Lead chromate (PbCrO4)

323.19

323.89700

231-846-0

AA3229AOUS

0003

3085|2291|3288

DTXSID1064792

C45891

Yellow or orange-yellow powder|Yellow-orange monoclinic crystals|Orthorhombic: yellow crystals; monoclinic: orange crystals; tetragonal: red crystals

80.26000

-0.85600

Yellow sintered

6.12 g/cm³

844 °C

482°F (Decomposes)

Index of refraction: 2.31, 2.37 (Li /lamp/), 2.66

H2O: Insoluble . <0.1 g/100 mL at 19 ºC

PRECAUTIONS FOR "CARCINOGENS": Storage site should be as close as practical to lab in which carcinogens are to be used, so that only small quantities required for ... expt need to be carried. Carcinogens should be kept in only one section of cupboard, an explosion-proof refrigerator or freezer (depending on chemicophysical properties ...) that bears appropriate label. An inventory ... should be kept, showing quantity of carcinogen & date it was acquired ... Facilities for dispensing ... should b

Approximately 0 mm Hg

Oral-Mouse LD50: > 12000 mg/kg

Non-combustible; toxic lead-containing, chromium compound fumes are produced in the fire

Odorless

Bivalent chromium compounds are basic

Lead chromate displays colors that indicate its trimorphism. The stable form is monoclinic and has an orange-yellow color. An unstable tetragonal orange-red form is isomorphous with, and stabilized by, PbMoO4. A second unstable yellow form is rthorhombic, isomorphous with and stabilized by PbSO4. The diversity shown by the lead salt is the key to its versatility as a pigment.|Strong oxidizing agent

Insoluble in water.

Salts, Basic

Strong Oxidizing Agent

LEAD CHROMATE reacts violently with ferric ferrocyanide (NTP, 1992). The mixture of sulfur and the chromate is pyrophoric, as is the case of tantalum and the chromate. Under certain conditions, combinations of dry mixtures of lead chromate pigment and azo-dyes (nitrobenzeneazo derivatives) may lead to explosions. When these materials are intimately mixed, violent reactions may result [Loss Prev. Bull., 1978, (022), 117].

III

6.1

UN 3077 9/PG 3

3

61-33-40-50/53-62-45

53-45-60-61

GB2975000

T,N

Warehouse low temperature, ventilated, dry

Stable below 7℃

Stable. Reacts violently with ferric ferrocyanide.

P201-P260-P280-P308 + P313

H350-H360Df-H373-H410

Generators of waste (equal to or greater than 100 kg/mo) containing this contaminant, EPA hazardous waste number D007, must conform with USEPA regulations in storage, transportation, treatment and disposal of waste. /Chromium/|Generators of waste (equal to or greater than 100 kg/mo) containing this contaminant, EPA hazardous waste number D008, must conform with USEPA regulations in storage, transportation, treatment and disposal of waste.|Product: Offer surplus and non-recyclable solutions to a licensed disposal company. Contact a licensed professional waste disposal service to dispose of this material. Dissolve or mix the material with a combustible solvent and burn in a chemical incinerator equipped with an afterburner and scrubber; Contaminated packaging: Dispose of as unused product.|Chemical Treatability of Lead; Concentration Process: Biological Treatment; Chemical Classification: Metal; Scale of Study: Respirometer Study; Results of Study: Oxygen uptake inhibited.|For more Disposal Methods (Complete) data for LEAD CHROMATE (18 total), please visit the HSDB record page.

Incompatible materials: Organic materials, powdered metals|During grinding operations, the intimate mixture /of lead chromate and iron(3+) hexacyanoferrate(4-)/ was ignited by a spark and burned fiercely. Spontaneous ignition of Brunswick Green pigment (which also contains lead sulfate) soon after grinding was not uncommon, and similar incidents had led to the loss of ships with cargoes of Prussian Blue or Brunswick Green in wooden casks. The mixture /of lead chromate and sulfur/ is pyrophoric. The mixture /of lead chromate and tantalum/ is a pyrotechnic composition.|Considerable energy is released by the mixture /of lead chromate and aluminum dinitronaphthalene/ derived from chromate-catalyzed exothermic decomposition of the nitro compound, coupled with a thermite-type reaction of the aluminum and chromate.|Under certain conditions, dry mixtures of lead chromate pigments with the G & O azo-dyes ... dinitroaniline orange or ... chlorinated para-red may lead to violent explosions during mixing or blending operations.|For more Hazardous Reactivities and Incompatibilities (Complete) data for LEAD CHROMATE (9 total), please visit the HSDB record page.

