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Prophylactic chelation is prohibited by the lead standard. Diagnostic and therapeutic chelation are permitted only under the supervision of a licensed physician with appropriate medical monitoring in an acceptable clinical setting. The decision to initiate chelation therapy must be made on an individual basis and must take into account the severity of symptoms felt to be a result of lead toxicity along with blood lead levels, ZPP levels, and other laboratory tests as appropriate. EDTA and penicillamine, which are the primary chelating agents used in the therapy of occupational lead poisoning, have significant potential side effects and their use must be justified on the basis of expected benefits to the worker. Unless frank and severe symptoms are present, therapeutic chelation is not recommended, given the opportunity to remove a worker from exposure and allow the body to naturally excrete accumulated lead. As a diagnostic aid, the chelation mobilization test using Ca-EDTA has limited applicability. According to some investigators, the test can differentiate between lead-induced and other nephropathies. The test may also provide an estimation of the mobile fraction of the total body lead burden.
Employers are required to assure that accurate records are maintained on exposure monitoring, medical surveillance, and medical removal for each employee. Exposure monitoring and medical surveillance records must be kept for 40 years or the duration of employment plus 20 years, whichever is longer, while medical removal records must be maintained for the duration of employment. All records required under the standard must be available upon request to the Chief of the Division of Occupational Safety and Health and the Director of the National Institute for Occupational Safety and Health. Employees must also make environmental and biological monitoring and medical removal records available to affected employees and to former employees or their authorized employee representatives. Employees or their specifically designated representatives have access to their entire medical surveillance records.
In addition, the standard requires that the employer inform all workers exposed to lead at or above the action level of the provisions of the standard and all its appendices, the purpose and description of medical surveillance and provisions for medical removal protection if temporary removal is required. An understanding of the potential health effects of lead exposure by all exposed employees along with full understanding of their rights under the lead standard is essential for an effective monitoring program.
II. Adverse health effects of inorganic lead
Although the toxicity of lead has been known for 2,000 years, the knowledge of the complex relationship between lead exposure and human response is still being refined. Significant research into the toxic properties of lead continues throughout the world, and it should be anticipated that our understanding of thresholds of effects and margin of safety will be improved in future years. The provisions of the lead standard are founded on two prime medical judgments: first, the prevention of adverse health effects from exposure to lead throughout a working lifetime requires that worker blood lead levels be maintained at or below 40 m g/100g; and second, the blood lead levels of workers, male or female, who intend to parent in the near future should be maintained below 30 m g/100g to minimize adverse reproductive health effects to the parents and developing fetus. The adverse effects of lead on reproduction are being actively researched and the physician is encouraged to remainabreast of recent developments in the area to best advise pregnant workers or workers planning to conceive children.
The spectrum of health effects caused by lead exposure can be subdivided into five developmental stages: normal, physiological changes of uncertain significance, overt symptoms (morbidity), and mortality. Within this process there are no sharp distinctions, but rather a continuum of effects. Boundaries between categories overlap due to the wide variation of individual responses and exposures in the working population. The development of the lead standard focused on pathophysiological changes as well as later stages of disease.
1. Heme Synthesis Inhibition. The earliest demonstrated effect of lead involves its ability to inhibit at least two enzymes of the heme synthesis pathway at very low blood lead levels. Inhibition of delta aminolevulinic acid dehydrase (ALA-D) which catalyzes the conversion of delta-aminolevulinic acid (ALA) to protoporphyrin is observed at a blood lead level below 20 m g/100g of whole blood. At a blood lead level of 40 m g/100g, more than 20% of the population would have 70% inhibition of ALA-D. There is an exponential increase in ALA excretion at blood lead levels greater than 40 m g/100g.
Another enzyme, ferrochelatase, is also inhibited at low blood lead levels. Inhibition of ferrochelatase leads to increase free erythrocyte protoporphyrin (FEP) in the blood which can then bind to zinc to yield zinc protoporphyrin (ZPP). At a blood lead level of 50 m g/100g or greater, nearly 100% of the population will have an increase in FEP. There is also an exponential relationship between blood lead levels greater than 40 m g/100g and the associated ZPP level, which has led to the development of the ZPP screening test for lead exposure.
While the significance of these effects is subject to debate, these enzymatic disturbances may be early stages of a disease process which eventually results in the clinical symptoms of lead poisoning. Whether or not the effects do progress to the later stages of clinical disease, disruption of these enzymatic processes over a working lifetime is considered to be a material impairment of health.
One of the eventual results of lead-induced inhibition of enzymes in the heme synthesis pathway is anemia which can be asymptomatic if mild but associated with a wide array of symptoms including dizziness, fatigue, and tachycardia when more severe. Studies have indicated that lead levels as low as 50 m g/100g can be associated with a definite decreased hemoglobin, although most cases of lead-induced anemia, as well as shortened red-cell survival times, occur at lead levels exceeding 80 m g/100g. Inhibited hemoglobin synthesis is more common in chronic cases whereas shortened erythrocyte life span is more common in acute cases.

