Chronic respiratory effects
    Kidney effects
    Skeletal effects
    Other effects
      Part 3. Biological Testing Methods For Cadmium Exposures
    Cadmium in the blood
    Cadmium in the urine
    Markers of early renal effects of cadmium exposure
    Direct measurement of cadmium concentration
    in liver and kidneys
      Part 4. Cadmium Exposure Limits


This paper accompanies a prototype "fact sheet" intended to help lay adjudicators dealing with claims for industrial disease or "poisoning" as a result of occupational exposure to cadmium. It provides the rationale for the information included on the fact sheet, as well as further references which an adjudicator might consult in the process of making a decision.


Cadmium has a large array of uses, and its production has climbed steadily during the last forty years, although certain applications have recently declined. Industrial exposure levels in some industries were very high through the 1950's and 60's. [12] In the last two decades, however, occupational exposures have dropped, following the dramatic reduction of exposure limits in most industrialized nations. [74] Many scientists and policy makers acknowledge the need to continue reducing exposures to this very toxic metal. Some jurisdictions have prohibited specific uses of cadmium.

Cadmium may be encountered in work other than that listed below. Because of the wide variety of uses for cadmium, it is not possible to provide an exhaustive list. Industries are listed in order of potential exposures, from higher to lower.








E.          CANCER



Three main tests are used for measuring cadmium exposures: cadmium in whole blood, cadmium in urine, and measurement of plasma proteins in urine. A number of other tests may be employed in investigating cadmium-related health effects. Some of these are mentioned in Part II. They will not be described further here.


Mainly because of ease of analysis, cadmium in whole blood has been used as a biological indicator of occupational exposures. [72] Cadmium concentrations in blood are mainly a reflection of recent exposure. [80] The ACGIH suggests that monitoring in blood is preferred during the initial year of exposure and whenever changes in the degree of exposure are suspected. [4] In workers not currently exposed, cadmium in blood decreases substantially. [95] When declining blood cadmium levels reach a steady state, they are considered to reflect body burden from previous exposures.

Normal values of cadmium in blood of non-smokers are generally less than 1 ug/l. [72] Higher average values of 1.4 to 4.2 ug/l are found in smokers, though individual blood cadmium levels in smokers may exceed these values. [27]

In 1991, the Ontario Ministry of Labour suggested medical assessment for exposed workers whose blood cadmium level reaches 11 ug/l. [76] However, OSHA recently chose 5 ug Cd/l of whole blood as a level at which further medical surveillance is required of American workers. If this level of cadmium in blood is accompanied by protein in the urine, then OSHA requires workers to be medically removed. [75] A level of 15 ug Cd/l is cause for removal without proteinuria. The ACGIH has also recently proposed a Biological Exposure Index of 5 ug/l of cadmium in blood. The BEI "is intended to prevent the potential for increased urinary excretion of markers of renal dysfunction in almost all workers". [4]


Cadmium concentration in urine is considered to be more reflective of body burden in currently-exposed workers than cadmium in blood, and is the most widely used biological measure of chronic exposure to cadmium. Cadmium in urine increases with age, cigarette smoking, and exposures in the general and occupational environments.

The normal concentration of cadmium in urine is from 0.1 to 1 ug/g creatinine. [27] Until recently, a measure of 10 ug Cd/g creatinine has been regarded as a threshold for kidney effects. However, a number of recent studies have cast doubt on this figure. [79, 92] Evidence of subtle kidney effects are demonstrated at levels a low as 2 ug Cd/g creatinine. [15, 79] Levels of 5 to 1ug Cd/g creatinine are associated with a 10% risk of increased excretion of enzymes and proteins. [78] OSHA recently chose a level of 3 ug Cd/g creatinine as a trigger for enhancing medical surveillance of cadmium. If this level of cadmium in urine is accompanied by proteinuria, then OSHA requires medical removal of the affected worker. A level of 15 ug/g creatinine is cause for removal without proteinuria. [75] The ACGIH has recommended a new Biological Exposure Index (BEI) of 5 ug/g creatinine for cadmium in urine.


While not a measure of cadmium exposure per se, the increase of proteins in urine is a marker of damage to the kidneys which precedes or accompanies most health effects associated with cadmium exposure. One particular protein -- beta2-microglobulin (BMG) -- has been extensively used as an indicator of cadmium-related damage to the proximal tubules of the kidney. BMG excretion may be elevated due to other causes: anti-cancer drugs, antibacterial antibiotics such as streptomycin, anti-inflammatory compounds, myeloma, flu and upper respiratory tract infections. [75] These factors can be readily identified, and need not confound the diagnosis of cadmium-related proteinuria.

