# I.
RECOMMENDATIONS FOR AN ACRYLAMIDE STANDARD 1 Sufficient technology exists to permit compliance with the recommended standard. Although the workplace environmental limit is considered to be a safe level based on current information, it should be regarded as the upper boundary of exposure and every effort should be made to maintain the exposure at levels as low as is technically feasible. The criteria and standard will be subject to review and revision as necessary.
Synonyms for acrylamide include propenamide, acrylic amide, and akrylamid. The terms "acrylamide" or "acrylamide monomer" are used in this document interchangeably. "Action level" is defined as a time-weighted average (TWA) concentration of one-half the environmental limit.
"Occupational exposure to acrylamide," because of systemic effects and dermal irritation produced by contact of acrylamide with the skin, is defined as work in an area where acrylamide is stored, produced, processed, or otherwise used, except as an unintentional contaminant in other materials at a concentration of less than 1% by weight.
If an employee is occupationally exposed to airborne concentrations of acrylamide in excess of the action level, then all sections of the recommended standard shall be complied with; if the employee is occupationally exposed at or below the action level, then all sections of the recommended standard shall be complied with except Section 8.

# Section 1 -Environmental (Workplace Air) (a) Concentration
The employer shall control workplace concentrations of acrylamide so that no employee is exposed at a concentration greater than 0. Procedures for the collection and analysis of environmental samples shall be as provided in Appendices I and II, or by any method shown to be at least equivalent in accuracy, precision, and sensitivity to the methods specified.

# Section 2 -Medical
Medical surveillance shall be made available to all persons subject to occupational exposure to acrylamide as described below.
(a) Preplacement medical examinations shall include:
(1) Comprehensive medical and work histories with special emphasis to such areas as weight loss and neurologic disturbances.
(2) Complete physical examination giving particular attention to the skin, eyes, and nervous system.
Judgment of the worker's ability to use positive-or negative-pressure respirators.
(b) Periodic examinations shall be made available on an annual basis, or as otherwise determined by the responsible physician. These examinations shall include at least:
(1) Interim medical and work histories.
(2) Weekly examination by trained personnel of the fingertips of hands and other portions of the body exposed to acrylamide for evidence of skin peeling.
(3) Physical examination as outlined in paragraph (a)(2) of this section.

# (c)
In an emergency involving exposure to acrylamide, all affected personnel shall be provided immediate first-aid assistance and prompt medical attention, especially with respect to the skin and eyes. Medical attendants shall be informed of the need of observation and followup for any delayed neurologic effects.
(d) In the event of skin contact with acrylamide, grossly contaminated clothing and shoes shall be removed. Any exposed body area shall be immediately and thoroughly washed with soap and water. In the case of eye contact with acrylamide, eyes shall be flushed with copious amounts of water and a physician shall be consulted promptly. (1) Appropriate protective clothing, including gloves, aprons, long-sleeved overalls, footwear, and face shields (8-inch minimum), shall be worn where needed to limit skin contact with acrylamide.
Impervious clothing may be needed in specialized operations. Appropriate eye protection (chemical safety goggles or face shields and safety glasses with side shields) shall be worn in any operation in which acrylamide (solid, liquid, or spray) may come in contact with eyes.
The employer shall provide the employee with the appropriate equipment specified in paragraph (a)(1) of this section.
(b) Respiratory Protection (I) Engineering controls shall be used if needed to keep acrylamide concentrations at or below the TWA environmental limit.
Respiratory protective equipment may be used:
(A) During the time necessary to install or test the required engineering controls.
(B) During emergencies or during the performance of nonroutine maintenance or repair activities which may cause exposures at concentrations in excess of the TWA environmental limit.
(2) When a respirator is permitted by paragraph (b)(1) of this section, it shall be selected and used pursuant to the following requirements:
(A)
The employer shall establish and enforce a respiratory protective program meeting the requirements of 29 CFR 1910.134.

# (B)
The employer shall provide respirators in accordance with Table 1-1 and shall ensure that the employee uses the respirator provided when necessary.
The respiratory protective devices provided in conformance with Table 1-1 shall comply with the standards jointly approved by NIOSH and the Mining Enforcement and Safety Administration (formerly Bureau of Mines) as specified under the provisions of 30 CFR 11.
(C) Respirators specified for use in higher concentrations of acrylamide may be used in atmospheres of lower concentrations.
(D)
The employer shall ensure that respirators are adequately cleaned and maintained, and that employees are instructed in the proper use and testing for leakage of respirators assigned to them.
(E) Respirators shall be easily accessible, and employees shall be informed of their location. (1) Supplied-air respirator, demand mode, with full facepiece (2) Self-contained breathing apparatus, demand mode, with full facepiece Less than or equal to 100 ppm (300 mg/cu m)
(1) Supplied-air respirator, continuousflow type or pressure-demand (positive pressure) mode, with half-mask or full facepiece (2) Supplied-air respirator, continuousflow type, with hood, helmet, or suit Greater than 100 ppm (300 mg/cu m)
(1) Self-contained breathing apparatus with full facepiece operated in pressuredeipand or other positive-pressure mode (2) Combination Type C supplied-air respirator with full facepiece operated in pressure-demand mode, with an auxiliary self-contained air supply Emergency entry (into an area of unknown concen tration)
(1) Self-contained breathing apparatus with full facepiece operated in pressuredemand or other positive-pressure mode (2) Combination Type C supplied-air respirator with full facepiece operated in pressure-demand mode, with an auxiliary self-contained air supply Escape (from an area of unknown concentration)
(1) Gas mask, full facepiece, equipped with a combination organic vapor canister and a high-efficiency filter (2) Self-contained breathing apparatus operated in either demand or pressuredemand mode (F)
In case of an accident which could result employee exposure to acrylamide in excess of the environmental limit, the employer shall provide respiratory protection as listed in Table 1-1.
Section 5 -Informing Employees of Hazards from Acrylamide (a)
The employer shall ensure that each employee occupationally exposed to acrylamide is informed at the beginning of employment or on assignment to an acrylamide area of the hazards, relevant symptoms such as skin peeling, numbness ("pins and needles" in fingers), sleepiness, loss of weight, and weakness, appropriate emergency procedures, and proper conditions and precautions for the safe use of acrylamide. People engaged in maintenance and repair shall be included in these training programs.
The employee shall be reinformed at least once a year. Each employee shall be advised of the availability of such relevant information kept on file, including the material safety data sheet. (1) Ventilation systems if used shall be designed to prevent the accumulation or recirculation of acrylamide in the workplace, to maintain acrylamide concentrations at or below the recommended environmental limit, and to effectively remove acrylamide from the breathing zones of employees.
Ventilation systems shall be subject to regular preventive maintenance and cleaning to ensure effectiveness, which shall be verified by periodic performance measurements.
(2) A partially enclosed, ventilated, and automated system should be used to empty and transfer bags of solid acrylamide into a bin, so that dust are effectively removed. The bag should be cut open automatically and any dust should be removed by local exhaust ventilation.
(3) Concrete floors in operations areas shall be sealed in a manner that minimizes permeation of acrylamide into the concrete. (.2) Acrylamide contact with skin and eyes of workers shall be prevented. Equipment, walls, and floors should be kept clean to limit worker exposure.
(3) Prior to maintenance work, sources of acrylamide and its vapor shall be eliminated to the extent feasible. If concentrations at or below the recommended workplace environmental limit cannot be ensured, respiratory protective equipment as specified in Table 1-1 shall be used during such maintenance work. (2) Individuals entering confined spaces where they may be exposed to acrylamide shall wear respirators as outlined in Section 4.
(3) Confined spaces shall be ventilated while work is in progress to keep the concentration of acrylamide at or below the workplace environmental limit.
(4) When a person enters a confined space, another properly protected worker shall be on standby outside.

