The Occupational Safety and Health Act of 1970 emphasizes the need for standards to protect the health of workers exposed to an ever-increasing number of potential hasards at their workplace. To provide relevant data from which valid criteria and effective stan dards can be deduced, the National Institute for Occupational Safety and Health has projected a formal system of research, with priorities determined on the basis of specified Indices. It is intended to present successive reports as research and epidemiologic studies are completed and sampling and analytic methods are developed. Criteria and standards will be reviewed periodically to ensure continuing protection of the worker. I am pleased to acknowledge the contributions to this report on chromic acid by members of my staff, by Robert B. O'Connor, M.D., NIOSH consultant In occupational medicine, and by Edwin C. Hyatt, MIOSH consultant on respiratory protection. Valuable and constructive comments were presented by the Review Consultants on Chromic A d d and by the ad hoc committees of the Industrial Medical Association and of the American Academy of Industrial Hygiene. The NIOSH recommendations for standards are not necessarily a consensus of all the consultants and professional societies that reviewed this criteria document on chromic a d d . Lists of the NIOSH Review Committee members and of the Review Consultants appear on the following pages.# I.

# RECOMMENDATIONS FOR A CHROMIC ACID STANDARD
The
Sampling and Analysis: Procedures for sampling and analysis of air samples shall be as provided in Appendices I and II, or by any method shown to be equivalent in precision, accuracy, and sensitivity to the methods specified.

# Section 2 -Medical
Medical surveillance shall be made available as outlined below for all workers occupationally exposed to chromic acid. Maintenance personnel periodically exposed during routine maintenance or emergency repair operations shall also be offered medical surveillance.
(a) Preplacement and annual medical examinations shall include :
A work history to elicit information on all past exposures to chromic acid and other hexavalent chromium compounds.
A medical history to elicit information on condi tions indicating the inadvisability of further exposure to chromic acid, eg, skin or pulmonary sensitization, or a skin or mucous membrane condition that may promote response to chromic acid.
(3) Thorough examination of the skin for evidence of dermatitis or chromic ulcers and of the membranes of the upper respiratory tract for irritation, bleeding, ulcerations or perforations.
(4) An evaluation of the advisability of the worker's using negative-or positive-pressure respirators. Do not get in eyes, on skin, on clothing.
Do not breathe dust or mist from solutions.
In case of contact, immediately flush skin or eyes with plenty of water for at least 15 minutes.
For eyes, get medical attention Immediately.
Wash clothing before reuse, Use fresh clothing daily. Take hot showers after work, using plenty of soap.

# (b)
The following warning sign shall be affixed in a readily visible location at or near entrances to areas in which there is occupational' exposure to chromic acid.  (1) For the purpose of determining the class of respirator to be used, the employer shall measure the atmospheric concentration of chromic acid in the workplace ben the initial application for variance is made and thereafter whenever process, worksite, climate, or control changes occur which are likely to affect the chromic acid concentration. The employer shall ensure that no worker is being exposed to chromic acid in excess of the standard because of improper respirator selection or fit.
(2) A respiratory protective program meeting the general requirements outlined in section 3.5 of American National Standard Practices for Respiratory Protection Z88.2-1969 shall be established and enforced by the employer.
Unless eye protection is afforded by a respirator hood or facepiece, protective goggles or face shields impervious to chromic acid shall be worn at operations where chromic acid splashes may contact the eyes.
(4) All protective equipment shall be maintained in a clean and satisfactory working condition. NIOSH estimates that 15,000 people are potentially exposed to chromic acid mist.

# Historical Reports
One of the first reports of injury to workers in this country from exposure to chromium compounds was in 1884 by MacKenzie.  He reported that factory workers employed in the chambers where bichromate was made invariably developed perforation of the nasal septum, generally within a few days of exposure. The characteristic development of septal perforation was described in detail. Although destruction of the cartilage was reported to be very extensive in many cases, the external appearance of the nose was said to be unchanged.
Other effects reported included ulceration of the turbinates and nasal pharynx, and inflammation of the lower respiratory tract. Perforation of the tympanic membrane was also reported, due either to passage of bichromates through the Eustachian tubes or to direct external contact.
