California Code of Regulations › Title 8 - Industrial Relations › Division 1 - Department of Industrial Relations › Chapter 4 - Division of Industrial Safety › Subchapter 7 - General Industry Safety Orders › Group 16 - Control of Hazardous Substances › Article 110 - Regulated Carcinogens › Appendix A - Substance Safety Data Sheet Cadmium

Current through Register 2024 Notice Reg. No. 28, July 12, 2024
I. Substance Identification
A. Substance: Cadmium.
B. 8-Hour, Time-weighted-average, Permissible Exposure
						  Limit (TWA PEL):
1. TWA PEL: Five micrograms of cadmium per cubic meter
						  of air 5 µg/m3, time-weighted average (TWA)
						  for an 8-hour workday.
C. Appearance: Cadmium metal - soft, blue-white,
						  malleable, lustrous metal or grayish-white powder. Some cadmium compounds may
						  also appear as a brown, yellow, or red powdery substance.
II. Health Hazard Data
A. Routes of Exposure.
Cadmium can cause local skin or eye irritation. Cadmium
						  can affect your health if you inhale it or if you swallow it.
B. Effects of overexposure.
1. Short-term (acute) exposure: Cadmium is much more
						  dangerous by inhalation than by ingestion. High exposures to cadmium that may
						  be immediately dangerous to life or health occur in jobs where workers handle
						  large quantities of cadmium dust or fume; heat cadmium-containing compounds or
						  cadmium-coated surfaces; weld with cadmium solders or cut cadmium-containing
						  materials such as bolts.
2. Severe exposure may occur before symptoms appear.
						  Early symptoms may include mild irritation of the upper respiratory tract, a
						  sensation of constriction of the throat, a metallic taste and/or a cough. A
						  period of 1 - 10 hours may precede the onset of rapidly progressing shortness
						  of breath, chest pain, and flu-like symptoms with weakness, fever, headache,
						  chills, sweating and muscular pain. Acute pulmonary edema usually develops
						  within 24 hours and reaches a maximum by three days. If death from asphyxia
						  does not occur, symptoms may resolve within a week.
3. Long-term (chronic) exposure. Repeated or long-term
						  exposure to cadmium, even at relatively low concentrations, may result in
						  kidney damage and an increased risk of cancer of the lung and of the
						  prostate.
C. Emergency First Aid Procedures
1. Eye exposure: Direct contact may cause redness or
						  pain. Wash eyes immediately with large amounts of water, lifting the upper and
						  lower eyelids. Get medical attention immediately.
2. Skin exposure: Direct contact may result in
						  irritation. Remove contaminated clothing and shoes immediately. Wash affected
						  area with soap or mild detergent and large amounts of water. Get medical
						  attention immediately.
3. Ingestion: Ingestion may result in vomiting,
						  abdominal pain, nausea, diarrhea, headache and sore throat. Treatment for
						  symptoms must be administered by medical personnel. Under no circumstances
						  should the employer allow any person whom he retains, employs, supervises or
						  controls to engage in therapeutic chelation. Such treatment is likely to
						  translocate cadmium from pulmonary or other tissue to renal tissue. Get medical
						  attention immediately.
4. Inhalation: If large amounts of cadmium are inhaled,
						  the exposed person must be moved to fresh air at once. If breathing has
						  stopped, perform cardiopulmonary resuscitation. Administer oxygen if available.
						  Keep the affected person warm and at rest. Get medical attention
						  immediately.
5. Rescue: Move the affected person from the hazardous
						  exposure. If the exposed person has been overcome, attempt rescue only after
						  notifying at least one other person of the emergency and putting into effect
						  established emergency procedures. Do not become a casualty yourself. Understand
						  your emergency rescue procedures and know the location of the emergency
						  equipment before the need arises.
III. Employee Information
A. Protective Clothing and Equipment
1. Respirators: You may be required to wear a
						  respirator for non-routine activities; in emergencies; while your employer is
						  in the process of reducing cadmium exposures through engineering controls; and
						  where engineering controls are not feasible. If respirators are worn in the
						  future, they must have a joint Mine Safety and Health Administration (MSHA) and
						  National Institute for Occupational Safety and Health (NIOSH) label of
						  approval. Cadmium does not have a detectable odor except at levels well above
						  the permissible exposure limits. If you can smell cadmium while wearing a
						  respirator, proceed immediately to fresh air. If you experience difficulty
						  breathing while wearing a respirator, tell your employer.
2. Protective Clothing: You may be required to wear
						  impermeable clothing, gloves, foot gear, a face shield, or other appropriate
						  protective clothing to prevent skin contact with cadmium. Where protective
						  clothing is required, your employer must provide clean garments to you as
						  necessary to assure that the clothing protects you adequately. The employer
						  must replace or repair protective clothing that has become torn or otherwise
						  damaged.
3. Eye Protection: You may be required to wear
						  splash-proof or dust resistant goggles to prevent eye contact with
						  cadmium.