# (e) Emergency Procedures
For all work areas where there is a reasonable potential for accidents involving acrylamide, the employer shall take all necessary steps to ensure that employees are instructed in and follow the procedures specified below and any others appropriate for a specific operation or process.
(1) Procedures shall include prearranged plans for obtaining emergency medical care and for the necessary transportation of injured workers.
Employees shall also be trained in administering immediate first aid and shall be prepared to render such assistance when necessary.
(2) Approved eye, skin, and respiratory protection as specified in Section 4 shall be used by persons involved in the cleaning procedure of the accident site.
(3) All persons who may be required to shut off sources of acrylamide, clean up spills, and repair leaks shall be properly trained in emergency procedures and shall be adequately protected against attendant hazards from exposure to acrylamide.
Employees not essential to clean-up operations shall be evacuated from exposure areas during emergencies. Perimeters of hazardous exposure areas shall be delineated, posted, and secured.
(5) Eyewash fountains and showers shall be provided in accordance with 29 CFR 1910.151.
If an employee is found to be exposed to acrylamide in excess of the recommended TWA environmental limit, the exposure of that employee shall be measured at least once a week, control measures shall be initiated, and the employee shall be notified of the exposure and of the control measures being implemented. Such monitoring shall continue until two consecutive determinations, at least 1 week apart, indicate that the employee's exposure no longer exceeds the recommended environmental limit;
routine monitoring may then be resumed.

# (b) Recordkeeping
Records of environmental monitoring shall be kept by the employer for at least 20 years. These records shall include the dates of measurements, the most popular and commercially useful method, by the use of free radical initiators of redox catalytic systems . Molten acrylamide polymerizes vigorously with i_he evolution of heat  .
Acrylonitrile is the major starting material used in all industrial methods for the manufacture of acrylamide . The starting material is mixed with sulfuric acid, an exothermic reaction, and then diluted with water. Acrylamide is then prepared from acrylamide sulfate either by the lime process, ammonia process, carbonate process, or ion-exchange process.
Acrylamide is difficult to recover at the aqueous stage since it may polymerize or undergo hydrolysis. Various processes have been devised by manufacturers to facilitate the recovery and to control the amount of heat generated in the procedure. Recently, a few manufacturers have developed pollution-and byproduct-free processes for direct production of acrylamide monomer via hydration of acrylonitrile over a catalyst .
Acrylamide monomer production has been estimated to have amounted to about 15-20 million pounds in 1966, 30 million in 1969, 32 million in 1972, 40 million in 1973, and approximately 70 million in 1974 . During the past 20 years, the use of acrylamide polymers has also increased very rapidly with the increased production of acrylamide monomer . In 1972, about 35 million pounds of acrylamide polymers were used in the United States alone. These are the latest years for which data are available.
The major use of acrylamide monomer is in the production of polymers . Aqueous solutions of the monomers and a redox catalyst are used for soil stabilization.
Polyacrylamides are very effective flocculants for finely divided solids in aqueous suspensions. AM-9 has found increasing application as a chemical grout. The largest market for acrylamide now is in the manufacture of polyacrylamides for waste and water treatment flocculants, in products for aiding sewage dewatering, and in a variety of products for the water treatment industry. These uses consumed more than 40% of the acrylamide used in 1973 . Acrylamide is also used to prepare polyacrylamides, which are used as strengtheners in papermaking and retention aids (to keep the fibers from being washed away). The pulp and paper industry accounted for about 20% of the acrylamide consumption in 1973. Some other uses of polyacrylamides are drilling-mud additives, textile treatment, and surface coatings.
In very small quantities, acrylamide polymers are also used for flocculation of ores , mine tailings and coal, friction reduction , thickening , soil stabilization, gel chromatography and electrophoresis, photography, fog dissipation, breaking of oil-in-water emulsions, dyeing, ceramics, and clarification and treatment of potable water and foods .
Several other uses for monomeric acrylamide have been proposed by various investigators. Compounds such as N,N'-ethylene-bis-acrylamide and some bromo combinations have shown promise as antitumor agents in mice , in tomato plant tumors , and in plant tissue cultures .
NIOSH estimates that approximately 20,000 workers are potentially exposed to acrylamide in the United States.
Interest was not shown in its preparation and properties until acrylonitrile became commercially available in 1940 . It was first offered by American Cyanamid Company for developmental consideration in 1952, and they began manufacture for the commercial market in 1954.
It was not until the advent of large-scale commercial production that some pharmacologic and toxicologic experiments were initiated by American Cyanamid Company at Hazleton Laboratories. After single large oral doses, death occurred as a consequence of convulsions and asphyxia in mice, rats, rabbits, and dogs. However, after repeated administration of acrylamide, a neurologic syndrome was characterized by postural and motor incoordination in these animals.
The single-dose toxicity of monomeric acrylamide in animals was also reported by Druckrey et al  in 1953.
The so-called average lethal dose by intraperitoneal (ip) injection was reported to be 120 mg/kg in rats which died within 1 or 2 days with severe pulmonary obstruction.
A toxicologic study reported by Hamblin  in 1956 showed that the oral administration of acrylamide monomer produced neuropathy in mice, rats, and dogs.