DHHS/ATSDR; Toxicological profile for chromium (September 2012).[DHHS/ATSDR; Toxicological profile for chromium (September 2012); Available from, as of February 8, 2016: ww.atsdr.cdc.gov/toxprofiles/tp7.pdf]

Flammability and Flash point data are unavailable; this compound is probably non-flammable. (NTP, 1992)|Not combustible. Gives off irritating or toxic fumes (or gases) in a fire. Risk of fire and explosion on contact with incompatible substances. See Chemical Dangers.

|Danger|H350: May cause cancer [Danger Carcinogenicity]|P201, P202, P260, P273, P281, P308+P313, P314, P391, P405, and P501|H350 (99.76%): May cause cancer [Danger Carcinogenicity]|Aggregated GHS information provided by 418 companies from 13 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.|H350 (100%): May cause cancer [Danger Carcinogenicity]|Aggregated GHS information provided by 350 companies from 10 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.|H317: May cause an allergic skin reaction [Warning Sensitization, Skin]|P201, P202, P260, P261, P271, P272, P273, P280, P281, P302+P352, P304+P340, P308+P313, P311, P314, P321, P333+P313, P363, P391, P403+P233, P405, and P501|P201, P202, P260, P261, P264, P270, P272, P280, P281, P285, P302+P352, P304+P341, P307+P311, P308+P313, P314, P321, P333+P313, P342+P311, P363, P405, and P501|P201, P202, P260, P264, P270, P281, P307+P311, P308+P313, P314, P321, P405, and P501|H341: Suspected of causing genetic defects [Warning Germ cell mutagenicity]

Excerpt from ERG Guide 140 [Oxidizers]: As an immediate precautionary measure, isolate spill or leak area in all directions for at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids. LARGE SPILL: Consider initial downwind evacuation for at least 100 meters (330 feet). FIRE: If tank, rail car or tank truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions. (ERG, 2016)

SMALL SPILLS AND LEAKAGE: Should a spill occur while you are handling this chemical, you should dampen the solid spill material with dilute acid or dilute alkali (e.g. dilute HNO3), then transfer the dampened material to a suitable container. Use absorbent paper dampened with the dilute acid or alkali to pick up any remaining material. Seal the absorbent paper and any of your clothing which may be contaminated in a vapor-tight plastic bag for eventual disposal. Solvent-wash all contaminated surfaces with dilute acid or alkali followed by washing with strong soap and water solution. Do not reenter the contaminated area until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned. STORAGE PRECAUTIONS: You should keep this material in a tightly-closed container under an inert atmosphere, and store it in a freezer. (NTP, 1992)

RECOMMENDED RESPIRATOR: Where the neat test chemical is weighed and diluted, wear a NIOSH-approved half face respirator equipped with an organic vapor/acid gas cartridge (specific for organic vapors, HCl, acid gas and SO2) with a dust/mist filter. (NTP, 1992)|Eye/face protection: Safety glasses with side-shields conforming to EN166. Use equipment for eye protection tested and approved under appropriate government standards such as NIOSH (US) or EN 166(EU).|Skin protection: Handle with gloves.|Body Protection: Complete suit protecting against chemicals, The type of protective equipment must be selected according to the concentration and amount of the dangerous substance at the specific workplace.|Respiratory protection: Where risk assessment shows air-purifying respirators are appropriate use a full-face particle respirator type N100 (US) or type P3 (EN 143) respirator cartridges as a backup to engineering controls. If the respirator is the sole means of protection, use a full-face supplied air respirator. Use respirators and components tested and approved under appropriate government standards such as NIOSH (US) or CEN (EU).|For more Personal Protective Equipment (PPE) (Complete) data for LEAD CHROMATE (13 total), please visit the HSDB record page.