Reporting on 12 cases in two plating plants, Blair  in 1928 described four electroplaters who experienced symptoms of a bad cold with coryza, sneezing, watery discharge from the eyes and nose, and itching and burning of the nose, especially when they left the plant and came in contact with outdoor air. Of these four men, one had a perforated nasal septum, one a large unilateral ulcer on the septum, and two had marked congestion of the nasal mucosa with hyperemia, swelling, mucoid discharge, and small ulcers. In this mortality study of employees from seven chromate plants with mixed exposures to trivalent and hexavalent chromium compounds, the crude death rate (ie, the death rate not adjusted for age) for lung cancer was 25 times greater than normal. This investigation was followed by others establishing an increased risk for lung cancer in workers in chromate plants.  Effects on Humans Chromium is a naturally occurring trace element found in human tissues. Imbus et al  reported normal levels of 2.65 yg/100 g of blood and 3.77 ^g/liter of urine. Schroeder et al  reported the normal level in adult tissue in the United States to be 2.3 yg/g of ash in the kidney and 1.6 yg/g ash in the liver. Levels were higher in persons from other countries. The element was found in relatively high concentrations in all tissues of newborns (51.8 yg/g ash and 17.9 yg/g ash in the kidney and liver, respectively) but the concentration fell during the first two decades of life and was stable thereafter, except in the lungs.  In the lungs, the chromium level was reported to be 85.2 yg/g ash in Infants. This decreased to a low of 6.8 yg/g ash during the second decade, after which the reported level gradually rose to 38.0 yg/g ash in the 70-80 year age group.  Chromium affects glucose and lipid metabolism in animals  as well as in man,  and is an essential micronutrient in mice and rats.  In workers occupationally exposed to mixed chromites and chromates in the chromate producing industry, the U.S. Public Health Service  reported median blood chromium levels of 0.004 and 0.006 mg/100 ml blood for white and black workers, respectively. No overall mean or median was reported. Median urine levels of 0.043 and 0.071 mg/liter, respectively, were reported for white and black workers.
Among similarly exposed production and maintenance workers, Mancuso  The exposure levels of chromic acid were not measured by the investigator. One worker was exposed to the chromic acid mist for approximately four days while concentrating chromic acid by boiling the acid in large vats. The first symptoms were coughing and wheezing, followed by severe frontal headaches, dyspnea, pain on deep inspiration, fever, and loss of weight.
After six months the worker had improved with respect to weight and cough but still had chest pains on deep inspiration. A bronchoscopic examination 6 months after exposure "revealed that the tracheal mucosa and the mucosa of the entire tracheobronchial tree was hyperemic and somewhat edematous." Eleven months after exposure, the worker still had complaints of Infrequent chills, cough, and mild pains located in the anterior part of the chest.
The second worker, though working at the same operation, was exposed for only one day. He stated that he had no immediate ill effects from inhalation of the mist, but during the following three or four days hoarseness developed, with a cough productive of whitish mucoid sputum.
A chest X-ray, hematologic studies, and urinalysis produced no abnormal results, but during the following three months the patient became anorexic and noted a gradual loss of 20 to 25 Pascale et al  in 1952 reported five cases of hepatic injury apparently due to exposure to chromic acid from plating baths. A person, who had been employed five years at a chromium plating factory, was hospitalized with jaundice and was found to be excreting significant amounts of chromium. Her lungs and cardiovascular system were normal. A liver biopsy showed histological changes resembling those found in toxic hepatitis. To investigate the possibility that the liver damage was of occupational origin, eight fellow workers were screened for urinary chromium excretion. Four of these were found to be excreting significant amounts and were examined in more detail. In three workers who had been exposed to chromic acid mists for 1 to 4 years, liver biopsies and a series of twelve hepatic tests showed mild to moderate abnormalities. No liver biopsy was taken from the fifth worker, who had been removed from further exposure because of nasal ulceration after 6 months at the plating bath. Only one of his liver function tests indicated a borderline abnormality. The urinary excretion of chromium (2.8 and 2.9 mg/24 hours) by the two workers employed four years was greater than the excretion (1.48 mg/24 hours) by the worker employed five years who suffered the greatest liver damage. The lowest urinary chromium excretion (0.184 mg/24 hours) was measured in the fifth worker, the individual with least exposure. All five exhibited some signs of damage to the nasal mucosa. This plus the levels of urinary excretion suggests that exposures were significant, but no environmental data were reported.

# Epidemiologic Studies
No epidemiologic data are available on the incidence of pulmon ary cancer in workers exposed only to chromic acid. The epidemiologic data that are available pertain to workers In the chromate-producing industry. These workers were subject to mixed exposures, and these data have only indirect and limited application to chromic acid exposures.