# Effects on Humans
In 1953, a new method of acrylamide production was undertaken at an American Cyanamid Company manufacturing plant  where acrylonitrile was hydrated by sulfuric acid to form acrylamide sulfate after which it was neutralized by ammonia, yielding free acrylamide. About 5 months after the new process was begun, a "handful" of the hundreds of potentially exposed plant workers noticed numbness and tingling of their hands and weakness of their hands and legs. Dermal contact of the workers was thought to have been limited because they wore protective clothing and gloves. The air in the plant was sampled and only traces of acrylamide were found. However, by the use of methods (not described) of detection then in use, it was calculated that the maximum amount of acrylamide which could have been inhaled by one worker in a 5-month period was approximately 1.8 mg/kg. The whole manufacturing process was altered and the exposure of the workers to acrylamide was reduced or eliminated. Further details were not presented. In some instances there was evidence of CNS involvement .
A pattern of reactions emerged when signs, symptoms, and results of neurologic examinations of the workers were compiled and compared (see  18,21], sleepiness , and complete collapse (which occurred in two people after drinking alcoholic beverages) . Still later, emotional changes  and finally, reactions typical of overt peripheral neuropathy, positive Romberg's sign 23,24], loss of vibration and position senses 23] Some of the incidents of acrylamide intoxication which occurred in Japan were reported by Fujita et al  . They described in considerable detail the signs and symptoms which resulted from acrylamide exposure in 10 workers in one factory. Nine men and one woman ranging in age from 17 to 43 years were exposed at a pilot plant where manufacturing procedures were being developed. The length of employment in that plant varied from 3 to of the typical signs and symptoms of acrylamide intoxication relating more to the legs than to the arms. Of the three workers who were hospitalized because they were the most severly affected, one had been employed for 12 months and the other two for 3 months in their present jobs. Those three workers had, in addition to the typical reactions (tremor and numbness of the hands and feet, dizziness, loss of the knee jerk, heavy feeling of the legs, staggering, and positive Romberg's sign), emotional changes which were also somewhat similar to, but very much less severe than those of the family reported by Igisu et al , which is described in detail later.
The symptoms were attributed to the presence of the peripheral neuropathy and the desquamation and sensitivity of the soles of the feet, which may also have been in contact with acrylamide. Fujita et al  also found sufficient signs and symptoms to postulate that the CNS and probably the cerebellum, in addition to peripheral nerves, were involved in acrylamide intoxication. All 10 workers improved during about 4 months of rest and supportive treatment.
Takahashi et al  described the reactions of 13 factory and 2 laboratory workers who were exposed to acrylamide from 2 months to 8 years.
All of the workers were males aged 18-32 years. They were exposed during the polymerization of the monomer in the manufacture of papercoating materials. The described reactions conformed to the typical ones (numbness of lower limbs, ataxia, dizziness, gastrointestinal upset, and hand peeling).
The authors  concluded that, although peripheral neuropathy was one of the most important effects in the patients, a few CNS effects also may have been present. When the work environment was changed to limit or prevent contact with acrylamide, the workers gradually recovered; however, the authors  did not describe the controls used. Takahashi et al  also performed special studies in which motor and sensory nerve conduction velocities and action potentials were determined in some of the peripheral nerves in arms and legs of the affected workers. The motor nerves tested had essentially normal reactions, whereas the sensory nerves' had decreased action potential amplitude. The authors  suggested that the defect in the action potential would precede decreases in conduction velocity and that this indicated sensory nerve injury.

# Garland
and Patterson  described six cases of acrylamide intoxication in workers in three factories in Great Britain where acrylamide flocculants were produced. The workers, all men and aged 19-59 years, had worked in the factories for periods varying from 1 to over 12 months. Although limited details of the medical histories and examinations were reported, the authors  suggested that what was recorded agreed with some of the signs and symptoms of the typical reactions (increased sweating of feet and hands, fatigue, muscle weakness and pain, hand peeling, sensory loss, and positive Romberg's sign). The authors stated that all of the men recovered after they were removed from exposure, although it took from 2 to 12 months. Garland and Patterson  interpreted that, because of the sleepiness of the men, the midbrain, as well as peripheral nerves, was involved. Fullerton  studied nerve conduction velocities in three of the patients reported by Garland and Patterson  while they were recovering from the ill effects of exposure.
Maximal motor nerve conduction in the distal ends of median and ulnar nerves was found to be normal or slightly reduced and response to nerve stimulation in small muscles was dispersed irregularly. Fullerton suggested that those changes were caused by degeneration and regeneration of the distal nerves (nerve endings near muscles). The action potentials of the sensory nerves were also decreased or absent; the author  indicated that the peripheral sensory nerves had been more severely damaged than their associated motor nerves.
In addition to the determination of the neurophysiologic phenomena, Fullerton  microscopically examined biopsy specimens of nerves from the calf muscles from two of the three patients. The author  concluded that simultaneous nerve degeneration and regeneration occurred immediately after, and probably during acrylamide exposure, and that most probably nerve function was impaired before structural changes were evident. obtained qualitatively similar results in adult Porton-strain albino rats.
Fullerton and Barnes  also observed that acrylamide administered to rats at a single dose of 100 mg/kg by stomach tube produced only fine tremors, but when repeated in 24 hours killed most of the animals within 3 days. General weakness was also observed in the dying rats. When intubated with 50-mg/kg doses, 12 times over a 15-day period, all rats (number not specified) developed severe weakness and died within a few days after the final dose. At necropsy, many rats (both males and females) had gross distention of the bladder. Ten-week-old rats given acrylamide orally at a dose of 25 mg/kg/day, 5 days/week, developed the first signs of weakness after the fourth week. A dose of 10 mg/kg/day, 5 days/week, given for about 5 months, produced no signs of toxicity in six female rats.