Suitable extinguishing media: Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide.|Advice for firefighters: Wear self-contained breathing apparatus for firefighting if necessary.|NFPA recommends the use of water on fire.|From a secure, explosion-proof location, use water spray to cool exposed containers, If cooling streams are ineffective (venting sound increases in volume and pitch, tank discolors, or shows any signs of deforming), withdraw immediately to a secure position.|For more Fire Fighting Procedures (Complete) data for LEAD CHROMATE (6 total), please visit the HSDB record page.

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid dust formation. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Avoid breathing dust; Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Discharge into the environment must be avoided; Methods and materials for containment and cleaning up: Pick up and arrange disposal without creating dust. Sweep up and shovel. Keep in suitable, closed containers for disposal.|Evacuate persons not wearing protective equipment from area of spill or leak until cleanup is complete. Remove all ignition sources. Collect powdered material in the most convenient and safe manner and deposit in sealed containers. Ventilate area after cleanup is complete. It may be necessary to contain and dispose of this chemical as a hazardous waste. If material or contaminated runoff enters waterways, notify downstream users of potentially contaminated waters.|Cr(VI) cmpd in waste sludge are completely removed by redn by carbon at 600 °C. /Chromium VI/|Persons not wearing protective equipment and clothing should be restricted from areas of spills until cleanup has been completed. If chromic acid or chromates are spilled, the following steps should be taken: 1. Ventilate area of spill. 2. Collect spilled material in the most convenient and safe manner and deposit in sealed containers for reclamation or for disposal in a secured sanitary landfill. Liquid containing chromic acid or chromates should be absorbed in vermiculite, dry sand, earth, or a similar material. /Chromic acid and chromates/|PRECAUTIONS FOR "CARCINOGENS": A high-efficiency particulate arrestor (HEPA) or charcoal filters can be used to minimize amt of carcinogen in exhausted air ventilated safety cabinets, lab hoods, glove boxes or animal rooms ... Filter housing that is designed so that used filters can be transferred into plastic bag without contaminating maintenance staff is avail commercially. Filters should be placed in plastic bags immediately after removal ... The plastic bag should be sealed immediately ... The sealed bag should be labelled properly ... Waste liquids ... should be placed or collected in proper containers for disposal. The lid should be secured & the bottles properly labelled. Once filled, bottles should be placed in plastic bag, so that outer surface ... is not contaminated ... The plastic bag should also be sealed & labelled. ... Broken glassware ... should be decontaminated by solvent extraction, by chemical destruction, or in specially designed incinerators. /Chemical Carcinogens/

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid dust formation. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Avoid breathing dust; Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Discharge into the environment must be avoided.|Precautions for safe handling: Avoid contact with skin and eyes. Avoid formation of dust and aerosols. Further processing of solid materials may result in the formation of combustible dusts. The potential for combustible dust formation should be taken into consideration before additional processing occurs. Provide appropriate exhaust ventilation at places where dust is formed.|Appropriate engineering controls: Handle in accordance with good industrial hygiene and safety practice. Wash hands before breaks and at the end of workday.|Gloves must be inspected prior to use. Use proper glove removal technique (without touching glove's outer surface) to avoid skin contact with this product. Dispose of contaminated gloves after use in accordance with applicable laws and good laboratory practices. Wash and dry hands.|For more Preventive Measures (Complete) data for LEAD CHROMATE (20 total), please visit the HSDB record page.

PRECAUTIONS FOR "CARCINOGENS": Procurement ... of unduly large amt ... should be avoided. To avoid spilling, carcinogens should be transported in securely sealed glass bottles or ampoules, which should themselves be placed inside strong screw-cap or snap-top container that will not open when dropped & will resist attack from the carcinogen. Both bottle & the outside container should be appropriately labelled. ... National post offices, railway companies, road haulage companies & airlines have regulations governing transport of hazardous materials. These authorities should be consulted before ... material is shipped. /Chemical Carcinogens/|PRECAUTIONS FOR "CARCINOGENS": When no regulations exist, the following procedure must be adopted. The carcinogen should be enclosed in a securely sealed, watertight container (primary container), which should be enclosed in a second, unbreakable, leakproof container that will withstand chem attack from the carcinogen (secondary container). The space between primary & secondary container should be filled with absorbent material, which would withstand chem attack from the carcinogen & is sufficient to absorb the entire contents of the primary container in the event of breakage or leakage. Each secondary container should then be enclosed in a strong outer box. The space between the secondary container & the outer box should be filled with an appropriate quantity of shock-absorbent material. Sender should use fastest & most secure form of transport & notify recipient of its departure. If parcel is not received when expected, carrier should be informed so that immediate effort can be made to find it. Traffic schedules should be consulted to avoid ... arrival on weekend or holiday ... /Chemical Carcinogens/