B. Employer Requirements
1. Medical: If you are exposed to cadmium at or above
						  the action level, your employer is required to provide a medical examination,
						  laboratory tests and a medical history according to the medical surveillance
						  provisions under paragraph (
l
) of this standard. (See summary
						  chart and tables in this Appendix A.) These tests shall be provided without
						  cost to you. In addition, if you are accidentally exposed to cadmium under
						  conditions known or suspected to constitute toxic exposure to cadmium, your
						  employer is required to make special tests available to you.
2. Access to Records: All medical records are kept
						  strictly confidential. You or your representative are entitled to see the
						  records of measurements of your exposure to cadmium. Your medical examination
						  records can be furnished to your personal physician or designated
						  representative upon request by you to your employer.
3. Observation of Monitoring: Your employer is required
						  to perform measurements that are representative of your exposure to cadmium and
						  you or your designated representative are entitled to observe the monitoring
						  procedure. You are entitled to observe the steps taken in the measurement
						  procedure, and to record the results obtained. When the monitoring procedure is
						  taking place in an area where respirators or personal protective clothing and
						  equipment are required to be worn, you or your representative must also be
						  provided with, and must wear the protective clothing and equipment.
C. Employee Requirements
You will not be able to smoke, eat, drink, chew gum or
						  tobacco, or apply cosmetics while working with cadmium in regulated areas. You
						  will also not be able to carry or store tobacco products, gum, food, drinks or
						  cosmetics in regulated areas because these products easily become contaminated
						  with cadmium from the workplace and can therefore create another source
						  unnecessary of cadmium exposure.
Some workers will have to change out of work clothes
						  and shower at the end of the day, as part of their workday, in order to wash
						  cadmium from skin and hair. Handwashing and cadmium-free eating facilities
						  shall be provided by the employer and proper hygiene should always be performed
						  before eating. It is also recommended that you do not smoke or use tobacco
						  products, because among other things, they naturally contain cadmium. For
						  further information, read the labeling on such products.
IV. Physician Information
A. Introduction
The medical surveillance provisions of paragraph
						  (
l
) generally are aimed at accomplishing three main
						  interrelated purposes: first, identifying employees at higher risk of adverse
						  health effects from excess, chronic exposure to cadmium; second, preventing
						  cadmium-induced disease; and third, detecting and minimizing existing
						  cadmium-induced disease. The core of medical surveillance in this standard is
						  the early and periodic monitoring of the employee's biological indicators of:
						  a) recent exposure to cadmium; b) cadmium body burden; and c) potential and
						  actual kidney damage associated with exposure to cadmium.
The main adverse health effects associated with cadmium
						  overexposure are lung cancer and kidney dysfunction. It is not yet known how to
						  adequately biologically monitor human beings to specifically prevent
						  cadmium-induced lung cancer. By contrast, the kidney can be monitored to
						  provide prevention and early detection of cadmium-induced kidney damage. Since,
						  for non-carcinogenic effects, the kidney is considered the primary target organ
						  of chronic exposure to cadmium, the medical surveillance provisions of this
						  standard effectively focus on cadmium-induced kidney disease. Within that
						  focus, the aim, where possible, is to prevent the onset of such disease and,
						  where necessary, to minimize such disease as may already exist. The by-products
						  of successful prevention of kidney disease are anticipated to be the reduction
						  and prevention of other cadmium-induced diseases.
B. Health Effects
The major health effects associated with cadmium
						  overexposure are described below.
1. Kidney
The most prevalent non-malignant disease observed among
						  workers chronically exposed to cadmium is kidney dysfunction. Initially, such
						  dysfunction is manifested as proteinuria. The proteinuria associated with
						  cadmium exposure is most commonly characterized by excretion of low-molecular
						  weight proteins (15,000 to 40,000 MW) accompanied by loss of electrolytes, uric
						  acid, calcium, amino acids, and phosphate. The compounds commonly excreted
						  include: beta-2-microglobulin (I2-M), retinol binding
						  protein (RBP), immunoglobulin light chains, and lysozyme. Excretion of low
						  molecular weight proteins are characteristic of damage to the proximal tubules
						  of the kidney (Iwao
et al
., 1980).
It has also been observed that exposure to cadmium may
						  lead to urinary excretion of high-molecular weight proteins such as albumin,
						  immunoglobulin G, and glycoproteins (Ex. 29). Excretion of high-molecular
						  weight proteins is typically indicative of damage to the glomeruli of the
						  kidney. Bernard
et al
., (1979) suggest that damage to the
						  glomeruli and damage to the proximal tubules of the kidney may both be linked
						  to cadmium exposure but they may occur independently of each other.