# Fullerton and Barnes
 also measured motor nerve conduction velocity in the fibers supplying the small muscles on the plantar surface of the hind paws in Porton-strain albino rats. Nerve conduction velocity in control animals was 56 (SD 5.8) meters/second compared with 44 (SD 2.2) meters/second in the 11 of the 15 rats fed acrylamide in their diets (200 ppm for 6 months or 400 ppm for 2-3 months) and showed severe neurologic abnormalities of the hindlimbs. The conduction velocities were normal in the remaining four rats recovering from the severe leg weakness.
The influence of age on acrylamide-induced leg weakness was investigated by Fullerton and Barnes  in groups of six rats (sex not specified) aged 5, 8, 26, and 52 weeks and fed 100 mg/kg of acrylamide at weekly intervals. After four doses, the youngest animals were only mildly affected, whereas those aged 26 weeks at the start of study were severely affected. The 52-week-old rats were severely affected after only three doses.
The authors stated that, when acrylamide feeding was discontinued, the recovery in young animals, which had shown weakness for only a few weeks, was rapid and complete. For the older rats, in which weakness had been present for months, recovery was slow, and mild ataxia continued for some months.
The effects of orally administered acrylamide on dogs were briefly reported by Hamblin  in 1956, but recently have been studied in more detail by Thomann et al . In the earlier investigation , groups of two dogs each were given acrylamide at doses of 1 mg/kg/day for 19 weeks, 5 mg/kg/day for 5 weeks, or 8 mg/kg/day for 4 weeks without overt signs of toxicity. However, a dose of 10 mg/kg/day for 4-5 weeks produced incoordination, weakness of the extremities, and impaired righting reflex.
A single dose of 100 mg/kg produced these same effects in 24 hours. In the 1974 report by Thomann et al , experiments were performed on 6-to 12-month-old beagles. The dogs were given acrylamide orally in gelatin capsules in daily doses of 5 or 15 mg/kg. The first group (three males and three females) received 5 mg/kg/day for 60 days; the second group (five males and five females) received 15 mg/kg/day for 22 days. After the first 3 weeks of the experiment, the dogs in the 5-mg/kg/day group were inactive and had muscular weakness, which was particularly noticeable in the jaw muscles.
In addition to muscular weakness, the animals in the 15-mg/kg/day group had dilated pupils, conjunctivitis, salivation, difficulty in breathing, muscular stiffness of the hindlegs, muscle twitching, head Hamblin  briefly described the effects on the growth of albino rats given acrylamide in the diet (10, 50, 100, or 300 ppm).
No effects were reported at the 10-and 50-ppm levels. Diets containing 100 and 300 ppm of acrylamide produced growth retardation within 6 and 4 weeks, respectively.
Fullerton and Barnes  studied the effects of acrylamide on 6-to 8-week-old male albino rats. The animals were fed diets containing 100, 200, 300, or 400 ppm of acrylamide. According to the authors , these represented daily intakes of about 6-9, 10-14, 15-18, or 20-30 mg/kg, respectively. Control rats received a similar diet without acrylamide.
Rats on the acrylamide diets developed slight leg weakness as follows: at 400 ppm after 3 weeks, at 300 ppm after 4 weeks, at 200 ppm after 12 weeks, and at 100 ppm after 40 weeks.
Severe leg weakness developed in all except the 100-ppm rats on continuation of dietary treatment; the slight leg weakness observed at week 40 did not increase during the remaining 8 weeks of the experiment. The only macroscopic findings at necropsy were wasting of the hindlimb musculature and distended urinary bladders in all rats.
Axons and myelin sheaths of the sciatic, tibial, median, and ulnar nerves examined microscopically at necropsy showed extensive degeneration in the peripheral nerves of all the clinically affected animals. Microscopic examination of kidney, spleen, pancreas, adrenal, lung, brain, and spinal cord tissues showed no abnormalities.
McCollister et al  studied the effects of acrylamide given at low concentrations in the diet. Groups of 10 male and 10 female 8-week-old rats of the Dow Wistar strain were maintained on diets containing 3, 9, or 30 ppm acrylamide for 90 days, and then killed and necropsied.
As judged by their appearance, behavior, growth, mortality, organ weights, and microscopic examination of tissues, there was no evidence of adverse effects in either male or female rats. No signs of neurotoxicity were seen in two other groups of animals maintained on diets containing either 70 or 110 ppm of acrylamide for 189 days. In the same experiment, McCollister et al  also studied the effects on male and female rats of acrylamide given at high concentrations in the diet. At a 300-ppm acrylamide dietary level, the rats began to show loss of control of the hindquarters after 21 days.
By day 42, all 10 males and 6 of 10 females were dead. Loss of hindquarter control was seen at 14 days in rats maintained at a diet containing 400 ppm of acrylamide. According to the authors , doses of 3, 9, 30, 70, 90, 110, 300, and 400 ppm of acrylamide in the diet were equivalent to 0.3, 0.9, 3, 7, 9, 11, 30, and 40 mg/kg/day, respectively. weeks, the cats showed slight weakness of the hindlimbs which progressed at variable rates to paralysis of the hindlimbs. Atrophy of the thigh and leg muscles was noticeable in severely paralyzed cats, and a few cats also had weakness of the forelimbs. The authors  reported that the cat cries became coarse, indicating possible involvement of the laryngeal nerves.
Cats showed marked improvement when returned to their normal diet.
Hindlimb strength was regained within 2-3 weeks, but complete recovery took several months and was directly related to the severity of the involvement.
Microscopic examination of the nerves revealed degeneration of the myelin and axons of all four limbs. There was a suggestion of actual axon loss in the distal third or fourth portion of the tibial nerve fibers. Atrophy was evident grossly in nearly all muscles of the caudal limbs; however, microscopically, it was marked only in the digital muscles.  weights of male Porton-strain albino rats weighing about 200 g. Acrylamide was injected ip, twice a week, for 1 month. At 32 days after the first injection, there was a 28% reduction in body weight in rats injected with 50 mg/kg; those injected with 100 mg/kg showed a weight reduction of 63%.
Rats in both groups were ataxic after 2 weeks.

# Suzuki and Pfaff
 studied the effects of acrylamide in white Osbome-Mendel strain suckling and adult rats. One group consisted of 30
suckling (1-day-old) rats weighing 5-8 g and the other of 28 adult rats weighing 150-300 g. The animals received ip injections of 50 mg/kg of acrylamide in saline, three times a week, for up to 18 injections; two additional adult rats each received a total of 26 injections. Controls were injected with saline only. Suckling rats, both experimental and control, gained weight normally until tlieir fifth or sixth injection, when weight gains of the ar.rylamide-injected animals slowed down. Slight weakness of the hindlimbs, noticeable in some of the young animals after five or six acrylamide injections, became more pronounced until the rats could no longer stand. In contrast to the results obtained In suckling rats, the body weights of the adults did not change. Weakness of the hindlimbs, noticeable after 7 or 8 injections, was followed by complete paralysis after 15-17 injections. At this time, wasting of the musculature of the hindlimbs was prominent. Weakness of the forelimbs was also noted in some rats. In the animals for which acrylamide treatment was terminated after the 16th injection, weakness of the extremities persisted for about 1 month but, in animals given 26 injections, it persisted for about 2 months.
Animals with clinical signs of neuropathy showed prominent distention of the urinary bladder in pups and adults at autopsy. The other organs were congested, but otherwise normal. With electron microscopy, the authors  found that the most common feature in suckling rats given nine injections of acrylamide was axons filled with fine filaments. Very few changes were noted in the adult rats killed after 10 or 12 injections. Many axons of the sciatic nerve were filled with neurofilaments; however, the myelin sheaths appeared normal.
In addition to accumulations of neurofilaments, degeneration of axons and myelin sheaths was observed in adult rats receiving 15-18 injections.
Sciatic nerves and their branches in adult rats which had received 26 injections had numerous Schwann cells and macrophages containing many myelin figures and fat droplets but very few myelinated fibers. There were many Schwann cells in the sections, but few of these sections contained axons. Microscopic examination of the nerves of adult rats killed 20 or 30 days after the last injection showed numerous axonal sprouts growing within the Schwann cells.