Irritates the respiratory tract. ... Irritation of nose, throat, or bronchial tubes can also occur, with cough and/or wheezing. Skin contact with concentrated lead chromate can cause burns, deep ulcers, or an allergic skin rash.|Chromic acid mist & chromate dusts may cause severe irritation of the nose, throat, bronchial tubes, and lung. /Chromic acid mist & chromate dusts/

Permissible Exposure Limit: (1) The employer shall assure that no employee is exposed to lead at concentrations greater than fifty micrograms per cubic meter of air (50 ug/cu m) averaged over an 8-hr period. (2) If an employee is exposed to lead for more than 8 hr in any work day, the permissible exposure limit, as a time weighted average (TWA) for that day, shall be reduced according to the following formula: Maximum permissible limit (in ug/cu m)=400 divided by the number of hours worked in the day. (3) When respirators are used to supplement engineering and work practice controls to comply with the PEL and all the requirements of paragraph (f) have been met, employee exposure, for the purpose of determining whether the employer has complied with the PEL, may be considered to be at the level provided by the protection factor of the respirator for those periods the respirator is worn. Those periods may be averaged with exposure levels during periods when respirators are not worn to determine the employee's daily TWA exposure. /Lead means metallic lead, all inorganic lead compounds, and organic lead soaps. Excluded from this definition are all other organic lead compounds./|Permissible Exposure Limit: Table Z-1 8-hr Time Weighted Avg: 1 mg/cu m. /Chromium metal and insoluble salts, as Cr/|Permissible Exposure Limit: Table Z-1 8-hr Time Weighted Avg: 0.5 mg/cu m. /Chromium(II) compounds, as Cr/|Permissible Exposure Limit: Table Z-1 8-hr Time Weighted Avg: 0.5 mg/cu m. /Chromium(III) compounds, as Cr/|Permissible Exposure Limit: Table Z-2 Acceptable Ceiling Concentration: 1 mg/10 cu m. /Chromic acid and chromates (as CrO3)/

Recommended Exposure Limit: 8-hour Time-Weighted Average: 0.5 mg Cr/cu m. /Chromium metal, chromium(II) and chromium(III) compounds/|Recommended Exposure Limit: 8-hour Time-Weighted Average: 0.0002 mg Cr(VI)/cu m. NIOSH considers all Cr(VI) compounds (including chromic acid, tert-butyl chromate, zinc chromate, and chromyl chloride) to be potential occupational carcinogens. /All hexavalent chromium (Cr(VI) compounds/|NIOSH usually recommends that occupational exposures to carcinogens be limited to the lowest feasible concentration. /Chromic acid and chromates/

Personal protection: particulate filter respirator adapted to the airborne concentration of the substance. Do NOT let this chemical enter the environment. Vacuum spilled material with specialist equipment. If appropriate, moisten first to prevent dusting. Carefully collect remainder. Then store and dispose of according to local regulations.

Separated from food and feedstuffs and incompatible materials. See Chemical Dangers. Store in an area without drain or sewer access. Provision to contain effluent from fire extinguishing.

Evaporation at 20 °C is negligible; a harmful concentration of airborne particles can, however, be reached quickly on spraying or when dispersed, especially if powdered.

The substance is irritating to the respiratory tract.

The substance may have effects on the blood, bone marrow, central nervous system, peripheral nervous system, kidneys and lungs. This may result in anaemia, peripheral nerve disease, abdominal cramps and kidney impairment. This substance is carcinogenic to humans. May cause toxicity to human reproduction or development.

NO contact with incompatible materials: See Chemical Dangers

PREVENT DISPERSION OF DUST! AVOID ALL CONTACT!