Several studies indicate that the onset of
						  low-molecular weight proteinuria is a sign of irreversible kidney damage
						  (Friberg
et al
., 1974; Roels
et al
., 1982;
						  Piscator 1984; Elinder
et al
., 1985; Smith
et
						  al
., 1986). Above specific levels of l2-M
						  associated with cadmium exposure it is unlikely that
						  l2-M levels return to normal even when cadmium exposure
						  is eliminated by removal of the individual from the cadmium work environment
						  (Friberg, Ex. 29, 1990).
Some studies indicate that such proteinuria may be
						  progressive; levels of l2-M observed in the urine
						  increase with time even after cadmium exposure has ceased. See, for example,
						  Elinder
et al
., 1985. Such observations, however, are not
						  universal, and it has been suggested that studies in which proteinuria has not
						  been observed to progress may not have tracked patients for a sufficiently long
						  time interval (Jarup, Ex. 8-661).
When cadmium exposure continues after the onset of
						  proteinuria, chronic nephrotoxicity may occur (Friberg, Ex. 29). Uremia results
						  from the inability of the glomerulus to adequately filter blood. This leads to
						  severe disturbance of electrolyte concentrations and may lead to various
						  clinical complications including kidney stones (L-140-50).
After prolonged exposure to cadmium, glomerular
						  proteinuria, glucosuria, aminoaciduria, phosphaturia, and hypercalciuria may
						  develop (Exs. 8-86, 4-28, 14-18). Phosphate, calcium, glucose, and amino acids
						  are essential to life, and under normal conditions, their excretion should be
						  regulated by the kidney. Once low molecular weight proteinuria has developed,
						  these elements dissipate from the human body. Loss of glomerular function may
						  also occur, manifested by decreased glomerular filtration rate and increased
						  serum creatinine. Severe cadmium- induced renal damage may eventually develop
						  into chronic renal failure and uremia (Ex. 55).
Studies in which animals are chronically exposed to
						  cadmium confirm the renal effects observed in humans (Friberg
et
						  al
., 1986). Animal studies also confirm problems with calcium
						  metabolism and related skeletal effects which have been observed among humans
						  exposed to cadmium in addition to the renal effects. Other effects commonly
						  reported in chronic animal studies include anemia, changes in liver morphology,
						  immunosuppression and hypertension. Some of these effects may be associated
						  with co- factors. Hypertension, for example, appears to be associated with diet
						  as well as cadmium exposure. Animals injected with cadmium have also shown
						  testicular necrosis (Ex. 8-86B).
2. Biological Markers
It is universally recognized that the best measures of
						  cadmium exposures and its effects are measurements of cadmium in biological
						  fluids, especially urine and blood. Of the two, CdU is conventionally used to
						  determine body burden of cadmium in workers without kidney disease. CdB is
						  conventionally used to monitor for recent exposure to cadmium. In addition,
						  levels of CdU and CdB historically have been used to predict the percent of the
						  population likely to develop kidney disease (Thun
et
al
., Ex. L-140-50; WHO, Ex. 8-674; ACGIH, Exs. 8-667,
						  140-50).
The third biological parameter upon which OSHA relies
						  for medical surveillance is Beta-2-microglobulin in urine
						  (l2-M), a low molecular weight protein. Excess
						  l2-M has been widely accepted by physicians and
						  scientists as a reliable indicator of functional damage to the proximal tubule
						  of the kidney (Exs. 8-447, 144-3-C, 4-47, L-140-45, 19-43-A).
Excess l2-M is found when the
						  proximal tubules can no longer reabsorb this protein in a normal manner. This
						  failure of the proximal tubules is an early stage of a kind of kidney disease
						  that commonly occurs among workers with excessive cadmium exposure. Used in
						  conjunction with biological test results indicating abnormal levels of CdU and
						  CdB, the finding of excess l2-M can establish for an
						  examining physician that any existing kidney disease is probably
						  cadmium-related (Trs. 6/6/90, pp. 82-86, 122, 134). The upper limits of normal
						  levels for cadmium in urine and cadmium in blood are 3 µg Cd/gram
						  creatinine in urine and 5 µg Cd/liter whole blood, respectively. These
						  levels were derived from broad-based population studies.