In lead-induced anemias, there is usually a reticulocytosis along with the presence of basophilic stippling, and ringed sideroblasts, although none of the above are pathognomonic for lead-induced anemia.
2. Neurological Effects. Inorganic lead has been found to have toxic effects on both the central and peripheral nervous systems. The earliest stages of lead-induced central nervous system effects are manifested by behavioral disturbances and central nervous system symptoms including irritability, restlessness, insomnia and other sleep disturbances, fatigue, vertigo, headache, poor memory, tremor, depression, and apathy. With more severe exposure, symptoms can progress to drowsiness, stupor, hallucinations, delirium, convulsions and coma.
The most severe and acute form of lead poisoning which usually follows ingestion or inhalation of large amounts of lead is acute encephalopathy which may arise precipitously with the onset of intractable seizures, coma, cardiorespiratory arrest, and death within 48 hours.
While there is disagreement about what exposure levels are needed to produce the earliest symptoms, most experts agree that symptoms definitely can occur at blood lead levels of 60 m g/100g whole blood and therefore recommend a 40 m g/100g maximum. The central nervous system effects frequently are not reversible following discontinued exposure or chelation therapy and when improvement does occur, it is almost always only partial.
The peripheral neuropathy resulting from lead exposure characteristically involves only motor function with minimal sensory damage and has a marked predilection for the extensor muscles of the most active extremity. The peripheral neuropathy can occur with varying degrees of severi ty. The earliest and mildest form which can be detected in workers with blood lead levels as low as 50 m g/100g is manifested by slowing of motor nerve conduction velocity often without clinical symptoms. With progression of the neuropathy there is development of painless extensor muscle weakness usually involving the extensor muscles of the fingers and hand in the most active upper extremity, followed in severe cases by wrist drop or, much less commonly, foot drop.
In addition to slowing of nerve conduction, electromyographical studies in patients with blood lead levels greater than 50 m g/100g have demonstrated a decrease in the number of acting motor unit potentials, an increase in the duration of motor unit potentials, and spontaneous pathological activity including fibrillations and fasciculations. Whether these effects occur at levels of 40 m g/100g is undetermined.

While the peripheral neuropathies can occasionally be reversed with therapy, again such recovery is not assured particularly in the more severe neuropathies and often improvement is only partial. The lack of reversibility is felt to be due in part to segmental demyelination.
3. Gastrointestinal. Lead may also affect the gastrointestinal system producing abdominal colic or diffuse abdominal pain, constipation, obstipation, diarrhea, anorexia, nausea and vomiting. Lead colic rarely develops at blood lead levels below 80 m g/100g.
4. Renal. Renal toxicity represents one of the most serious health effects of lead poisoning. In the early stages of disease nuclear inclusion bodies can frequently be identified in proximal renal tubular cells. Renal function remains normal and the changes in this stage are probably reversible. With more advanced disease there is progressive interstitial fibrosis and impaired renal function. Eventually extensive interstitial fibrosis ensues with sclerotic glomeruli and dilated and atrophied proximal tubules; all represent end stage kidney disease. Azotemia can be progressive, eventually resulting in frank uremia necessitating dialysis. There is occasionally associated hypertension and hyperuricemia with or without gout.

Early kidney disease is difficult to detect. The urinalysis is normal in early lead nephropathy and the blood urea nitrogen and serum creatinine increase only when two-thirds of kidney function is lost. Measurement of creatinine clearance can often detect earlier disease as can other methods of measurement of glomerular filtration rate. An abnormal Ca-EDTA mobilization test has been used to differentiate between lead-induced and other nephropathies, but this procedure is not widely accepted. A form of Fanconi syndrome with aminoaciduria, glycosuria, and hyperphosphaturia indicating severe injury to the proximal renal tubules is occasionally seen in children.
5. Reproductive effects. Exposure to lead can have serious effects on reproductive function in both males and females. In male workers exposed to lead there can be a decrease in sexual drive, impotence, decreased ability to produce healthy sperm, and sterility. Malformed sperm (teratospermia), decreased number of sperm (hypospermia), and sperm with decreased motility (asthenospermia) can all occur. Teratospermia has been noted at mean blood lead levels of 53 m g/100g and hypospermia and asthenospermia at 41 m g/100g. Furthermore, there appears to be adose-response relationship for teratospermia in lead exposed workers.