Use local exhaust or breathing protection.

Protective gloves. Protective clothing.

Wear safety goggles or eye protection in combination with breathing protection if powder.

... Substances for which a Federal Register notice has been published that included consideration of the serious health effects, including cancer, from ambient air exposure to the substance. Chromium is included on this list. /Chromium/|Listed as a hazardous air pollutant (HAP) generally known or suspected to cause serious health problems. The Clean Air Act, as amended in 1990, directs EPA to set standards requiring major sources to sharply reduce routine emissions of toxic pollutants. EPA is required to establish and phase in specific performance based standards for all air emission sources that emit one or more of the listed pollutants. Chromium compounds is included on this list. /Chromium compounds/

D008; A waste containing lead may or may not be characterized as a hazardous waste following testing by the Toxicity Characteristic Leaching Procedure as prescribed by the Resource Conservation and Recovery Act (RCRA) regulations. /Lead/|D007; A waste containing chromium may or may not be characterized as a hazardous waste following testing by the Toxicity Characteristic Leaching Procedure as prescribed by the Resource Conservation and Recovery Act (RCRA) regulations. /Chromium/

D008; A solid waste containing lead may or may not become characterized as a hazardous waste when subjected to the Toxicity Characteristic Leaching Procedure listed in 40 CFR 261.24, and if so characterized, must be managed as a hazardous waste. /Lead/|D007; A solid waste containing chromium may or may not become characterized as a hazardous waste when subjected to the Toxicity Characteristic Leaching Procedure listed in 40 CFR 261.24, and if so characterized, must be managed as a hazardous waste. /Chromium/

practically nontoxic

IDENTIFICATION AND USE: Lead chromate is a yellow or orange-yellow powder. It is used as a pigment for paints and inks; in oil and water colors; printing fabrics; decorating china and porcelain; in chemical analysis of organic substances; and in traffic paints. HUMAN EXPOSURE AND TOXICITY: Lead chromate is toxic by ingestion and inhalation. Although no evidence has been found that lead-chromate causes lung cancer in lead chromate workers, it cannot be unequivocally stated that heavy exposures to lead chromate does not present a cancer hazard. One possible mechanism for lead chromate-induced carcinogenesis is through centrosome dysfunction, leading to the induction of aneuploidy. Lead in lead chromate could cause possible neurotoxicity. Increasing concentrations of lead chromate induced increasing amounts of cytotoxicity and clastogenicity in human skin cells. ANIMAL STUDIES: A single sc injection of 30 mg lead chromate(VI) oxide in water to 2 groups of 40 rats gave rise to 26/40 & 27/40 sarcomas, respectively, at site of injection within 117-150 weeks. No local sarcoma occurred in 60 vehicle-treated control rats. Lead chromate induced 14 fibrosarcomas & 17 rhabdomyosarcomas at the site of injection in 31/47 rats given monthly im injections of lead chromate. In addition, 3/24 lead chromate-treated rats had renal carcinomas. No such tumors appeared in a similar group of 22 controls injected with the vehicle. No lung tumors were found in rabbits and guinea pigs after intratracheal instillation. The potential mutagenicity of lead chromate was tested by following battery of microbial tests: the Escherichia coli pola+/pola- survival test; the Salmonella/microsome his+ reversion assay; the E coli trp+ reversion test plate assay; the E coli gal+ forward mutation test; & the Saccharomyces cerevisiae assay for mitotic recombination. Lead chromate was mutagenic in Salmonella & in Saccharomyces. Metabolic activation by rat liver homogenate (S9) was not required. Apparently, chromate ion is responsible for mutagenicity of lead chromate. An insoluble chromic compound, lead chromate (PbCrO4), was not cytotoxic nor mutagenic on V79 cells, probably because it is taken up by the cells very slowly. ECOTOXICITY STUDIES: Lead chromate was both cytotoxic and genotoxic to sea turtle cells. Concentrations of 0.1, 0.5, 1, and 5 ug/sq cm lead chromate induced 108, 79, 54, and 7% relative survival, respectively. Additionally, concentrations of 0, 0.1, 0.5, 1, and 5 ug/sq cm lead chromate induced damage in 4, 10, 15, 26, and 36% of cells and caused 4, 11, 17, 30, and 56 chromosome aberrations in 100 metaphases, respectively. Increasing concentrations of lead chromate induce increasing amounts of cytotoxicity and clastogenicity in sperm whale skin cells.