Levels of BMG are considered elevated by most investigators at 300 ug/g creatinine, [22, 78] although levels as low as 200 or as high as 500 ug/g creatinine have been suggested as abnormal. [32, 60] OSHA mandates a removal level of 1500 ug BMG/g creatinine, if cadmium levels in blood or urine are elevated.

Exposures to cadmium for 20 years at a level 50 ug/m3 (0.05 mg/m3), the current Ontario limit, give rise to a greatly increased incidence of tubular proteinuria as indicated by output of BMG. [65]

In recent years, a number of other markers for cadmium effects have been recommended. Several of these markers appear to be more sensitive to the early effects of cadmium on the kidney, and/or more stable than BMG in urine. The following markers have been assessed and shown to have significant association with cadmium exposure:

Conventional indicators of renal function such as total urinary protein, serum urea, and serum creatinine are considered insensitive indicators of early renal dysfunction, but may indicate the progression of cadmium-related damage. [15, 50, 55]


Neutron activation analysis is a new method which allows for the direct measurement of the cadmium burden in the liver and kidney. The technique involves use of an ultrasonic scan to precisely locate the target organs, followed by irradiation with a neutron beam which allows assessment of organ burden by measurement of cadmium-specific gamma rays. [14, 30, 31, 37] The radiation dosage is less than most conventional x-rays. [32]

For workers who have been out of exposure for some time or who have suffered kidney damage, this technique can provide a more accurate measure of body burden and may help in determining if non-specific diseases such as emphysema are cadmium-related. This equipment has been employed in England to resolve compensation disputes. [14] Only one Canadian facility is currently equipped to carry out this kind of analysis -- at McMaster University in Hamilton.

Estimation of liver burden is considered more appropriate because once renal damage occurs, cadmium excretion increases and the kidneys lose their cadmium burden. Liver and kidney burdens increase until a 40 ppm concentration is reached in the liver, after which kidney levels decrease while liver burden continues to rise. One study measured a mean liver cadmium burden of 0.6 ppm in non-exposed controls. [65]

X-ray fluorescence, another technique for in vivo measurement of cadmium body burden, has also been developed recently, but is not generally available at this time. [13]


Exposure limits for cadmium and its compounds have declined steadily over time, as the knowledge about cadmium-related diseases has grown. The current Ontario time-weighted average limit of 0.05 mg/m3 is considered too high by many scientists. Ontario is currently considering a new limit of 0.02 mg/m3, to match the lower Dutch limit. The Dutch Working Group of Experts which reviewed cadmium's toxicity in 1980, actually proposed a health-based limit of 0.01 mg/m3. [96] However, this limit was not considered feasible at the time. The cadmium limit is again under review in the Netherlands.

In Sweden, a limit of 0.01 mg/m3 is in effect for all new industries employing cadmium or its compounds.

In 1990, the American Conference of Governmental Industrial Hygienists (ACGIH), an influential body which produces a list of Threshold Limit Values adopted by many governments as enforceable occupational exposure limits, proposed a new total dust limit of 0.01 mg/m3 for cadmium, and a 0.002 mg/m3 respirable dust limit. [3]

In 1992, after an exhaustive review of occupational exposures, toxicity and feasibility issues, the U.S. Occupational Safety and Health Administration adopted a new cadmium limit of 0.005 mg/m3, one-tenth of the current Ontario limit, in order to prevent kidney effects and cancer in exposed workers. [75]

In 1991 and 1992, a lively debate occurred in the scientific literature on the question of a protective occupational exposure limit. [13, 53, 67, 91] Proposed protective limits varied from a low of 0.001 mg/m3 [89] through 0.01 mg/m3 [13]. One author suggested a limit in the range of 0.01 - 0.1 mg/m3 might be protective, but put some emphasis on 0.02 mg/m3 [67]. Although there is not consensus on the level of a protective limit, there is considerable agreement in the scientific community that a limit of 0.05 mg/m3 does not provide sufficient protection, and that kidney effects occur at this level of exposure.


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A.          Sources of Exposure (The following list not exhaustive. Industries are ranked from most to least exposed.)

B.          Health Effects of Cadmium Exposure

C.          Biological Testing Methods

D.          Occupational Exposure Limits