Three issues confront the physicians in the use of
						  l2-M as a marker of kidney dysfunction and material
						  impairment. First, there are a few other causes of elevated levels of
						  l2-M not related to cadmium exposures, some of which may
						  be rather common diseases and some of which are serious diseases (e.g., myeloma
						  or transient flu, Exs. 29 and 8-086). These can be medically evaluated as
						  alternative causes (Friberg, Ex. 29). Also, there are other factors that can
						  cause l2-M to degrade so that low levels would result in
						  workers with tubular dysfunction. For example, regarding the degradation of
						  l2-M, workers with acidic urine (pH < 6) might have
						  l2-M levels that are within the "normal" range when in
						  fact kidney dysfunction has occurred (Ex. L-140-1) and the low molecular weight
						  proteins are degraded in acid urine. Thus, it is very important that the pH of
						  urine be measured, that urine samples be buffered as necessary (See Appendix
						  F.), and that urine samples be handled correctly, i.e., measure the pH of
						  freshly voided urine samples, then if necessary, buffer to pH > 6 (or above
						  for shipping purposes), measure pH again and then, perhaps, freeze the sample
						  for storage and shipping. (See also Appendix F.) Second, there is debate over
						  the pathological significance of proteinuria, however, most world experts
						  believe that l2-M levels greater than 300 µg/g Cr
						  are abnormal (Elinder, Ex. 55, Friberg, Ex. 29). Such levels signify kidney
						  dysfunction that constitutes material impairment of health. Finally, detection
						  of l2-M at low levels has often been considered
						  difficult, however, many laboratories have the capability of detecting excess
						  l2-M using simple kits, such as the Phadebas Delphia
						  test, that are accurate to levels of 100 µg l2-M/g
						  Cr U (Ex. L-140-1).
Specific recommendations for ways to measure
						  l2-M and proper handling of urine samples to prevent
						  degradation of l2-M have been addressed by OSHA in
						  Appendix F, in the section on laboratory standardization. All biological
						  samples must be analyzed in a laboratory that is proficient in the analysis of
						  that particular analyte, under paragraph (
l
)(1)(iv). [See
						  Appendix F]. Specifically, under paragraph (
l
)(1)(iv), the
						  employer is to assure that the collecting and handling of biological samples of
						  cadmium in urine (CdU), cadmium in blood (CdB), and beta-2 microglobulin in
						  urine (l2-M) taken from employees is collected in a
						  manner that assures reliability. The employer must also assure that analysis of
						  biological samples of cadmium in urine (CdU), cadmium in blood (CdB), and
						  beta-2 microglobulin in urine (l2-M) taken from
						  employees is performed in laboratories with demonstrated proficiency for that
						  particular analyte. (See Appendix F.)
3. Lung and Prostate Cancer
The primary sites for cadmium-associated cancer appear
						  to be the lung and the prostate (L-140-50). Evidence for an association between
						  cancer and cadmium exposure derives from both epidemiological studies and
						  animal experiments. Mortality from prostate cancer associated with cadmium is
						  slightly elevated in several industrial cohorts, but the number of cases is
						  small and there is not clear dose-response relationship. More substantive
						  evidence exists for lung cancer.
The major epidemiological study of lung cancer was
						  conducted by Thun
et al
., (Ex. 4-68). Adequate data on cadmium
						  exposures were available to allow evaluation of dose-response relationships
						  between cadmium exposure and lung cancer. A statistically significant excess of
						  lung cancer attributed to cadmium exposure was observed in this study even when
						  confounding variables such as co-exposure to arsenic and smoking habits were
						  taken into consideration (Ex. L-140-50).
The primary evidence for quantifying a link between
						  lung cancer and cadmium exposure from animal studies derives from two rat
						  bioassay studies; one by Takenaka
et al
., (1983), which is a
						  study of cadmium chloride and a second study by Oldiges and Glaser (1990) of
						  four cadmium compounds.
Based on the above cited studies, the U.S.
						  Environmental Protection Agency (EPA) classified cadmium as "B1", a probable
						  human carcinogen, in 1985 (Ex. 4-4). The International Agency for Research on
						  Cancer (IARC) in 1987 also recommended that cadmium be listed as "2A", a
						  probable human carcinogen (Ex. 4-15). The American Conference of Governmental
						  Industrial Hygienists (ACGIH) has recently recommended that cadmium be labeled
						  as a carcinogen. Since 1984, NIOSH has concluded that cadmium is possibly a
						  human carcinogen and has recommended that exposures be controlled to the lowest
						  level feasible.
4. Non-carcinogenic Effects
Acute pneumonitis occurs 10 to 24 hours after initial
						  acute inhalation of high levels of cadmium fumes with symptoms such as fever
						  and chest pain (Exs. 30, 8-86B). In extreme exposure cases pulmonary edema may
						  develop and cause death several days after exposure. Little actual exposure
						  measurement data is available on the level of airborne cadmium exposure that
						  causes such immediate adverse lung effects, nonetheless, it is reasonable to
						  believe a cadmium concentration of approximately 1
						  mg/m3 over an eight hour period is "immediately
						  dangerous" (55 FR 4052, ANSI; Ex. 8-86B).
In addition to acute lung effects and chronic renal
						  effects, long term exposure to cadmium may cause other severe effects on the
						  respiratory system. Reduced pulmonary function and chronic lung disease
						  indicative of emphysema have been observed in workers who have had prolonged
						  exposure to cadmium dust or fumes (Exs. 4-29, 4-22, 4-42, 4-50, 4-63). In a
						  study of workers conducted by Kazantzis
et al
., a
						  statistically significant excess of worker deaths due to chronic bronchitis was
						  found, which in his opinion was directly related to high cadmium exposures of 1
						  mg/m3 or more (Tr. 6/8/90, pp. 156-157).