13 lead chromate-based pigments were assayed for mutagenicity and toxicity using Salmonella typhimurium TA100. The compounds were assayed with and without S9, both in the presence and absence of the chelating agent, nitrilotriacetic acid (NTA). In general, the use of NTA to solubilize the compounds resulted in mutagenicity and/or toxicity being observed where it had not in the absence of NTA, or being observed at lower concentrations than when water alone was used. Encapsulation of pigments with amorphous silica rendered these pigments non-mutagenic and non-toxic, indicating that the active moieties were biologically unavailable to the bacteria. Varying the percentage of silica encapsulation on one pigment, medium chrome yellow, indicated that 5% encapsulation did not alter the mutagenicity while 10% encapsulation inhibited the mutagenicity without or with NTA.

LD50 Mouse oral >12 g/kg

/AQUATIC SPECIES/ Sea turtles are a charismatic and ancient ocean species and can serve as key indicators for ocean ecosystems, including coral reefs and sea grass beds as well as coastal beaches. Genotoxicity studies in the species are absent, limiting our understanding of the impact of environmental toxicants on sea turtles. Hexavalent chromium (Cr(VI)) is a ubiquitous environmental problem worldwide, and recent studies show it is a global marine pollutant of concern. Thus, ...the cytotoxicity and genotoxicity of soluble and particulate Cr(VI) in hawksbill sea turtle cells /was evaluated/. Particulate Cr(VI) was both cytotoxic and genotoxic to sea turtle cells. Concentrations of 0.1, 0.5, 1, and 5 ug/sq cm lead chromate induced 108, 79, 54, and 7% relative survival, respectively. Additionally, concentrations of 0, 0.1, 0.5, 1, and 5 ug/sq cm lead chromate induced damage in 4, 10, 15, 26, and 36% of cells and caused 4, 11, 17, 30, and 56 chromosome aberrations in 100 metaphases, respectively. For soluble Cr, concentrations of 0.25, 0.5, 1, 2.5, and 5 uM sodium chromate induced 84, 69, 46, 25, and 3% relative survival, respectively. Sodium chromate induced 3, 9, 9, 14, 21, and 29% of metaphases with damage, and caused 3, 10, 10, 16, 26, and 39 damaged chromosomes in 100 metaphases at concentrations of 0, 0.25, 0.5, 1, 2.5, and 5uM sodium chromate, respectively. These data suggest that Cr(VI) may be a concern for hawksbill sea turtles and sea turtles in general.|/AQUATIC SPECIES/ Chromium (Cr) is a global marine pollutant, present in marine mammal tissues. Hexavalent chromium [Cr(VI)] is a known human carcinogen. In this study, we compare the cytotoxic and clastogenic effects of Cr(VI) in human (Homo sapiens) and sperm whale (Physeter macrocephalus) skin fibroblasts. Our data show that increasing concentrations of both particulate /lead chromate/ and soluble /sodium chromate/ Cr(VI) induce increasing amounts of cytotoxicity and clastogenicity in human and sperm whale skin cells. Furthermore, the data show that sperm whale cells are resistant to these effects exhibiting less cytotoxicity and genotoxicity than the human cells. Differences in Cr uptake accounted for some but not all of the differences in particulate and soluble Cr(VI) genotoxicity, although it did explain the differences in particulate Cr(VI) cytotoxicity. Altogether, the data indicate that Cr(VI) is a genotoxic threat to whales, but also suggest that whales have evolved cellular mechanisms to protect them against the genotoxicity of environmental agents such as Cr(VI).

Crocoite, a natural lead chromate, found use as a pigment because of its beautiful, permanent orange-red color(1). However, this mineral was very rare(1). Lead chromate occurs in nature as the minerals crocoite and phoenicochroite(2).