The first report of lung cancer from exposure to chromium was given in 1932 by Lehmann.  He reported two cases of workers with lung cancer out of several hundred workers who had been employed in a chrornate plant in Germany. No information was given on the length of exposure or on the nature and airborne concentration of the exposure to chromium compounds. Lehmann did not consider these two cases to be occupationally related.
Machle and Gregorius  gave the first report on the incidence of cancer of the respiratory system in the chromate industry in the United States.
The workers had been exposed to chromite ore and a mixture of trivalent and hexavalent chromium compounds. Available records from seven chromate plants for the preceding 10-15 years (1933)(1934)(1935)(1936)(1937)(1938)(1939)(1940)(1941)(1942)(1943)(1944)(1945)(1946)(1947)(1948) were studied. Of the 193 deaths in all plants, 66 (34.2%)
were due to cancer of any type or at any site, a rate over twice that for a control industrial group. This increase was attributable to an excessive proportion of deaths from cancer of the respiratory system.
Lung cancers comprised 60% of all cancers as compared to an expected rate of 9%. In five of the seven plants, (no deaths due to lung cancer were recorded in two plants) lung cancer rates varied from 13 to 31 times normal. The mean duration of exposure prior to onset was 14.5 years.
One plant (plant C in Machle and Gregorius ) with no cancer deaths was small and no deaths from any cause were seen among its workers during the period covered. The second was one of two plants (D1 and D2 ) in the study owned by a single company. In plant D2
there were 33 deaths in 1,853 male-years (a term used by the authors to Indicate that only males were included in the group studied) of exposure. Four of the 33 deaths (.12.1%) were cancer deaths; none were cancer of the respiratory system. In contrast, in plant Dl there were 29 deaths in 2,491 male-years of exposure, of which five were due to lung cancer. These five deaths represented 17.4% of all deaths, or 71.4% (5 of 7) of all cancer deaths.  Although the best available data had been used, the Machle and Gregorius report   The percentage of lung cancer patients who were employed at the chromate-producing plant was compared with the percentage of the employed male population of Baltimore who were employed at the plant.
Statistical analysis again indicated that the percentage of chromate workers in the lung cancer series was significantly higher than the percentage of chromate workers in the employed male population of Baltimore.
This study therefore confirmed the earlier conclusions of Machie and Gregorius  that the number of deaths due to cancer of the lungs and bronchi was greater in the chromate-producing Industry than was normally expected.
Mancuso and Hueper in 1951  reported on a study of occupational cancer in workers in a chromate plant. The workers were exposed to a mixture of trivalent and hexavalent chromium compounds including chromic acid. Of 33 deaths from all causes, nine (27.2%)
were from all types of cancers. Six of these (18.2% of all deaths)
were from cancer of the respiratory system. The mean latent period was 10.6 years.
In comparison, out of 2,931 deaths in Lake County, Ohio, In which the plant was located, 34 were due to lung cancer. The ratio of lung cancer to total deaths in the chromate plant was 17 times that of Lake County.
This was followed with a report by Mancuso  on the clinical and toxicologic aspects of 97 workers examined in a chromateproduction plant: 63% showed perforations of the nasal septum or ulcers of the mucosa, 87% had chronic rhinitis, 42% had chronic phar yngitis, 10% had hoarseness, and 12% had polyps or cysts. Thirtyseven percent of the 97 examined had some involvement of the nose, throat, and sinuses.
A total of 17.5% of those given gastrointestinal X-ray exami nations had evidence or ulcers, gastritis, or gastrointestinal tumor.
In comparison, X-ray examinations of a group of cement workers showed that 4 of 41 (9.8%) had similar evidence. The author stated "workers The great majority of these were air samples, but material and settled dust samples were also collected.
It was found that the milling, roasting, and leaching processes generated dusts containing chromite ore, soda ash, roast, residue, and of a mask, petrolatum in the nostrils, and nasal douching was judged to be the most effective protection.  The authors concluded that the prevalence of nasal perforation was not a valid index of the prevalence of pulmonary carcinoma.
Ten of the 897 chromate workers examined were diagnosed as having bronchogenic carcinoma (3 of the 10 had been diagnosed before the survey).  The mean age of these 10 workers was 54. 5  Expected deaths from the selected causes were determined from the agecause specific mortality rates for the U.S. civilian male population.