# Suzuki and Pfaff
 concluded that, since degenerative changes of sciatic nerve axons seen only in adult rats in advanced stages of neuropathy were also frequently observed in suckling rats at the onset of paralysis, the peripheral nerves of suckling rats were more susceptible to acrylamide than were those of adults. The authors  suggested that the higher susceptibility of suckling rats could be a result of the incomplete development of the barrier system of peripheral nerves.    seen at any of these intervals. However, more radioactivity from labeled lysine was counted in proteins of the spinal cords of treated than of control rats after 4 weeks of feeding and the difference continued to increase, particularly in the lower cord, until 6 or 8 weeks.
In the sciatic nerve, a slight decrease in radioactivity was noted after 2 or 3 weeks, but was followed by a larger increase beginning at 4 weeks.
The effects of acrylamide on the incorporation of 35S-methionine into proteins were studied at weekly intervals from weeks 2 to 6 of feeding .
The incorporation by the controls was highest at all times in the sciatic nerve followed by the liver, brain cortex, and spinal cord. A significant increase in incorporation was demonstrated at 6 weeks after start of the feeding in the spinal cord and sciatic nerve, but not in the brain or liver.
In contrast to the results obtained with lysine, when methionine was used, no decrease in radioactivity was seen in the sciatic nerve protein at the early stages.  Six male Porton-strain albino rats weighing about 200 g were injected iv with radioactive acrylamide at a dose of 100 mg/kg.
The 14C-radioactivity was measured in the expired air and in the urine.
About 6% of the injected dose was exhaled as carbon dioxide in the first 8 hours; excretion was very low after that (reaching only slightly more than 6% in 24 hours). Urinary excretion of the 14C-radioactive material was very rapid, 40% of the injected dose excreted over the first day and a maximum of about 65% reached by day 4; the excreted metabolites were not identified. The distribution of 14C-radioactivity was studied in whole blood, plasma, brain, spinal cord, sciatic nerve, liver, and kidney at 1, 4, and 14 days after injection. At each of these intervals, the radioactive material was found in all tissues examined, with high counts in the blood. A considerable amount of radioactivity was present at 14 days; most of it was not extractable by 5% trichloroacetic acid and so was presumably protein-bound.
Edwards  recently reported on the half-life of acrylamide in the blood of male Porton-strain rats weighing 200 g. Acrylamide dissolved in 0.9% saline was injected iv at a dose of 100 mg/kg. The drop in the blood concentration of acrylamide was exponential and its half-life was 1.9 hours.  ; in the handling of a 10% aqueous solution in a mine ; in the production of flocculators from the monomer ; in the use of a resin mixture that apparently contained residual monomer in sealing processes ; and in the production of polymers while manufacturing papercoating materials .
The exposure of a Japanese family to acrylamide-contaminated well water, which they drank, cooked with, and bathed in (the latter for a few days only) was the single nonoccupational incident .
In all of the occupational incidents Other workers who were filling pumps or working in areas where there were leaks in the pressurized delivery system were splashed with a resin containing an unknown amount of monomers. In contrast to those exposures, workers in a flocculator plant where all skin contact was avoided exhibited no signs of intoxication . The authors  also stated that the crystalline monomer was heavy (large particle size) and did not form stable aerosols. The vapor pressure of solid monomeric acrylamide is 0.007 mmHg at 25 C , equivalent to a saturation concentration of 27 mg/cu m, so acrylamide vapor may pose a hazard in confined or poorly ventilated spaces.
The more likely inhalation ha ard from acrylamide solution is from aerosolization of the solution.
Although signs and symptoms that developed in some workers who were exposed dermally to monomeric acrylamide have been well documented 23], the exact time of the appearance of symptoms after dermal exposure was not. The times of onset that were reported varied from 4 weeks  to about 24 months  except for one worker  ; however, these effects were more evident in those humans who ingested acrylamide-contaminated water  than in those dermally exposed. Another manifestation, which occurred in adults who ingested acrylamide, was retention of feces and urine that resulted in constipation and overflow urinary incontinence , Distended urinary bladders were also reported in animals . Reddened skin from dermal contact with acrylamide has been reported in humans  and in rabbits .
It is notable and in marked contrast to the reactions of those people who were occupationally exposed (mainly dermally) to acrylamide 23] that the initial complaints of those exposed by ingestion  were not directed toward the extremities or the skin. When symptoms of mild dysesthesia did occur by oral ingestion and probably also by dermal absorption, the three adults  had been hospitalized for emotional problems for 2-4 weeks.
Electromyography and nerve conduction studies were performed on humans before  and during  recovery from acrylamide intoxication. Muscle response to nerve stimulation was abnormal, indicating damage of distal nerve terminals . Conduction velocity was affected in only a few units of each motor nerve . Structural abnormalities were also found in the distal portions of the long nerves .
Because both the action potentials and conduction times in the sensory nerves were more extensively affected than in the motor nerves, the author  concluded that the sensory fibers were damaged earlier and more severely than the motor fibers.
Microscopic examination by Fullerton  of biopsied sensory nerves from two patients in the Garland and Patterson  study showed the presence of simultaneous degeneration and regeneration of the sensory nerves which seemed to have occurred before the onset of symptoms- Neuroanatomic and physiologic studies  on animals, performed on a much more extensive scale than in humans, confirmed these results. Excretion of 14C-acrylamide and the effects of hepatic microsomal enzyme inducers on the toxicity of acrylamide also have been studied.
While these results have added to the information concerning the effects of acrylamide on various life processes, they do not describe the initial process whereby acrylamide produces peripheral neuropathy in humans and animals.
Other important and diagnostic manifestations of the acrylamide effect on humans are: dizziness ; vertigo ; positive Romberg's sign and inability to stand on one leg ; slurring of speech ; confusion, insecurity, and bizarre behavior ; poor memory and orientation ; writing inability or difficulty ; muscle pain  ; adiadochokinesis ; gastrointestinal disturbance and dysphagia ; loss of temperature and touch and vibration senses ; dysarthria ; and paresthesia, dysesthesia, and hyperesthesia .
In summary, in the absence of pertinent exposure data, no useful correlation can be made between the type and extent of exposure and the degree of human intoxication produced by acrylamide in the industrial  , when compiled and summarized, are very valuable for the recognition of the sequence and characterization of adverse effects produced on humans by exposure to monomeric acrylamide.
The animal studies also are pertinent in understanding human effects since they are very similar. In the single report of a nonoccupational episode  found, three of five family members were hospitalized after ingesting well water containing an acrylamide concentration of 400 ppm. Just how much each ingested is unknown.
It is evident that effects on the CNS, rhinorrhea, and coughing were the first symptoms which were noticed by the people who ingested acrylamide, while those dermally exposed first noticed paresthesias, skin changes, and muscle weakness of the extremities. In all known recorded human cases of and in all types of exposures to acrylamide, persons recovered in 2 weeks-2 years (latter associated with peripheral nerve defects); most persons recovered in 1-12 months after cessation of exposure to acrylamide.