Women exposed to lead may experience menstrual disturbances including dysmenorrhea, menorrhagia and amenorrhea. Following exposure to lead, women have a higher frequency of sterility, premature births, spontaneous miscarriages, and stillbirths.
Germ cells can be affected by lead and cause genetic damage in the egg or sperm cells before conception and result in failure to implant, miscarriage, stillbirth, or birth defects.
Infants of mothers with lead poisoning have a higher mortality during the first year and suffer from lowered birth weights, slower growth, and nervous system disorders.
Lead can pass through the placental barrier and lead levels in the mother's blood are comparable to concentrations of lead in the umbilical cord at birth. Transplacental passage becomes detectable at 12-14 weeks of gestation and increases until birth.
There is little direct data on damage to the fetus from exposure to lead but it is generally assumed that the fetus and newborn would be at least as susceptible to neurological damage as young children. Blood lead levels of 50- 60 m g/100g in children can cause significant neurobehavioral impairments and there is evidence of hyperactivity at blood lead levels as low as 25 m g/100g. Given the overall body of literature concerning the adverse health effects of lead in children, it is recommended that the blood lead level in children should be maintained below 30 m g/100g with a population mean of 15 m g/100g. Blood lead levels in the fetus and newborn likewise should not exceed 30 m g/100g.
Because of lead's ability to pass through the placental barrier and also because of the demonstrated adverse effects of lead on reproductive function in both the male and female as well as the risk of genetic damage of lead on both the ovum and sperm, a 30 m g/100g maximum permissible blood lead level is recommended for both males and females who wish to bear children.
6. Other toxic effects. Debate and research continue on the effects of lead on the human body. Hypertension has frequently been noted in occupationally exposed individuals although it is difficult to assess whether this is due to lead's adverse effects on the kidney or if some other mechanism is involved. Vascular and electrocardiographic changes have been detected but have not been well characterized. Lead is thought to impair thyroid function and interfere with the pituitary-adrenal axis, but again these effects have not been well defined.
III. Medical Evaluation
The most important principle in evaluating a worker for any occupational disease including lead poisoning is a high index of suspicion on the part of the examining physician. As discussed in Section II, lead can affect numerous organ systems and produce a wide array of signs and symptoms, most of which are non-specific and subtle in nature at least in the early stages of disease. Unless serious concern for lead toxicity is present, many of the early clues to diagnosis may easily be overlooked.
The crucial initial step in the medical evaluation is recognizing that a worker's employment can result in exposure to lead. The worker will frequently be able to define exposures to lead and lead-containing materials but often will not volunteer this information unless specifically asked. In other situations the worker may not know of any exposures to lead but the suspicion might be raised on the part of the physician because of the industry or occupation of the worker. Potential occupational exposure to lead and its compounds occur in at least 120 occupations, including lead smelting, the manufacture of lead storage batteries, the manufacture of lead pigments and products containing pigments, solder manufacture, shipbuilding and ship repair, auto manufacturing, construction, and painting.
Once the possibility for lead exposure is known, the focus can then be directed toward eliciting information from the medical history, physical examination, and finally from laboratory data to evaluate the worker for potential lead toxicity.
A complete and detailed work history is important in the initial evaluation. A listing of all previous employment with information on work processes, exposure to fumes or dust, known exposures to lead or other toxic substances, respiratory protection used, and previous medical surveillance should all be included in the worker's record. Where exposure to lead is suspected, information concerning on-the-job personal hygiene, smoking or eating habits in work areas, laundry procedures, and use of any protective clothing or respiratory protection equipment should be noted. A complete work history is essential in the medical evaluation of a worker with suspected lead toxicity, especially when long term effects such as neurotoxicity and nephrotoxicity are considered.
The medical history is also of fundamental importance and should include a listing of all past and current medical conditions, current medications including proprietary drug intake, previous surgeries and hospitalizations, allergies, smoking history, alcohol consumption, and also non-occupational lead exposures such as hobbies (hunting, riflery). Also known childhood exposures should be elicited. Any previous history of hematological, neurological, gastrointestinal, renal, psychological, gynecological, genetic, or reproductive problems should be specifically noted.
A careful and complete review of systems must be performed to assess both recognized complaints and subtle or slowly acquired symptoms which the worker might not appreciate as being significant. The review of symptoms should include the following:
General weight loss, fatigue, decreased appetite.
Head, Eyes, Ears, Nose, Throat (HEENT) headaches, visual disturbances or decreased visual acuity, hearing deficits or tinnitus, pigmentation of the oral mucosa, or metallic taste in mouth.
Cardiopulmonary shortness of breath, cough, chest pains, palpitations, or orthopnea.