Cadmium need not be respirable to constitute a hazard.
						  Inspirable cadmium particles that are too large to be respirable but small
						  enough to enter the tracheobronchial region of the lung can lead to
						  bronchoconstriction, chronic pulmonary disease, and cancer of that portion of
						  the lung. All of these diseases have been associated with occupational exposure
						  to cadmium (Ex. 8- 86B). Particles that are constrained by their size to the
						  extra-thoracic regions of the respiratory system such as the nose and maxillary
						  sinuses can be swallowed through mucocillary clearance and be absorbed into the
						  body (ACGIH, Ex. 8-692). The impaction of these particles in the upper airways
						  can lead to anosmia, or loss of sense of smell, which is an early indication of
						  overexposure among workers exposed to heavy metals. This condition is commonly
						  reported among cadmium-exposed workers (Ex. 8-86-B).
C. Medical Surveillance
In general, the main provisions of the medical
						  surveillance section of the standard, under paragraphs
						  (
l
)(1)-(17) of the regulatory text, are as follows:
1. Workers exposed above the action level are
						  covered;
2. Workers with intermittent exposures are not
						  covered;
3. Past workers who are covered receive biological
						  monitoring for at least one year;
4. Initial examinations include a medical questionnaire
						  and biological monitoring of cadmium in blood (CdB), cadmium in urine (CdU),
						  and Beta-2-microglobulin in urine (l2-M);
5. Biological monitoring of these three analytes is
						  performed at least annually; full medical examinations are performed
						  biennially;
6. Until five years from the effective date of the
						  standard, medical removal is required when CdU is greater than 15 µg/gram
						  creatinine (g Cr), or CdB is greater than 15 µg/liter whole blood (lwb),
						  or l2-M is greater than 1500 µg/g Cr, and CdB is
						  greater than 5 µg/lwb or CdU is greater than 3 µg/g Cr;
7. Beginning five years after the standard is in
						  effect, medical removal triggers will be reduced;
8. Medical removal protection benefits are to be
						  provided for up to 18 months;
9. Limited initial medical examinations are required
						  for respirator usage;
10. Major provisions are fully described under section
						  (
l
) of the regulatory text; they are outlined here as
						  follows:
A. Eligibility
B. Biological monitoring
C. Actions triggered by levels of CdU, CdB, and
						  l2-M (See Summary Charts and Tables in
						  Attachment-1.)
D. Periodic medical surveillance
E. Actions triggered by periodic medical surveillance
						  (See Appendix A Summary Chart and Tables in Attachment-1.)
F. Respirator usage
G. Emergency medical examinations
H. Termination examination
I. Information to physician
J. Physician's medical opinion
K. Medical removal protection
L. Medical removal protection benefits
M. Multiple physician review
N. Alternate physician review
O. Information employer gives to employee
P. Recordkeeping
Q. Reporting on OSHA form 200
11. The above mentioned summary of the medical
						  surveillance provisions, the summary chart, and tables for the actions
						  triggered at different levels of CdU, CdB and l2-M (in
						  Appendix A Attachment-1) are included only for the purpose of facilitating
						  understanding of the provisions of paragraphs (
l
)(3) of the
						  final cadmium standard. The summary of the provisions, the summary chart, and
						  the tables do not add to or reduce the requirements in paragraph
						  (
l
)(3).
D. Recommendations to Physicians
1. It is strongly recommended that patients with
						  tubular proteinuria are counseled on: the hazards of smoking; avoidance of
						  nephrotoxins and certain prescriptions and over-the-counter medications that
						  may exacerbate kidney symptoms; how to control diabetes and/or blood pressure;
						  proper hydration, diet, and exercise (Ex. 19-2). A list of prominent or common
						  nephrotoxins is attached. (See Appendix A Attachment-2.)
2. DO NOT CHELATE; KNOW WHICH DRUGS ARE NEPHROTOXINS OR
						  ARE ASSOCIATED WITH NEPHRITIS.
3. The gravity of cadmium-induced renal damage is
						  compounded by the fact there is no medical treatment to prevent or reduce the
						  accumulation of cadmium in the kidney (Ex. 8-619). Dr. Friberg, a leading world
						  expert on cadmium toxicity, indicated in 1992, that there is no form of
						  chelating agent that could be used without substantial risk. He stated that
						  tubular proteinuria has to be treated in the same way as other kidney disorders
						  (Ex. 29).
4. After the results of a workers' biological
						  monitoring or medical examination are received the employer is required to
						  provide an information sheet to the patient, briefly explaining the
						  significance of the results. (See Attachment 3 of this Appendix A.)
5. For additional information the physician is referred
						  to the following additional resources:
a. The physician can always obtain a copy of the
						  preamble, with its full discussion of the health effects, from OSHA's
						  Computerized Information System (OCIS).
b. The Docket Officer maintains a record of the
						  rulemaking. The Cadmium Docket (H-057A), is located at 200 Constitution Ave.