No data were presented on levels of worker exposure to chromates.
All of the preceding reports 16,32]  Bidstrup and Case  reported a follow-up study of the remaining 723 workers, conducted almost six years after the first study.
In the follow-up, it was found that 217 workers had left the industry and were lost to the follow-up. A total of 59 men were known to have died, 12 of these by lung cancer. This compared to 3.3 expected lung cancer deaths, or an incidence of 360% of expected. The difference was statistically significant, but as the authors pointed out, by the time all the men at risk have lived their life span, the lung cancer increase probably will be found to be very much higher. The possi bility that the increase was due to nonoccupational factors such as diagnostic bias, place of residence, social class, or smoking habits was examined and discarded. It was not possible to form an opinion about the identity of the occupational carcinogen.
The chromate workers in the above studies 32] had exposures to a mixture of trivalent and hexavalent chromium compounds of which chromic acid was only a minor part. The workers were exposed to chromite ore, chromlte-chromate intermediates and chromates as well as trace metals and minerals associated with the processing of the chromite ore. These studies suggest that exposure to the roasted chromite ore complex may be important as a causative agent of the lung cancer observed In chromate workers.
In the literature, there is no direct evidence that exposure to chromic acid per se at the measured concentrations and under the conditions of industrial exposure has led to cancer. However, no study of this nature has been undertaken. More definitive data are needed on this subject.
Bloomfield and Blum  in 1928 reported on a study of health hazards in chromium plating. In the study 19 workers were examined General room ventilation was provided through the use of room fans and opened windows. Four of the nine workers examined with exposure times ranging from 2 to 12 months had perforated nasal septa, three workers with exposure times ranging from 1 to 10 months had ulcerated nasal septa, and two workers with exposure times of 0.5 and 9 months, respectively, had moderate injection of the nasal septa. The air sampling was done at the breathing zone level near where the worker stood.
In 1972 Gomes  made a study of the incidence of cutaneousmucous lesions in workers exposed to chromic acid in the State of Sao Paulo, Brazil. He found that only 50% of the industries used exhaust protection and that the threshold limit for workers in electroplating with hot chromic acid was frequently surpassed. Clinical examination of the 303 workers exposed to chromic acid revealed that 24% had perforated nasal septa and 38.4% ulceration of the same. Together, these lesions of the nasal septum affected more than 50% of the workers.
More than 50% of the workers examined showed ulcerous scars not only on the hands, but also on forearms, arms, and feet. Ulcerous scars on the feet were due to working without boots and the wearing of Japanese type sandals.

# Animal Toxicity
In order to study in animals the reported cancer hazard due to chromium, Hueper  attempted to identify a species and tissue sensitive to the carcinogenic action of chromium or its compounds.
Chromium and chromite ore were introduced in a powdered form suspended in two different vehicles (lanolin, gelatin) by various routes (in the femur, intrapleural, intraperitoneal, Intravenous, Intramuscular,
Intranasal sinus) into mice, rats, guinea pigs, rabbits, and dogs.
Results were equivocal at best as to evidence supporting a carcinogenic action of metallic chromium and chromite ore. Only in rats were tumors observed which might have been causally related to the chromium deposits. In the series with thigh implants, three developed tumors (one benign) remote from the implant. This suggested to the investigator that the chromite ore roast contained carcinogenic material, possibly the water insoluble-acid soluble chromium compounds present. The author concluded that the carcinogenic action of chromium was dependent on the solubility of the compound and the amount present, stating that if hexavalent chromium in the form of chromate ion is available in too large a dose, acute effects result, but that a smaller dose can result in malignancy.
These results and conclusions were corroborated by Roe and
Carter  who injected rats intramuscularly with calcium chromate in arachis oil. Twenty once-weekly injections were given. The first two Injections contained 5.0 mg of calcium chromate, but signs of severe local Inflammation developed, so the dosage in the last 18 injections was 0.5 mg. Of 24 test rats, 11 developed spindle cell sarcomas and seven developed pleomorphic sarcomas at the injection site. No tumors were seen in 16 controls.
Laskin et al in 1969  reported studies of selected chromium compounds in a cholesterol carrier using an intrabronchial implanta tion technique.
Compounds under investigation included chromic chromate, chromic oxide, chromium trioxide, calcium chromate, and process residue. Pellets were prepared from molten mixtures of materials dispersed in equal quantities of cholesterol carrier. These studies included materials of differing solubilities and valences, and have involved over 500 rats that were under observation for periods of up to 136 weeks.