Gastrointestinal nausea, vomiting, heartburn, abdominal pain, constipation or diarrhea.
Neurologic irritability, insomnia, weakness (fatigue), dizziness, loss of memory, confusion, hallucinations, incoordination, ataxia, decreased strength in hands or feet, disturbances in gait, difficulty in climbing stairs, or seizures.
Hematologic pallor, easily fatigued, abnormal blood loss, melena.
Reproductive (male and female and spouse where relevant) history of infertility, impotence, loss of libido, abnormal menstrual periods, history of miscarriages, stillbirths, or children with birth defects.
Musculo-skeletal muscle and joint pains.
The physical examination should emphasize the neurological, gastrointestinal, and cardiovascular systems. The worker's weight and blood pressure should be recorded and the oral mucosa checked for pigmentation characteristic of a possible Burtonian or lead line on the gingiva. It should be noted, however, that the lead line may not be present even in severe lead poisoning if good oral hygiene is practiced.
The presence of pallor on skin examination may indicate an anemia, which if severe might also be associated with a tachycardia. If an anemia is suspected, an active search for blood loss should be undertaken including potential blood loss through the gastrointestinal tract.
A complete neurological examination should include an adequate mental status evaluation including a search for behavioral and psychological disturbances, memory testing, evaluation for irritability, insomnia, hallucinations, and mental clouding. Gait and coordination should be examined along with close observation for tremor. A detailed evaluation of peripheral nerve function including careful sensory and motor function testing is warranted. Strength testing particularly of extensor muscle groups of all extremities is of fundamental importance.
Cranial nerve evaluation should also be included in the routine examination.
The abdominal examination should include auscultation for bowel sounds and abdominal bruits and palpation for organomegaly, masses, and diffuse abdominal tenderness.
Cardiovascular examination should evaluate possible early signs of congestive heart failure. Pulmonary status should be addressed particularly if respirator protection is contemplated.
As part of the medical evaluation, the lead standard requires the following laboratory studies:
1. Blood lead level.
2. Hemoglobin and hematocrit determinations, red cell indices, and examination of the peripheral blood smear to evaluate red blood cell morphology.
3. Blood urea nitrogen.
4. Serum creatinine.
5. Routine urinalysis with microscopic examination.
6. A zinc protoporphyrin level.