According to the 2012 TSCA Inventory Update Reporting data, 1 reporting facility estimate the number of persons reasonably likely to be exposed during the manufacturing, processing, or use of lead chromate oxide (7758-97-6) in the United States as <10 workers per plant; the data may be greatly underestimated due to confidential business information (CBI) or unknown values(1).|NIOSH (NOES Survey 1981-1983) has statistically estimated that 31,932 workers (8,639 of these are female) were potentially exposed to lead chromate in the US(1). Occupational exposure to lead chromate may occur through inhalation of dust and partuculates and dermal contact with this compound at workplaces where lead chromate is produced or used(2). Exposure to lead chromate may occur during the removal of lead paints containing lead chromate(3).

The mean chromium level in the urine of 10 production workers working in a pigment plant making lead chromate was 265 nmol/mmol creatinine (range 41-1250)(1).

Chemicals and substances that impart color including soluble dyes and insoluble pigments. They are used in INKS; PAINTS; and as INDICATORS AND REAGENTS. (See all compounds classified as Coloring Agents.)

(51)Cr-labelled sodium, zinc and lead chromates were studied. Sodium chromate and the less soluble zinc chromate were absorbed by the blood, resulting in increased urinary excretion of chromium. ... The less water-soluble the chromate, the higher was its elimination via the feces. Absorbed chromium was retained in the spleen and bone marrow in all three cases, and also in the liver and kidneys in the case of sodium chromate. Chromium levels in blood and urine are not indicative of inhalation exposure to insoluble chromates.|Transmission electron microscopy (TEM) equipped with energy-dispersive x-ray analysis (EDX), electron spectroscopy for chemical analysis (ESCA), secondary ion mass spectrometry (SIMS), and laser microprobe for mass analysis (LAMMA) were used to follow the fate of chromium compounds deposited in the sheep tracheal lobe. Four chromium compounds were used: two chromium(VI) compounds (lead chromate and chromium trioxide) and two chromium(III) compounds (chronic oxide and chromium sulfate). Chromium trioxide is very soluble and the other three are slightly soluble. The compositions, concentrations, and sizes of particles were determined in the bronchoalveolar lavages (BAL) at d 2, 3, 5, and 30 after instillation and on the lung samples collected at d 31. The concentrations of particles in the BAL samples separated the chromium compounds in two groups where Cr2O3 and PbCrO4 (as Pb) were higher than Cr2(SO4)3, PbCrO4 (as Cr), and CrO3. The half-life for alveolar clearance of Cr2O3 and Cr2(SO4)3 has been calculated respectively at 11 and 80 d. Prismatic PbCrO4 particles break up in the lung and sustain a high concentration of isometric particles of lead chromate and another lead-containing compound in the BAL. The CrO3 instilled particles react with endogenous compounds or are transformed to insoluble hydroxyl complexes instead of diffusing very rapidly through the alveolar-capillary barrier. The alveolar clearance as measured in the BAL is not different from the control.