# Carcinogenicity, Mutagenicity, and Teratogenicity
No reports which address the subject of possible carcinogenic, mutagenic, or teratogenic properties of acrylamide monomer were found.

# Summary Tables of Exposure and Effect
The effects of dermal and oral exposures on humans to acrylamide that were presented in Chapter III are summarized in Table III   However, the major manufacturers and users of monomeric acrylamide have provided some insight into a few sampling procedures. A direct readout method for analysis of airborne monomeric acrylamide dust and vapor has not been found.
One method for the sampling of acrylamide dust involving the use of a portable pump with an 0.8-jum membrane filter (open face) at an air flowrate of 2-3 liters/minute has been recommended for breathing zone sampling .
The minimum sampling time at a concentration of 0.3 mg/cu m was 30 minutes.
No information is available on different concentration ranges over which this method is applicable. Unless the membrane filter is properly stored after sampling either by refrigerating or in a sealed cassette, sample loss by sublimation  could cause an error. Also, sampling with a membrane filter does not collect the vapor portion of acrylamide in the air and tends to underestimate the total exposure. There is insufficient information regarding concentrations that were tested, the concentration ranges over which this method is applicable, and a minimum sampling time.
Although this method can be used for collection of acrylamide vapor, it probably does not collect acrylamide particulates efficiently.
In addition, glasswool plugs at both ends of the tube would probably collect some dust particles since they are inefficient filters.
In any case, this system is not useful for collection of total acrylamide in air.
Another method of sampling for determination of acrylamide vapor in air was developed by using a midget fritted glass bubbler . The bubbler was filled to the 20-ml mark with distilled water and air was passed at a flowrate of 1 liter/minute for 100 minutes. Data concerning concentrations of acrylamide in the air that were collected are not available. However, the sampling adsorption efficiency of one bubbler with a flowrate of 1 liter/minute and a sampling period of 100 minutes was reported to be 98%, but without supporting data.
Midget impingers, as well as silica gel tubes, have been used to sample airborne dust and vapor of acrylamide . Two midget impingers, each containing 15 ml of distilled water, were connected in series. The recommended sampling time was a minimum of 60 minutes with an air pump adjusted to a flowrate of up to 1.75 liters/minute . It was indicated that this sampling method is applicable to any acrylamide monomer which may be present in the air in an industrial environment . It was also stated that, since the sample size is essentially unlimited, the limit of detection of acrylamide in air is determined by the amount of interference present. Details such as efficiency of collection by the impingers and concentration ranges over which this sampling technique is valid were not given.
A variety of sampling methods have been discussed, such as the portable pump with a membrane filter, silica gel tube, midget fritted glass bubbler, and midget impingers.
There is no one method that is uniquely applicable for collecting acrylamide aerosol and vapor. A membrane filter has been used to collect samples of acrylamide aerosol and the midget fritted glass bubbler has been used for determinations of acrylamide vapor in air. Silica gel tubes and midget impingers can be used to collect both dust and vapor with the latter method having less vapor loss. Therefore, despite the disadvantages of handling glassware and liquid solutions in field measurements, the sampling technique of using a midget impinger is recommended for personal breathing-zone sampling of airborne acrylamide dust and vapor to guard against losses attendant with filter sampling. Analysis of monomeric acrylamide solutions was also determined by measuring the refractive index of a sample solution at 35 C with an Abbe refractometer and converting the reading to percent acrylamide using a standard curve . Duplicate determinations were within 0.4% and the method could be applied for an aqueous acrylamide solution range of 5-60%.

# Samples
The usual concentration range of acrylamide monomer solutions in previously discussed analytical procedures is much lower than 5% and lacks specificity and sensitivity for a determination of acrylamide at the environmental limit.
A more sensitive, but nonspecific, analysis of monomeric acrylamide solutions can be performed by a titrimetric method . This method was based on the reaction of acrylamide with bromine which is obtained from an acidified bromate-bromide solution. The excess bromine was treated with potassium iodide which generates free iodine. The iodine was then titrated with thiosulfate to yield an indirect measure of acrylamide. Any reducible substance may interfere with this method. The titrimetric method gave a relative standard deviation of 0.1 and 0.01% for concentrations above and below 2% of acrylamide in solution, respectively. To prepare for infrared spectroscopy, a portion of the polymer extract equivalent to about 2 mg of acrylamide was evaporated to dryness onto potassium bromide and pressed into a disc. The infrared spectrum of this sample was so intense that other contaminants were obviously interfering.
After the sample was separated by thin-layer chromatography and the acrylamide portion of the chromatogram removed with methanol, the potassium bromide disc prepared from the extract gave an infrared spectrum identical to that of the pure acrylamide standard. Direct infrared analysis is subject to interferences from unspecified contaminants from the polymers.
Another disadvantage of the method is the large amount of acrylamide required for measurement. and a platinum wire auxiliary electrode as the anode. Recovery of acrylamide in the polyacrylamides was reported to be greater than 90%. The detection limit for acrylamide was less than 1 jug/ml. However, the presence of some nonionic species, substituted acrylamide, or acrylates would be electroactive in the same potential region as that of acrylamide and would thus interfere with polarographic acrylamide analysis.
Acrylonitrile also interfered but, because of its high volatility, it was purged readily by nitrogen from the solution with no adverse effects on acrylamide concentration. Acrolein, acrylic acid, acetone, vinyl-benzyl chloride, vinyl-benzyl alcohol, styrene, and beta-hydroxypropionitrile did not interfere in polarographic analysis of acrylamide. Resin treatment of the methanolic extract of polyacrylamide for 20 minutes removed the ionic species, such as sodium and potassium ions, without causing any detectable loss of acrylamide concentration.
The analysis of monomeric acrylamide by differential pulse polarography has been adapted for determining airborne acrylamide .
The sampling solution for dust and vapor from impingers was analyzed for acrylamide polarographically after ion-exchange resin treatment and the addition of the supporting electrolyte tetra-n-butylammonium hydroxide. No information on the accuracy or the precision for this analytical method was provided.
The method was claimed to be reasonably specific for acrylamide and to have relatively few interferences. It was also reported that an acrylamide concentration as low as 0.5 jug/ml could be determined by analysis.
A major factor for identifying the most appropriate analytical Engineering controls should be complimented with good work practices for more effective control of exposure to acrylamide. Respiratory protective equipment should not be used as a substitute for proper engineering controls but must be worn when the worker is exposed to dust or vapor concentrations exceeding the environmental exposure limit.