						  N.W., Room N-2625, Washington, D.C. 20210; telephone: 202-523-7894.
c. The following articles and exhibits in particular
						  from that docket (H-057A):
Exhibit
									 number
Author and paper
									 title
8-447
Lauwerys et. al., Guide for
								  physicians, Health Maintenance of Workers Exposed to Cadmium published by the
								  Cadmium Council
4-67.
Takenaka, S., H. Oldiges, H. Konig,
								  D. Hochrainer, G. Oberdorster. "Carcinogenicity of Cadmium Chloride Aerosols in
								  Wistar Rats". JNCI 70:367-373, 1983. (32)
4-68.
Thun, M.J., T.M. Schnoor, A.B.
								  Smith, W.E. Halperin, R.A. Lemen. "Mortality Among a Cohort of U.S. Cadmium
								  Production Workers - An Update." JNCI 74(2):325-33, 1985. (8)
4-25.
Elinder, C.G., Kjellstrom, T.,
								  Hogstedt, C.,
et al
., "Cancer Mortality of Cadmium Workers.
								  Brit. J. Ind. Med. 42:651-655, 1985. (14)
4-26.
Ellis, K.J.
et
								  al
., "Critical Concentrations of Cadmium in Human Renal Cortex: Dose
								  Effect Studies to Cadmium Smelter Workers." J. Toxicol. Environ. Health
								  7:691-703, 1981. (76)
4-27.
Ellis, K.J., S.H. Cohn and T.J.
								  Smith. "Cadmium Inhalation Exposure Estimates: Their Significance with Respect
								  to Kidney and Liver Cadmium Burden." J. Toxicol. Environ. Health 15:173-187,
								  1985.
4-28.
Falck, F.Y., Jr., Fine, L.J.,
								  Smith, R.G., McClatchey, K.D., Annesley, T., England, B., and Schork, A.M.
								  "Occupational Cadmium Exposure and Renal Status." Am J.Ind.Med. 4:541, 1983.
								  (64)
8-86A.
Friberg, L., C.G. Elinder,
et al
., Cadmium and Health a Toxicological and Epidemiological
								  Appraisal Volume I Exposure, Dose, and Metabolism. CRC Press, Inc., Boca Raton,
								  FL, 1986. (Available from the OSHA Technical Data Center)
8-86B.
Friberg, L., C.G. Elinder, et al.
								  Cadmium and Health: A Toxicological and Epidemiological Appraisal Volume II
								  Effects and Response. CRC Press, Inc., Boca Raton, FL, 1986. (Available from
								  the OSHA Technical Data Center)
L-140-45.
Elinder, C.G., "Cancer Morality
								  of Cadmium Workers", Brit. J. Ind. Med., 42, 651-655, 1985.
L-140-50.
Thun, M., Elinder, C.G.,
								  Friberg, L, "Scientific Basis for an Occupational Standard for Cadmium, Am. J.
								  Ind. Med., 20; 629-642, 1991.
V. Information Sheet
The information sheet (Appendix A Attachment-3.) or an
						  equally explanatory one should be provided to you after any biological
						  monitoring results are reviewed by the physician, or where applicable, after
						  any medical examination.
Appendix A--Attachment 1
Summary Chart And Tables A And B Of Actions
						  Triggered By Biological Monitoring
Appendix A Summary Chart: Section (1)(3) Medical
						  Surveillance
CATEGORIZING BIOLOGICAL MONITORING RESULTS
(A) Biological monitoring results categories are set
						  forth in Appendix A Table A for the periods ending December 31, 1998 and for
						  the period beginning January 1, 1999.
(B) The results of the biological monitoring for the
						  initial medical exam and the subsequent exams shall determine an employee's
						  biological monitoring result category.
ACTIONS TRIGGERED BY BIOLOGICAL MONITORING
(A)(i) The actions triggered by biological monitoring
						  for an employee are set forth in Appendix A Table B.
(ii) The biological monitoring results for each
						  employee under section (1)(3) shall determine the actions required for that
						  employee. That is, for any employee in biological monitoring category C, the
						  employer will perform all of the actions for which there is an X in column C of
						  Appendix A Table B.
(iii) An employee is assigned the alphabetical category
						  ("A" being the lowest) depending upon the test results of the three biological
						  markers.
(iv) An employee is assigned category A if monitoring
						  results for all three biological markers fall at or below the levels indicated
						  in the table listed for category A.
(v) An employee is assigned category B if any
						  monitoring result for any of the three biological markers fall within the range
						  of levels indicated in the table listed for category B, providing no result
						  exceeds the levels listed for category B.
(vi) An employee is assigned category C if any
						  monitoring result for any of the three biological markers are above the levels
						  listed for category C.