In addition to the above, the physician is authorized to order any further laboratory or other tests which he or she deems necessary in accordance with sound medical practice. The evaluation must also include pregnancy testing or laboratory evaluation of male fertility if requested by the employee.
Additional tests which are probably not warranted on a routine basis but may be appropriate when blood lead and ZPP levels are equivocal include delta-aminolevulinic acid and coproporphyrin concentrations in the urine, and dark-field illumination for detection of basophilic stippling in red blood cells.
If an anemia is detected further studies including a careful examination of the peripheral smear, reticulocyte count, stool for occult blood, serum iron, total iron binding capacity, bilirubin, and, if appropriate, vitamin B12 and folate may be of value in attempting to identify the cause of the anemia.
If a peripheral neuropathy is suspected, nerve conduction studies are warranted both for diagnosis and as a basis to monitor any therapy.
If renal disease is questioned, a 24-hour urine collection for creatinine clearance, protein, and electrolytes may be indicated. Elevated uric acid levels may result from lead-induced renal disease and a serum uric acid level might be performed.
An electrocardiogram and chest X-ray may be obtained as deemed appropriate.
Sophisticated and highly specialized testing should not be done routinely and where indicated should be under the direction of a specialist.
IV. Laboratory Evaluation
The blood lead level at present remains the single most important test to monitor lead exposure and is the test used in the medical surveillance program under the lead standard to guide employee medical removal. The ZPP has several advantages over the blood lead level, but because of its relatively recent development and the lack of extensive data concerning its interpretation, the ZPP currently remains an ancillary test.
This section will discuss the blood lead level and ZPP in detail and will outline their relative advantages and disadvantages. Other blood tests currently available to evaluate lead exposure will also be reviewed.
The blood lead level is a good index of current or recent lead absorption when there is no anemia present and when the worker has not taken any chelating agents. However, blood lead levels along with urinary lead levels do not necessarily indicate the total body burden of lead and are not adequate measures of past exposure. One reason for this is that lead has a high affinity for bone and up to 90% of the body's total lead is deposited there. A very important component of the total lead body burden is lead in soft tissue (liver, kidney, and brain). This fraction of the lead body burden, the biologically active lead, is not entirely reflected by blood lead levels since it is a function of the dynamics of lead absorption, distribution, deposition in bone and excretion. Following discontinuation of exposure to lead, the excess body burden is only slowly mobilized from bone and other relatively stable body stores and excreted. Consequently, a high blood lead level may only represent recent heavy exposure to lead without a significant total body excess and likewise a low blood lead level does not exclude an elevated total body burden of lead.
Also, due to its correlation with recent exposures, the blood lead level may vary considerably over short time intervals.
To minimize laboratory error and erroneous results due to contamination, blood specimens must be carefully collected (after thorough cleaning of the skin with appropriate methods) using lead-free blood containers and analyzed by a reliable laboratory. Under the standard, samples must be analyzed in laboratories which are approved by the Center of Disease Control (CDC) or which have received satisfactory grades in proficiency testing by the CDC in the previous year. Analysis is to be made using atomic absorption spectrophotometry, anodic stripping voltammetry or any method which meets the accuracy requirements set forth by the standard.
The determination of lead in urine is generally considered a less reliable monitoring technique than analysis of whole blood primarily due to individual variability in urinary excretion capacity as well as the technical difficulty of obtaining accurate 24-hour urine collections. In addition, workers with renal insufficiency,whether due to lead or some other cause, may have decreased lead clearances and consequently urine lead levels may underestimate the true lead burden. Therefore, urine lead levels should not be used as a routine test.
The zinc protoporphyrin test, unlike the blood lead determination, measures an adverse metabolic effect of lead and as such is a better indicator of lead toxicity than the level of blood lead itself. The level of ZPP reflects lead absorption over the preceding 3 to 4 months, and therefore is a better indicator of lead body burden. The ZPP requires more time than the blood lead to reach significantly elevated levels; the return to normal after discontinuing lead exposure is also slower. Furthermore, the ZPP test is simpler, faster, and less expensive to perform and no contamination is possible. Many investigators believe it is the most reliable means of monitoring chronic lead absorption.
Zinc protoporphyrin results from the inhibition of the enzyme ferrochelatase which catalyzes the insertion of an iron molecule into the protoporphyrin molecule, which then becomes heme. If iron is not inserted into the molecule then zinc, having a greater affinity for protoporphrin, takes the place of the iron, forming ZPP.
An evaluation in the level of circulating ZPP may occur at blood lead levels as low as 20-30 m g/100g in some workers. Once the blood lead level has reached 40 m g/100g there is more marked rise in the ZPP value from its normal range of less than 100 g/100ml. Increases in blood lead levels beyond 40 m g/100g are associated with exponential increases in ZPP.
Whereas blood lead levels fluctuate over short time spans, ZPP levels remain relatively stable. ZPP is measured directly in red blood cells and is present for the cell's entire 120-day life span. Therefore, the ZPP level in blood reflects the average ZPP production over the previous 3-4 months and consequently the average lead exposure during that time interval.
It is recommended that a hematocrit be determined whenever a confirmed ZPP of 50 m g/100ml whole blood is obtained to rule out a significant underlying anemia. If the ZPP is in excess of 100 g/100ml and not associated with abnormal elevations in blood lead levels, the laboratory should be checked to be sure that blood leads were determined using atomic absorption spectrophotometry, anodic stripping voltammetry or other method meeting the accuracy requirements set forth by the standard and by a CDC-approved laboratory which is experienced in lead level determinations. Repeat periodic blood lead studies should be obtained in all individuals with elevated ZPP levels to be certain that an associated elevated blood lead level has not been missed due to transient fluctuations in blood leads.
ZPP has a characteristic fluorescence spectrum with a peak at 594 nm which is detectable with a hematofluorimeter. The hematofluorimeter is accurate and portable and can provide on-site, instantaneous results for workers who can be frequently tested via a finger prick.
However, careful attention must be given to calibration and quality control procedures. Limited data on blood leadZPP correlations and the ZPP levels which are associated with the adverse health effects discussed in Section II are the major limitations of the test. Also it is difficult to correlate ZPP levels with environmental exposure and there is some variation of response with age and sex. Nevertheless, the ZPP promises to be an important diagnostic test for the early detection of lead toxicity and its value will increase as more data are collected regarding its relationship to other manifestations of lead poisoning.
Levels of delta-aminolevulinic acid (ALA) in the urine are also used as a measure of lead exposure. Increasing concentrations of ALA are believed to result from the inhibition of the enzyme delta-aminolevulinic acid dehydrase (ALA-D). Although the test is relatively easy to perform, inexpensive, and rapid, the disadvantages include variability in results, the necessity to collect a complete 24-hour urine sample which has a specific gravity greater than 1.010, and also the fact that ALA decomposes in the presence of light.
The pattern of porphyrin excretion in the urine can also be helpful in identifying lead intoxication. With lead poisoning, the urine concentrations of coproporphyrins I and II, porphobilinogen and uroporphyrin I rise. The most important increase, however, is that of coproporphyrin III; levels may exceed 5,000 m g/1 in the urine in lead poisoned individuals, but its correlation with blood lead levels and ZPP are not as good as those of ALA. Increases in urinary prophyrins are not diagnostic of lead toxicity and may be seen in porphyria, some liver diseases, and in patients with high reticulocyte counts.
Summary. The standard for inorganic lead places significant emphasis on the medical surveillance of all workers exposed to levels of inorganic lead above the action level of 30 m g/M [FN3] TWA. The physician has a fundamental role in this surveillance program, and in the operation of the medical removal protection program.
Even with adequate worker education on the adverse health effects of lead and appropriate training in work practices, personal hygiene and other control measures, the physician has a primary responsibility for evaluating potential lead toxicity in the worker. It is only through a careful and detailed medical and work history, a complete physical examination and appropriate laboratory testing that an accurate assessment can be made. Many of the adverse health effects of lead toxicity are either irreversible or only partially reversible and therefore early detection of disease is very important.
This document outlines the medical monitoring program as defined by the occupational safety and health standard for inorganic lead. It reviews the adverse health effects of lead poisoning and describes the important elements of the history and physical examinations as they relate to these adverse effects.