# V. DEVELOPMENT OF A STANDARD
Basis for Previous Standards
The acrylamide environmental limit was first introduced in 1966 in the United States by the American Conference of Governmental Industrial Hygienists (ACGIH) as a tentative Threshold Limit Value (TLV) of 0.3 mg of acrylamide/cu m of air with the notation "Skin" . This designation is intended to suggest the need for appropriate measures for the prevention of dermal or other local contact or absorption. The tentative TLV of 0.3 mg/cu m was adopted as the recommended value by the ACGIH the following year  , and has remained unchanged since 1967 .
According to the 1971 (third) edition of Documentation of the Threshold Limit Values for Substances In Workroom Air , the basis for the ACGIH TLV was extrapolation from long-term feeding experiments on cats reported by McCollister et al  in 1964. The oral LD50 for laboratory animals (rats, guinea pigs, and rabbits) was in the range of 150-180 mg/kg and the document  further stated that "toxic effects may be produced by any route of administration-ingestion, inhalation, injection, skin contact, or contact with the eye." The cat was described in this document as the most sensitive species.
Cats given acrylamide at a dose of 1 mg/kg/day by iv or ip injection developed the neurologic effects in about 6 months; however, long-term feeding experiments (0.3 and 1 mg/kg/day, 5 days/week, for 1 year) in this same species apparently did not produce any ill effect. From the results of long-term feeding experiments in the most sensitive species, the cat, the ACGIH recommended "that no more than 0.05 mg/kg/day be absorbed by workmen" .
According to this 1971 ACGIH Documentation of TLV's , an absorption of 0.05 mg/kg/day, assuming a ventilation rate of 10 cu m of air for each 8-hour workday, corresponds to an environmental limit of 0.3 mg/cu m, or about 0.1 ppm. The present federal standard for acrylamide, 0.3 mg/cu m as a TWA concentration with the notation "Skin" (29 CFR 1910.1000), is based on the 1968 ACGIH Threshold Limit Value.
According to a 1968 joint report of the International Labour Office and the World Health Organization  , no standards for acrylamide had been promulgated by countries other than the United States.

# Basis for the Recommended Standard
The studies of human intoxication with acrylamide have indicated that dermal absorption 20,21,23] and ingestion   Graveleau et al , and Morviller  in France and by Fujita et al  and Takahashi et al  in Japan. However, all of these reports on human effects are qualitative and deal only with clinical signs and symptoms of acrylamide intoxication.
Igisu et al  described a nonoccupational exposure to monomeric acrylamide in a family of five persons who used acrylamide contaminated well water for cooking, drinking, washing, and bathing. Three adults in the family showed signs of CNS toxicity manifested by ataxia.
This was followed in 2-4 weeks by symptoms of peripheral neuropathy. The well water was analyzed by gas chromatography and shown to contain 400 ppm of acrylamide and a trace of dimethylaminoproprionitrile. Although slightly more quantitative information was presented in this report than in the reports on occupational exposures , no information is available which would allow estimation of dermal or airborne exposure limits from this report.
There is abundant documentation that experimental administration of acrylamide has produced peripheral neuropathy in many animal species: hens demonstrated the dermal penetration of a 10-30% solution of acrylamide which subsequently appeared in the blood.
In rabbits, application of aqueous solutions of acrylamide (10 and 12.5%) killed one of two rabbits at a dose of 1 g/kg and resulted in slight toxicity at 0.5 g/kg .
McCollr'ster et al  also studied the effects of 10 and 40% aqueous solutions of acrylamide instilled into the eyes of rabbits. The 10% aqueous solution caused signs of slight pain and slight conjuctival irritation, while the 40% aqueous solution caused moderate pain, slight conjunctival irritation, and marked corneal injury.
McCollister et al  found that acrylamide in the feed at 0.3 mg/kg/day, 5 days/week, for 1 year produced no adverse effect on cats.
A dose of 1 mg/kg/day caused questionable effects, whereas the higher doses of 3 and 10 mg/kg/day resulted in definite signs of neurotoxicity. The authors  found that one monkey fed with 0.1 mg/kg/day, two with 0.3 mg/kg/day, and one with 1 mg/kg/day, 5 days/week, for one year also showed no adverse effects. However, 3 and 10 mg/kg/day levels did cause signs of neurotoxicity in monkeys. The authors  concluded that the "no adverse effect" level for monkeys on a diet containing acrylamide lay between 1 and 3 mg/kg/day. It was the authors '  suggestion that the summation of industrial exposures should be so controlled that it will be almost impossible for a worker to absorb more than 0.05 mg/kg/day of acrylamide on a day-to-day basis.
As previously stated, studies of human intoxication with acrylamide have indicated that dermal contact and ingestion may have been the main routes of exposure without neglecting the possible contribution of inhalation of aerosol or vapor. Consequently, without knowing the airborne acrylamide concentrations at which skin and neurologic symptoms manifest themselves, and also in the absence of information as to the primary routes of exposure, ie, dermal, inhalation, or ingestion, by which these symptoms may be produced, it is difficult to correlate dermal or neurologic symptoms with worker exposure to airborne acrylamide. The available human and animal studies do not provide enough information to alter the existing federal standard for acrylamide of 0.3 mg/cu m of air as a TWA value. NIOSH, therefore, recommends that the present federal standard be kept. Engineering controls must be used whenever feasible to control airborne concentrations of acrylamide monomer within the recommended TWA limit.
Where acrylamide monomer is present, a closed system of control should be used. During the time required to install adequate controls and equipments, to make process changes, to perform routine maintenance and operations, or to make repairs, overexposure to acrylamide can be prevented by the use of respirators and protective clothing and in some cases by administrative controls.
Because acrylamide produces delayed neuropathy, it is recommended that all medical and other pertinent records involving acrylamide exposure be maintained for 20 years after termination of employment. This will allow enough time for future detection of chronic neurotoxicity of acrylamide which may be related to the employee's known occupational exposure.
The technology is currently available to sample and analyze the present environmental limit to institute appropriate engineering controls.
As was discussed in greater detail in Chapter IV, a midget impinger is recommended for personal breathing zone sampling of airborne acrylamide aerosol and vapor to guard against losses attendant with filter sampling.
Current analytical techniques commonly used for the determination of acrylamide in the industrial environment are differential pulse polarography and gas chromatography.
As was discussed in Chapter IV, differential pulse polarography is the analytical method of choice for airborne acrylamide since gas chromatography involves complex derivative formations of unknown efficiencies and sample preparation.
Concern for worker health requires that protective measures be instituted below the enforceable limit to ensure that exposures stay below that limit. An action level is set as a TWA concentration of one-half the environmental limit. It has been chosen on the basis of professional judgment rather than on quantitative data that delineate nonhazardous areas from areas in which a hazard may exist. However, in the case of acrylamide it is also recognized that many employees work with solid or liquid forms of the substance in situations where there may be skin contact with the