(B) The user of Appendix A Tables A and B should know
						  that these tables are provided only to facilitate understanding of the relevant
						  provisions of paragraph (
l
)(3) of this section. Appendix A
						  Tables A and B are not meant to add to or subtract from the requirements of
						  those provisions.
Appendix A--Table A
Categorization Of Biological Monitoring Results
						  Applicable Through 1998 Only
Biological
Monitoring Result
									 Categories
Marker
A
B
C
cadmium in urine (CdU) (µg/g
								  creatinine)
[LESS THAN EQUAL TO]3
> 3 and [LESS THAN EQUAL
								  TO] 15
> 15
ß2-microglobulin
								  (ß2-M) (µg/g creatinine) cadium in blood
								  (CdB)
[LESS THAN EQUAL TO]300
> 300 and [LESS THAN EQUAL
								  TO]1500
> 1500*
(µg/liter whole blood)
[LESS THAN
								  EQUAL TO]5
> 5 and [LESS THAN EQUAL TO] 15
> 15
* If an employee's ß2-M
						  levels are above 1,500 µg/g creatinine, in order for mandatory medical
						  removal to be required (See Appendix A Table B.), either the employee's CdU
						  level must also be > 3 µg/g creatinine or CdB level must also be >
						  5 µg/liter whole blood
Applicable Beginning January 1,
						  1999
Biological
Monitoring Result
									 Categories
Marker
A
B
C
cadmium in urine (CdU) (µg/g
								  creatinine)
[LESS THAN EQUAL TO] 3
> 3 and [LESS THAN EQUAL
								  TO] 7
> 7
ß2-microglobulin
								  (ß2-M) (µg/g creatinine) cadium in blood
								  (CdB)
[LESS THAN EQUAL TO] 300
> 300 and [LESS THAN EQUAL
								  TO] 750
> 750*
(µg/liter whole blood)
[LESS THAN
								  EQUAL TO] 5
> 5 and [LESS THAN EQUAL TO] 10
> 10
* If an employee's ß2-M
						  levels are above 1,500 µg/g creatinine, in order for mandatory medical
						  removal to be required (See Appendix A Table B.), either the employee's CdU
						  level must also be > 3 µg/g creatinine or CdB level must also be >
						  5 µg/liter whole blood.
Appendix A--Table B
Actions Determined By Biological
						  Monitoring
This table presents the actions required based on the
						  monitoring result in Appendix A Table A. Each item is a separate requirement in
						  citing non-compliance. For example, a medical examination within 90 days for an
						  employee in category B is separate from the requirement to administer a
						  periodic medical examination for category B on an annual basis.
Required
								  Actions
Monitoring Result
								  Category
A*
B*
C*
(1)
Biological Monitoring
(a) Annual
X
(b) Semiannual
X
(c) Quarterly
X
(2)
Medical Examination
(a) Biennial
X
(b) Annual
X
(c) Semiannual
X
(d) Within 90 days
X
X
(3)
Assess Within Two Weeks
(a) Excess Cadmium Exposure
X
X
(b) Work Practices
X
X
(c) Personal Hygiene
X
X
(d) Respirator Usage
X
X
(e) Smoking History
X
X
(f) Hygiene Facilities
X
X
(g) Engineering Controls
X
X
(h) Correct within 30 days
X
X
(i) Periodically Assess
								  Exposures
X
(4)
Discretionary Medical
								  Removal
X
X
(5)
Mandatory Medical Removal
X**
__________
* For all employees covered by medical surveillance
						  exclusively because of exposures prior to the effective date of this standard,
						  if they are in Category A, the employer shall follow the requirements of
						  paragraphs (
l
)(3)(i)(B) and (l)(4)(v)(A). If they are in
						  Category B or C, the employer shall follow the requirements of paragraphs
						  (l)(4)(v)(B)-(C).
** See footnote Appendix A Table A.
Appendix A--Attachment 2
List Of Medications
A list of the more common medications that a physician,
						  and the employee, may wish to review is likely to include some of the
						  following: (1) anticonvulsants: paramethadione, phenytoin, trimethadone; (2)
						  antihypertensive drugs: captopril, methyldopa; (3) antimicrobials:
						  aminoglycosides, amphotericin B, cephalosporins, ethambutol; (4) antineoplastic
						  agents: cisplatin, methotrexate, mitomycin-C, nitrosoureas, radiation; (4)
						  sulfonamide diuretics: acetazolamide, chlorthalidone, furosemide, thiazides;
						  (5) halogenated alkanes, hydrocarbons, and solvents that may occur in some
						  settings: carbon tetrachloride, ethylene glycol, toluene; iodinated
						  radiographic contrast media; nonsteroidal anti-inflammatory drugs; and, (7)
						  other miscellaneous compounds: acetominophen, allopurinol, amphetamines,
						  azathioprine, cimetidine, cyclosporine, lithium, methoxyflurane, methysergide,
						  D-penicillamine, phenacetin, phenendione. A list of drugs associated with acute
						  interstitial nephritis includes: (1) antimicrobial drugs: cephalosporins,
						  chloramphenicol, colistin, erythromycin, ethambutol, isoniazid,
						  para-aminosalicylic acid, penicillins, polymyxin B, rifampin, sulfonamides,
						  tetracyclines, and vancomycin; (2) other miscellaneous drugs: allopurinol,
						  antipyrene, azathioprine, captopril, cimetidine, clofibrate, methyldopa,
						  phenindione, phenylpropanolamine, phenytoin, probenecid, sulfinpyrazone,
						  sulfonamid diuretics, triamterene; and, (3) metals: bismuth, gold.