Appendix D
Qualitative Fit Test (QLFT) Protocols

[See Section 5144, Appendix A]



Note: Authority cited: Section 142.3, Labor Code. Reference: Section 142.3, Labor Code.






s 5217. Formaldehyde.
(a) Scope and application. This standard applies to all occupational exposures to formaldehyde, i.e. from formaldehyde gas, its solutions, and materials that release formaldehyde.
(b) Definitions. For purposes of this standard, the following definitions shall apply:
Action level. Action level means a concentration of 0.5 part formaldehyde per million parts of air (0.5 ppm) calculated as an eight (8)-hour time-weighted average (TWA) concentration.
Authorized Person. Authorized person means any person required by work duties to be present in regulated areas, or authorized to do so by the employer, by this section, or by the California Occupational Safety and Health Act of 1973.
Chief. The Chief of the Division of Occupational Safety and Health, or designee.
Director. Director means the Director of the National Institute for Occupational Safety and Health, U.S. Department of Health and Human Services, or designee.
Emergency. An emergency is any occurrence, such as but not limited to equipment failure, rupture of containers, or failure of control equipment that results in an uncontrolled release of a significant amount of formaldehyde.
Employee exposure. Employee exposure means the exposure to airborne formaldehyde which would occur without corrections for protection provided by any respirator that is in use.
Formaldehyde. Formaldehyde means the chemical substance, HCHO, Chemical Abstracts Service Registry No. 50-00-0.
(c) Permissible Exposure Limit (PEL)
(1) Time Weighted Average (TWA): The employer shall assure that no employee is exposed to a concentration of airborne formaldehyde which exceeds 0.75 parts formaldehyde per million parts of air (0.75 ppm) as an 8-hour TWA.
(2) Short Term Exposure Limit (STEL): The employer shall assure that no employee is exposed to a concentration of airborne formaldehyde which exceeds two parts formaldehyde per million parts of air (2 ppm) as a 15 minute STEL.
(d) Exposure monitoring
(1) General.

(A) Each employer who has a workplace covered by this standard shall monitor employees to determine their exposure to formaldehyde.
(B) Exceptions.
Where the employer documents, using objective data, that the presence of formaldehyde or formaldehyde-releasing products in the workplace cannot result in concentrations of airborne formaldehyde that would cause any employee to be exposed at or above the action level or at or above the STEL under foreseeable conditions of use, the employer will not be required to measure employee exposure to formaldehyde.
(C) When an employee's exposure is determined from representative sampling, the measurements used shall be representative of the employee's full shift or short-term exposure to formaldehyde, as appropriate.
(D) Representative samples for each job classification in each work area shall be taken for each shift unless the employer can document with objective data that exposure levels for a given job classification are equivalent for different work shifts.

(2) Initial monitoring. The employer shall identify all employees who may be exposed at or above the action level or at or above the STEL and accurately determine the exposure of each employee so identified.
(A) Unless the employer chooses to measure the exposure of each employee potentially exposed to formaldehyde, the employer shall develop a representative sampling strategy and measure sufficient exposures within each job classification for each workshift to correctly characterize and not underestimate the exposure of any employee within each exposure group.
(B) The initial monitoring process shall be repeated each time there is a change in production, equipment, process, personnel, or control measures which may result in new or additional exposure to formaldehyde.
(C) If the employer receives reports of signs or symptoms of respiratory or dermal conditions associated with formaldehyde exposure, the employer shall promptly monitor the affected employee's exposure.
(3) Periodic monitoring.
(A) The employer shall periodically measure and accurately determine exposure to formaldehyde for employees shown by the initial monitoring to be exposed at or above the action level or at or above the STEL.
(B) If the last monitoring results reveal employee exposure at or above the action level, the employer shall repeat monitoring of the employees at least every 6 months.
(C) If the last monitoring results reveal employee exposure at or above the STEL, the employer shall repeat monitoring of the employees at least once a year under worst conditions.
(4) Termination of monitoring. The employer may discontinue periodic monitoring of employees if results from two consecutive sampling periods taken at least 7 days apart show that employee exposure is below the action level and the STEL.The results must be statistically representative and consistent with the employer's knowledge of the job and work operation.
(5) Accuracy of monitoring. Monitoring shall be accurate, at the 95 percent confident level, to within plus or minus 25 percent for concentrations of airborne formaldehyde at the TWA and the STEL, and to within plus or minus 35 percent for concentrations of airborne formaldehyde at the action level.