# VI. WORK PRACTICES
Occupational exposures can occur in the manufacture of solid forms of acrylamide , in the preparation and utilization of aqueous solutions of acrylamide , in the polymerization process , and in the handling of polymerized products which contain the residual monomer .
The conventional way of cutting bags of solid monomeric acrylamide manually with a knife and dumping the pellets or flakes into the reactor for polymerization should be replaced with a method that limits exposure to acrylamide. One method that has been used is a mechanized, maximally If there is any chance of skin contact with acrylamide, then the protective clothing worn should be impervious to acrylamide. At the present time, the suitability of impervious clothing for the protection of the worker has not been adequately established.
In addition, it is difficult for workers to wear this clothing for extended periods of time. Tomcufcik et al  found that various acrylamide compounds inhibited the growth of tumors in mice.
Ismaylova  also found the same inhibition property in tomato plant tumors and Ismaylova et al  in plant tissue cultures. This property might be interesting to investigate in mammals.
The recommended impinger sampling method for acrylamide has several disadvantages when used for personal monitoring. These include breakage of the glass impinger and spillage of the absorption solution during sampling and subsequent shipment to the laboratory unless extreme care is taken. A method of personal monitoring using a membrane filter followed by a silica gel tube or other adsorbent tubes should be evaluated. Instructions for calibration with the soapbubble meter follow. If another calibration device is selected, equivalent procedures should be used. Since the flowrate given by a pump is dependent on the pressure drop of the sampling device, in this case an impinger, the pump must be calibrated while operating with a representative filled impinger in line.
The calibration system should be assembled in series following this order: soapbubble meter, water manometer, midget impinger, and pump as shown in The trapped acrylamide is analyzed as described in Appendix II.
Other collection methods shown to be equivalent may be used.

# X. APPENDIX II
The following analytical method for acrylamide is adapted from those described by Betso and McLean  and presented in the Dow Chemical Company analytical method PAA No. 46 .

# Scope
This method is applicable to the determination of acrylamide monomer which may be present in the air in an industrial environment. The procedure is described for measuring potential employee exposure. Amounts of 5-200 Mg of acrylamide/10 ml of aqueous solution can be determined; larger amounts of acrylamide may be determined by appropriate dilution . Chemical substances should be listed according to their complete name derived from a recognized system of nomenclature.

# Principle of the Method
Where possible, avoid using common names and general class names such as "aromatic amine,"
"safety solvent," or "aliphatic hydrocarbon" when the specific name is known.
The may be the approximate percentage by weight or volume (indicate basis) which each hazardous ingredient of the mixture bears to the whole mixture. This may be indicated as a range or maximum amount, ie, "10-40% vol" or "10% max wt" to avoid disclosure of trade secrets.
Toxic hazard data shall be stated in terms of concentration, mode of exposure or test, and animal used, eg, "100 ppm LC50-rat," "25 mg/kg LD50skin-rabbit," "75 ppm LC man," or "permissible exposure from 29 CFR The "Health Hazard Data" should be a combined estimate of the hazard of the total product. This can be expressed as a TWA concentration, as a permissible exposure, or by some other indication of an acceptable standard. Other data are acceptable, such as lowest LC50 if multiple components are involved.
Under "Routes of Exposure," comments in each category should reflect the potential hazard from absorption by the route in question. Comments should indicate the severity of the effect and the basis for the statement if possible. The basis might be animal studies, analogy with similar products, or human experiences. Comments such as "yes" or "possible" are not helpful. Comments pertinent to acrylamide might be:
Skin Contact-single short contact, no adverse effects likely; prolonged or repeated contact, possibly mild irritation, erythema, and skin peeling.

# Eye
Contact-some pain and mild transient irritation; conjunctival injury. "Emergency and First Aid Procedures" should be written in lay language and should primarily represent first-aid treatment that could be provided by paramedical personnel or individuals trained in first aid.
Information in the "Notes to Physician" section should include any special medical information which would be of assistance to an attending physician including required or recommended preplacement and periodic medical examinations, diagnostic procedures, and medical management of overexposed employees. Respirators shall be specified as to type and NIOSH or US Bureau of Mines approval class, ie, "Supplied air," "Organic vapor canister," etc.
Protective equipment must be specified as to type and materials of construction.

# Range and Sensitivity
The polarographic detection limit for acrylamide in a clean system is less than 1 pg of acrylamide/ml of acrylamide solution , Even at this low concentration, the acrylamide reduction peak is well-defined and resolved from the background.

# Interferences
Differential pulse polarography is reasonably specific and relatively free from interferences. In addition, the ion-exchange resin treatment removes most common interferences, such as acrylic acid, acrylonitrile, and sodium and potassium ions. However, any compounds which are reducible in the same potential region (-2.0 v) will interfere. Substituted acrylamides and acrylate esters are reducible in the same potential region and, if present, will interfere.

# Apparatus (a)
Glass-fiber filter disc, or equivalent.

# Ill (i)
To the sample, add 0.1 ml of acrylamide standard solution (20 jug) with a 100-jul Eppendorf pipet to each of the samples and repeat (f) and (g). Record micrograms of acrylamide added.
(j) Measure the peak height of the sample at about -2.0 v, correcting for any blank reading, both before (value "A") and after (value "B") adding acrylamide (i).

# Calculations

# FIG U R E X II-1 C A LIB R A TIO N SETUP FOR PERSONAL SAMPLING PUMP W ITH M ID G E T IMPINGER