This list have been derived from commonly available
						  medical textbooks (e.g., Ex. 14-18). The list has been included merely to
						  facilitate the physician's, employer's, and employee's understanding. The list
						  does not represent an official OSHA opinion or policy regarding the use of
						  these medications for particular employees. The use of such medications should
						  be under physician discretion.
Appendix A--Attachment 3
Biological Monitoring and Medical Examination
						  Results
Employee ____________________
Testing Date ____________________
Normal
									 Levels
Cadmium in Urine
µg/g
								  Cr
[LESS THAN EQUAL TO] 3 µg/g Cr
Cadmium in
								  Blood
µg/lwb
[LESS THAN EQUAL TO] 5 µg/lwb
Beta-2-microglobulin in
								  Urine
µg/g Cr [LESS THAN EQUAL TO] 300 µg/g Cr
Physical Examination Results: N/A _________________
						  Satisfactory _________________ Unsatisfactory _________________ (see physician
						  again)
Physician's Review of Pulmonary Function Test: N/A
						  _________________
Normal __________ Abnormal __________
Next biological monitoring or medical examination
						  scheduled for
___________________________
The biological monitoring program has been designed for
						  three main purposes: 1) to identify employees at risk of adverse health efforts
						  from excess, chronic exposure to cadmium; 2) to prevent cadmium-induced
						  disease(s); and 3) to detect and minimize existing cadmium-induced
						  disease(s).
The levels of cadmium in the urine and blood provide an
						  estimate of the total amount of cadmium in the body. The amount of a specific
						  protein in the urine (beta-2-microglobulin) indicates changes in kidney
						  function. All three tests must be evaluated together. A single mildly elevated
						  result may not be important if testing at a later time indicates that the
						  results are normal and the workplace has been evaluated to decrease possible
						  sources of cadmium exposure. The levels of cadmium or beta-2-microglobulin may
						  change over a period of days to months and the time needed for those changes to
						  occur is different for each worker.
If the results for biological monitoring are above
						  specific "high levels" [cadmium urine greater than 10 micrograms per gram of
						  creatinine (µg Cr), cadmium blood greater than 10 micrograms per liter of
						  whole blood (µg/lwb), or beta-2-microglobulin greater than 1000
						  micrograms per gram of creatinine (µg Cr)], the worker has a much greater
						  chance of developing other kidney diseases.
One way to measure for kidney function is by measuring
						  beta-2- microglobulin in the urine. Beta-2-microglobulin is a protein which is
						  normally found in the blood as it is being filtered in the kidney, and the
						  kidney reabsorbs or returns almost all of the beta-2-microglobulin to the
						  blood. A very small amount (less than 300 µg/g Cr in the urine) of
						  beta-2-microglobulin is not reabsorbed into the blood, but is released in the
						  urine. If cadmium damages the kidney, the amount of beta-2-microglobulin in the
						  urine increases because the kidney cells are unable to reabsorb the
						  beta-2-microglobulin normally. An increase in the amount of
						  beta-2-microglobulin in the urine is a very early sign of kidney dysfunction. A
						  small increase in beta-2-microglobulin in the urine will serve as an early
						  warning sign that the worker may be absorbing cadmium from the air, cigarettes
						  contaminated in the workplace, or eating in areas that are cadmium
						  contaminated.
Even if cadmium causes permanent changes in the
						  kidney's ability to reabsorb beta-2-microglobulin, and the beta-2-
						  microglobulin is above the "high levels", the loss of kidney function may not
						  lead to any serious health problems. Also, renal function naturally declines as
						  people age. The risk for changes in kidney function for workers who have
						  biological monitoring results between the "normal values" and the "high levels"
						  is not well known. Some people are more cadmium-tolerant, while others are more
						  cadmium-susceptible.
For anyone with even a slight increase of
						  beta-2-microglobulin, cadmium in the urine, or cadmium in the blood, it is very
						  important to protect the kidney from further damage. Kidney damage can come
						  from other sources than excess cadmium-exposure so it is also recommended that
						  if a worker's levels are "high" he/she should receive counseling about drinking
						  more water; avoiding cadmium- tainted tobacco and certain medications
						  (nephrotoxins, acetaminophen); controlling diet, vitamin intake, blood pressure
						  and diabetes; etc.