Lung cancers that closely simulate lung cancer in man were found in these studies. With the calcium chromate, eight cancers were found in an exposed group of 100 animals. Six of these were squamous cell carcinomas. In all the experimental groups except the one exposed to chromium trioxide, there was evidence of atypical squamous metaplasia of the bronchus. In the 100 rats implanted with chromium trioxide, two tumors were observed, both hepato-cell carcinomas.
Since these studies Implicated calcium chromate as a lung carcinogen, inhalation studies using this compound were begun.  The study is not yet completed, but preliminary results suggest a carcinogenic action in rats after chronic exposure to aerosols at a concentration of 2.0 mg/cu m. These results may be significant for the human experience in the chromate-producing industry. As noted by this researcher,  calcium chromate exists in the residue step to the extent of 3% in no-lime roasts and at significantly higher levels when lime is used.

# Correlation of Exposure and Effect
Only five studies are available which report both the effects in man of chromic acid exposure and atmospheric levels of chromic acid. 29,41] All these reported the atmospheric levels as measured at the time of the study. Consequently, all share a common weakness, in that effects were reported which were cumulative effects of past exposures to chromic acid concentrations which may have been different
from the levels reported. Nevertheless, limited correlations can be drawn.
In the study by Bloomfield and Blum,  six plating plants were surveyed and the atmospheric concentration of chromic acid was determined in each, based on a total of 39 air samples. Using these data and the occupational histories of the workers, the investigators estimated the amount of chromic acid to which some workers were exposed daily during the time employed in the plating room. When the worker had been employed only a short time, "the estimated degree of exposure was more than an approximation" In the authors' opinion, since the ventilation system in use at the time of the purvey had been in use throughout the individual's employment.
Exposures were estimated for 23 workers who were given physical examinations. Four of these were controls with no known exposure to chromic acid. Estimated exposures for the remaining 19 ranged from 0.12 to 5.6 mg/cu m. Six platers were exposed to chromic acid estimated at a level of 0.12 mg/cu m. Employment had ranged from one week to seven months. All had inflamed mucosa and three had nosebleed.
The exposures in the past may have been different from those observed at the time of the study, but the data do indicate that distinct Injury to the nasal tissues can result after relatively short exposures. Some of these six platers were exposed such a short time that their experience strongly suggests that, assuming an accurate estimate was made, a concentration of 0.12 mg/cu m can cause inflammation of the nasal mucosa and nosebleed. This was the conclusion of the authors,  who stated that continuous daily exposure to concentrations greater than 0.1 mg/cu m is likely to cause definite injury to the nasal tissues. Because these reports all fail to give long-term environmental data, the effects observed cannot be directly related to the en vironmental data reported. Nevertheless, the five papers consistently illustrate that adverse effects can result after relatively short periods of employment and therefore short periods of exposure to 42 chromic acid.
The papers also consistently Indicate that nasal
Irritation does occur at atmospheric concentrations of 0.1 mg/cu m and may occur at lower levels.

# IV. ENVIRONMENTAL DATA AND ENGINEERING CONTROLS
Measurements of atmospheric concentrations of chromic acid around Industrial operations before and after controls were Instituted attest to the marked effect of controls In lowering the airborne levels of this contaminant. In 1928, Bloomfield and Blum  studied six plating plants with varying degrees of ventilation control and changing operating conditions. In one plant, concentrations were as high as 6.9 mg of chromic acid per cubic meter of air with no ventila tion in use while plating with a current density of 300 amperes per square foot. However, at the same current density but with ventilation operating at an air velocity of 1700 feet per minute at the face of the slot, there was no detectable chromic acid in the workers' breathing zone. In order to insure a reasonable safety factor, they recommended a lateral slot-type exhaust system operating at an air velocity of 2,000 fpm at the face of the slot, drawing air no more than 18 inches laterally. They also recommended that the exhaust slots be flush with the top of the tank and that the plating solution be at least 8 Inches below the top of the tanks to allow ample time for the mist to be directed to the exhaust slot.