(6) Employee notification of monitoring results. Within 15 days of receiving the results of exposure monitoring conducted under this standard, the employer shall notify the affected employees of these results. Notification shall be in writing, either by distributing copies of the results to the employees or by posting the results. If the employee exposure is over either PEL, the employer shall develop and implement a written plan to reduce employee exposure to or below both PELs, and give written notice to employees. The written notice shall contain a description of the corrective action being taken by the employer to decrease exposure.
(7) Observation of monitoring.
(A) The employer shall provide affected employees or their designated representatives an opportunity to observe any monitoring of employee exposure to formaldehyde required by this standard.
(B) When observation of the monitoring of employee exposure to formaldehyde requires entry into an area where the use of protective clothing or equipment is required, the employer shall provide the clothing and equipment to the observer, require the observer to use such clothing and equipment, and assure that the observer complies with all other applicable safety and health procedures.
(e) Regulated areas
(1) The employer shall establish regulated areas where the concentration of airborne formaldehyde exceeds either the TWA or the STEL, and post all entrances and accessways with signs bearing the following information:
DANGER FORMALDEHYDE IRRITANT AND POTENTIAL CANCER HAZARD AUTHORIZED PERSONNEL
ONLY

(2) The employer shall limit access to regulated areas to authorized persons who have been trained to recognize the hazards of formaldehyde.
(3) An employer at a multi-employer worksite who establishes a regulated area shall communicate the access restrictions and locations of these areas to other employers with work operations at that worksite.
(f) Methods of compliance

(1) Engineering controls and work practices. The employer shall institute engineering and work practice controls to reduce and maintain employee exposures to formaldehyde at or below the TWA and the STEL.
(2) Exception. Whenever the employer has established that feasible engineering and work practice controls cannot reduce employee exposure to or below either of the PELs, the employer shall apply these controls to reduce employee exposures to the extent feasible and shall supplement them with respirators which satisfy this standard.
(g) Respiratory protection
(1) General. For employees who are required to use respirators by this section, the employer must provide respirators that comply with the requirements of this subsection. Respirators must be used during:
(A) Periods necessary to install or implement feasible engineering and work practice controls;
(B) Work operations, such as maintenance and repair activities or vessel cleaning, for which the employer establishes that engineering and work practice controls are not feasible;
(C) Work operations for which feasible engineering and work practice controls are not yet sufficient to reduce exposure to or below the PELS; and
(D) Emergencies.
(2) Respirator program.
(A) The employer must implement a respiratory protection program in accordance with section 5144 (b) through (d) (except (d)(1)(C), (d)(3)(C)2.a and b.), and (f) through (m).
(B) If air-purifying chemical-cartridge respirators are used, the employer must:
1. Replace the cartridge after three (3) hours of use or at the end of the workshift, whichever occurs first, unless the cartridge contains a NIOSH-approved end-of-life-service life indicator (ELSI) to show when breakthrough occurs.

2. Unless the canister contains a NIOSH-approved ELSI to show when breakthrough occurs, replace canisters used in atmospheres up to 7.5 ppm (10 x PEL) every four (4) hours and industrial sized canisters used in atmospheres up to 75 ppm (100 x PEL) every two (2) hours or at the end of the workshift, whichever occurs first.
(3) Respirator selection.
(A) The employer must select the appropriate respirators as specified in Table 1.
(B) The employer shall make available a powered air purifying respirator, adequate to protect against formaldehyde exposure to any employee who experiences difficulty wearing a negative pressure respirator to reduce exposure to formaldehyde.
TABLE 1. MINIMUM REQUIREMENTS FOR RESPIRATORY PROTECTION AGAINST FORMALDEHYDE


-------------------------------------------------------------------------------
Condition of use or Minimum respirator

formaldehyde
concentration (ppm) required [FN1]
-------------------------------------------------------------------------------
Up to 7.5 ppm (10 x Full facepiece with cartridges or canisters specifically
PEL) approved for protection against formaldehyde [FN2]
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Up to 75 ppm (100 x Full-face mask with chin style or chest or
PEL)
back mounted type with industrial size
canister specifically approved for
protection against formaldehyde. Type C
supplied air respirator, pressure-demand or
continuous flow type, with full facepiece,
hood, or helmet.
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Above 75 ppm or Self-contained breathing apparatus
unknown
(emergencies) (100 x (SCBA) with positive pressure full face-piece.
PEL) Combination supplied-air, full face-piece positive
pressure respirator with auxiliary self-contained air
supply.

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Firefighting SCBA with positive pressure in full face-piece.
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Escape SCBA in demand or pressure demand mode. Full-face mask,
front or back mounted type with industrial size
canister specifically approved for protection against
formaldehyde.
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[FN1] Respirators specified for use at higher concentrations may be used at
lower concentrations.
[FN2] A half-mask respirator with cartridges specifically approved for
protection against formaldehyde can be substituted for the full facepiece
respirator providing that effective gas-proof goggles are provided and used
in combination with the half-mask respirator.