# Basis for Recommended Environmental Standard
Industrial exposure to mixed chromite and chromate compounds has been shown to cause ulceration of the skin,  dermatitis,  ulceration and perforation of the nasal septum,  inflamed mucosa,  irritation of the conjunctiva,  and cancer of the lung. 32] Other effects  reported as a result of mixed exposures include nasal mucosal polyps, chromitotic pneumoconiosis, chronic rhinitis, sinusitis, mucosal polyps and hydrops of nasal sinuses, inflammatory and ulcerative conditions of the gastrointestinal tract, and, often, an imbalanced ratio of the formed elements of the blood as well as lengthened bleeding time.
Occupational exposure to chromic acid has been shown to cause ulceration of the skin,  ulceration and perforation of the nasal septum, 30,31] inflamed or bleeding nasal mucosa,  and ulceration or congestion of the turbinates.
 Erosion and discoloration of the teeth has been attributed to chromic acid exposure  as has discoloration of the skin.  Apparent liver damage has been reported,  but other reports have indicated there was no evidence either of hepatic or of renal damage after acute  and chronic  exposure. An increased incidence of lung cancer has not been found reported from exposure to chromic acid alone.
In one epidemiologic study  of seven chromate plants, it is suggested that the carcinogen is a monochromate found in the process ing of the chromite ore.
In that study, the crude death rate (ie, the death rate not corrected for age) from cancer of the lung was 25 times higher than normal, but all observed lung cancer deaths were confined to five of the seven plants. One plant was quite small and there were no deaths among its employees during the nine years surveyed. There were no lung cancer deaths in another plant which was one of two plants in the study owned by a single company. The worker populations of the two plants were "similar with respect to age distribution, exposure history, color, geographic location, and were not greatly different in size." There was, however, an obvious difference in exposure, since one plant produced sodium bichromate from chromite ore, while the second plant produced chromic acid and basic chromic sulfate from the sodium bichromate. The incidence of death by lung cancer was 18 times normal in the plant producing sodium bichromate, while there were no lung cancer deaths in the plant processing the bichromate. Monochromates were suggested as the etiologic agent on the basis that the lung cancer was widely distributed in the first plant among all occupations entailing exposure to monochromates.
Thus, there is ample evidence that workers with mixed exposure in the chromate-producing industry have been at Increased risk of lung cancer. 32] Unfortunately, no epidemiological study of workers exposed only to chromic acid has been undertaken.
There is reason to suspect other chromium compounds as the carcinogens responsible for the increased lung cancer observed in chromate plants.
The chromite ore Itself has been suggested as the etiologic agent,  as have the monochromates,  and Intermediate water insolubleacid soluble compounds.  The animal studies by Hueper, Payne,  Hueper and Payne,  and Roe and Carter  suggest that the etiologic agent is a moderately soluble chromate which can be slowly released from a tissue "reservoir" in amounts which are not sufficiently toxic to cause necrosis. Calcium chromate has been implicated as a lung carcinogen by Laskin et al  and by Kuschner.
Hueper  has indicated the risk of cancer is negligible when chromic acid is used medicinally. This judgment was based in part on the "extreme rarity of such sequelae" to chronic ulcerative defects of the skin and nasal mucous membranes in workers having occupational contact with chromic acid mist and chromates.
 Therefore, while there is no positive evidence that chromic acid in the workplace has contributed to an increase in cancer, neither is there definitive evidence that absolves chromic acid.
At least one report  has suggested that liver damage is a possible consequence of exposure to chromic acid. Other reports have indicated that neither hepatic nor renal Involvement was observed after acute  and chronic  exposure.
In the one report of liver damage, urinary excretion of chromium and the clinical findings of nasal ulceration or mucosal injection and hyperemia suggest significant exposures to chromic acid.
The 1928 report by Bloomfield and Blum  has served to a great extent as the basis for the previously recommended chromic acid standards of 0.1 mg/cu m. In that paper, the authors concluded that "Continuous daily exposure to concentrations of chromic acid greater than 1 milligram in 10 cubic meters of air is likely to cause definite injury to the nasal tissues of the operators."
The lowest concentration to which chromium platers were estimated to have been exposed was 0.12 mg/cu m. Six platers were estimated to have been exposed to that level. One of these had been employed in the plating room approximately one week and two approximately three weeks, yet all six platers suffered slightly (2 of 6) to markedly (4 of 6) Inflamed mucosa. Three of these six, Including the Individual employed only one week, suffered nosebleeds. One plater who had been employed one year was estimated to be exposed to 2.8 mg/cu m at the time of the survey, but suffered no 111 effects, apparently due to personal prophylactic measures.