(h) Protective equipment and clothing. Employers shall comply with the provisions of Sections 3380, 3382, 3383 and 3384. When protective equipment or clothing is provided under these provisions, the employer shall provide these protective devices at no cost to the employee and assure that the employee wears them.

(1) Selection. The employer shall select protective clothing and equipment based upon the form of formaldehyde to be encountered, the conditions of use, and the hazard to be prevented.
(A) All contact of the eyes and skin with liquids containing 1 percent or more formaldehyde shall be prevented by the use of chemical protective clothing made of material impervious to formaldehyde and the use of other personal protective equipment, such as goggles and face shields, as appropriate to the operation.
(B) Contact with irritating or sensitizing materials shall be prevented to the extent necessary to eliminate the hazard.
(C) Where a face shield is worn, chemical safety goggles are also required if there is a danger of formaldehyde reaching the area of the eye.
(D) Full body protection shall be worn for entry into areas where concentrations exceed 100 ppm and for emergency reentry into areas of unknown concentration.
(2) Maintenance of protective equipment and clothing.

(A) The employer shall assure that protective equipment and clothing that has become contaminated with formaldehyde is cleaned or laundered before its reuse.
(B) When ventilating formaldehyde contaminated clothing and equipment, the employer shall establish a storage area so that employee exposure is minimized. Containers for contaminated clothing, equipment, and storage areas shall have labels and signs containing the following information:
DANGER FORMALDEHYDE-CONTAMINATED (CLOTHING) EQUIPMENT AVOID INHALATION AND SKIN
CONTACT

(C) The employer shall assure that only persons trained to recognize the hazards of formaldehyde remove the contaminated material from the storage area for purposes of cleaning, laundering, or disposal.
(D) The employer shall assure that no employee takes home equipment or clothing that is contaminated with formaldehyde.
(E) The employer shall repair or replace all required protective clothing and equipment for each affected employee as necessary to assure its effectiveness.

(F) The employer shall inform any person who launders, cleans, or repairs such clothing or equipment of formaldehyde's potentially harmful effects and of procedures to safely handle the clothing and equipment.
(i) Hygiene protection.
(1) The employer shall provide change rooms, as described in Section 3367 for employees who are required to change from work clothing into protective clothing to prevent skin contact with formaldehyde.
(2) If employee's skin may become splashed with solutions containing 1 percent or greater formaldehyde, for example because of equipment failure or improper work practices, the employer shall provide conveniently located quick drench showers and assure that affected employees use these facilities immediately.
(3) If there is any possibility that an employee's eyes may be splashed with solutions containing 0.1 percent or greater formaldehyde, the employer shall provide acceptable eyewash facilities within the immediate work area for emergency use.
(j) Housekeeping. For operations involving formaldehyde liquids or gas, the employer shall conduct a program to detect leaks and spills, including regular visual inspections.
(1) Preventative maintenance of equipment, including surveys for leaks, shall be undertaken at regular intervals.
(2) In work areas where spillage may occur, the employer shall make provisions to contain the spill, to decontaminate the work area, and to dispose of the waste.
(3) The employer shall assure that all leaks are repaired and spills are cleaned promptly by employees wearing suitable protective equipment and trained in proper methods for cleanup and decontamination.
(4) Formaldehyde contaminated waste and debris resulting from leaks or spills shall be placed for disposal in sealed containers bearing a label warning of formaldehyde's presence and of the hazards associated with formaldehyde.
(k) Emergencies. For each workplace where there is the possibility of an emergency involving formaldehyde, the employer shall assure appropriate procedures are adopted to minimize injury and loss of life. Appropriate procedures shall be implemented in the event of an emergency.
(l) Medical surveillance
(1) Employees covered.
(A) The employer shall institute medical surveillance programs for all employees exposed to formaldehyde at concentrations at or exceeding the action level or exceeding the STEL.
(B) The employer shall make medical surveillance available for employees who develop signs and symptoms of overexposure to formaldehyde and for all employees exposed to formaldehyde in emergencies. When determining whether an employee may be experiencing signs and symptoms of possible overexposure to formaldehyde, the employer may rely on the evidence that signs and symptoms associated with formaldehyde exposure will occur only in exceptional circumstances when airborne exposure is less than 0.1 ppm and when formaldehyde is present in materials in concentrations less than 0.1 percent.
(2) Examination by a physician. All medical procedures, including administration of medical disease questionnaires, shall be performed by or under the supervision of a licensed physician and shall be provided without cost to the employee, without loss of pay, and at a reasonable time and place.
(3) Medical disease questionnaire. The employer shall make the following medical surveillance available to employees prior to assignment to a job where formaldehyde exposure is at or above the action level or above the STEL, and annually thereafter. The employer shall also make the following medical surveillance available promptly upon determining that an employee is experiencing signs and symptoms indicative of possible overexposure to formaldehyde. (continued)