The mucous membranes can be protected, therefore, even against high concentrations of the mist. If the estimates were accurate, the experience of the six platers exposed to 0.12 mg/cu m demonstrates that adverse effects result fairly rapidly from exposures only slightly higher than 0.1 mg/cu m. Thus, the conclusion of the authors that damage Is likely at concentrations above 0.1 mg/cu m seems less an endorsement of that as a safe exposure level, but rather an Indication of the level at which adverse effects can be expected.
Zvalfler  and Gresh  In 1944 reported on over 100 cases observed In an anodizing plant. The majority of these Involved superficial greyish ulceration of the nasal mucosa with engorgement of the vessels and small areas of bleeding in workers not directly associated with the anodizing tanks. Among those working directly ht the tanks, the ulceration involved more of the septum, was deeper, and involved the turbinates and nasal septum as well as the mucosa. The chronic effects reported, lung cancer 32] and liver damage,  have not been proved to be a result of exposure to chromic acid, but the possibility of a correlation cannot be rejected.
Without better data, it is not possible to establish with confidence what atmospheric concentration will protect against chronic effects if a correlation does exist. Nevertheless, because chronic effects are a possibility, it is recommended that the worker be afforded an additional factor of protection by supplementing the allowable ceiling Of the methods of collection, filtration offers the greatest collection efficiency and ease of collection of breathing zone samples.
The AA type of membrane filter has a 0.8 micron pore size and provides a highly retentive matrix for particulates. The use of scrubbing liquids is inconvenient for personal breathing-zone sampling and is thus not recommended.
- The iodide-thiosulfate method is subject to Interferences from a wide variety of compounds with its nonspecific iodide reaction and the color definition is subject to a slight error. .The hematoxylin method is suggested only as a check for very small amounts of chromium and is a visual colorimetric method. The use of the colorimetric field analysis technique involving a grab sample and visual analysis must be considered to be only semiquantitatlve, and useful only for that purpose.
The colorimetric diphenylcarbazlde method does not react with trivalent chromium but produces a color with only the hexavalent form (present in chromic acid). However, cyanides, organic matter and other reducing agents, iron, copper, and molybdenum at concentrations above 200 ppm and vanadium above 4 ppm, interfere and must be separated or complexed before this method may be expected to provide chromic acid analytical data of an acceptable degree of accuracy precision.
The atomic absorption spectrophotometric method, applied directly, determines the total chromium and cannot make the desired distinction between the hexavalent chromium in chromic acid and the trivalent forms of chromium which may be present in the collected sample.
Hence, it is necessary to separate the hexavalent from the trivalent chromium compounds by extracting the chelated complex of hexavalent chromium with ammonium pyrrolidine dithiocarbamate into methyl isobutyl ketone and then applying the atomic absorption spectrophotometric method to the extract for a specific determination of hexavalent chromium.  Detailed procedures to be followed with emphasis on precautions to be taken in cleaning up and safe disposal of materials leaked or spilled. This includes proper labeling and disposal of containers containing residues, contaminated absorbants, etc.
j _ m _ _ l u c i i i hi i i    >    i 1 1 in " iiifiiif'-  ii  u u  n n u UTimn c r
(1) Section VIII. Special Protection Information.
Requirements for personal protective equipment, such as respirators, eye protection, and protective clothing, and ventilation such as local exhaust (at site of product use or application), general, or other special types.
(j) Section IX. Special Precautions.
Any other general precautionary information such as personal protective equipment for exposure to the thermal decomposition products listed in Section VI, and to particulates formed by abrading a dry coating, such as by a power sanding disc.

# (k)
The signature of the responsible person filling out the data sheet, his address, and the date on which it is filled out.
gas meter can be used. The actual set-up will be the same for these Instruments.
Instructions for calibration with the wet-test meter follow. If another calibration device is used, equivalent procedures should be followed.
(a)
The calibration device used shall be in good working con dition and shall have been calibrated against a spirometer (or other primary standard) upon procurement, after each repair, and at least annually.
(b) Calibration curves shall be established for each sampling pump and shall be used in adjusting the pumps prior to field use.

# (c)
The volumetric flowrate through the sampling system shall be spot checked and the proper adjustments made before and during each study to assure obtaining accurate airflow data.
(d) Flowmeter Calibration Test Method (see Figure 1)
Allow the layers to separate and add demineralized water until the ketone layer is completely in the neck of the flask.
The Cr-APDC complex is stable for at least 36 hours.