Hexavalent chromium compounds are known carcinogens for the respiratory tract in humans. The mechanism of cell transformation by hexavalent chromium compounds is not fully understood although a role for intracellular reduction is sought. The aim of this study was to determine the distribution of Cr valence states in human cells after in vitro exposure to soluble or particulate chromium compounds. A synchrotron X-ray-based microprobe was used to investigate the cellular reduction of Cr(VI) and to image chromium oxidation states in cells. It was shown that soluble Cr(VI) compounds are fully reduced to Cr(III) in cells. Cr(III) is homogeneously distributed within the cell volume and therefore present within the nucleus. In the case of low solubility particulate chromate compounds, Cr(VI) can coexist in the cell environment, as particles in the perinuclear region, together with intracellular and intranuclear Cr(III). Chemical distribution maps also suggest that intracellular Cr(III) originates from extracellular dissolution and reduction of lead chromate rather than from intracellular engulfed particles. The possible stronger carcinogenicity of low solubility chromate vs soluble chromate compounds may derive from the combinative genotoxic effects of intranuclear Cr(III) and the persistent exposure to a strong oxidant, Cr(VI). /Soluble and particulate chromates/|Exposure to certain particulate hexavalent chromium [Cr(VI)] compounds, such as lead chromate (PbCrO4), has been associated with lung cancer and respiratory tract toxicity. Previous studies indicate that the solubility of Cr(VI)-compounds is an important factor in Cr(VI)-induced carcinogenesis. The present study investigates reactive oxygen species (ROS) generation by PbCrO4 particles and cellular responses using RAW 264.7 cells. A mixture containing PbCrO4 and RAW 264.7 cells generated hydroxyl radical ((.)OH), using cellularly generated H2O2 as a precursor, as measured by electron spin resonance (ESR) spin trapping in combination with H2O2 and (.)OH scavengers, catalase and sodium formate. The effect of ascorbic acid on (.)OH radicals was also measured using ESR. Confocal microscopy showed that particles could become either bound to the cell surface or engulfed over a 120 min time period. H2O2 generation and O2 consumption were also increased after treatment of the cells with PbCrO4. Both NF-kappaB and AP-1 were activated after exposure to PbCrO4 particles as measured by the NF-kappaB or AP-1 luciferase reporter plasmid assay. Our investigation thus demonstrated that the RAW 264.7 cells phagocytized the PbCrO4 particles leading to accumulation of the particles within vacuoles in the cytoplasm. These particles could induce chronic production of ROS and activation of NF-kappaB and AP-1. Such induction of transcription pathways may be involved in the inflammatory and carcinogenic responses induced by Cr(VI)-containing particles. /Lead chromate oxide/|Free radical reactions are believed to play an important role in the mechanism of Cr(VI)-induced carcinogenesis. Most studies concerning the role of free radical reactions have been limited to soluble Cr(VI). Various studies have shown that solubility is an important factor contributing to the carcinogenic potential of Cr(VI) compounds. Here, we report that reduction of insoluble PbCrO4 by glutathione reductase in the presence of NADPH as a cofactor generated hydroxyl radicals (.OH) and caused DNA damage. The .OH radicals were detected by electron spin resonance (ESR) using 5,5-dimethyl-N-oxide as a spin trap. Addition of catalase, a specific H2O2 scavenger, inhibited the .OH radical generation, indicating the involvement of H2O2 in the mechanism of Cr(VI)-induced .OH generation. Catalase reduced .OH radicals measured by electron spin resonance and reduced DNA strand breaks, indicating .OH radicals are involved in the damage measured. The H2O2 formation was measured by change in fluorescence of scopoletin in the presence of horseradish peroxidase. Molecular oxygen was used in the system as measured by oxygen consumption assay. Chelation of PbCrO4 impaired the generation of .OH radical. The results obtained from this study show that reduction of insoluble PbCrO4 by glutathione reductase/NADPH generates .OH radicals. The mechanism of .OH generation involves reduction of molecular oxygen to H2O2, which generates .OH radicals through a Fenton-like reaction. The .OH radicals generated by PbCrO4 caused DNA strand breakage.

... The half-life for alveolar clearance of Cr2O3 and Cr2(SO4)3 has been calculated respectively at 11 and 80 d. ...

ACUTE/CHRONIC HAZARDS: This compound is toxic by ingestion and inhalation. (NTP, 1992)|Carcinogens

EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop. SKIN: IMMEDIATELY flood affected skin with water while removing and isolating all contaminated clothing. Gently wash all affected skin areas thoroughly with soap and water. If symptoms such as redness or irritation develop, IMMEDIATELY call a physician and be prepared to transport the victim to a hospital for treatment. INHALATION: IMMEDIATELY leave the contaminated area; take deep breaths of fresh air. IMMEDIATELY call a physician and be prepared to transport the victim to a hospital even if no symptoms (such as wheezing, coughing, shortness of breath, or burning in the mouth, throat, or chest) develop. Provide proper respiratory protection to rescuers entering an unknown atmosphere. Whenever possible, Self-Contained Breathing Apparatus (SCBA) should be used; if not available, use a level of protection greater than or equal to that advised under Protective Clothing. INGESTION: Some heavy metals are VERY TOXIC POISONS, especially if their salts are very soluble in water (e.g., lead, chromium, mercury, bismuth, osmium, and arsenic). IMMEDIATELY call a hospital or poison control center and locate activated charcoal, egg whites, or milk in case the medical advisor recommends administering one of them. Also locate Ipecac syrup or a glass of salt water in case the medical advisor recommends inducing vomiting. Usually, this is NOT RECOMMENDED outside of a physician's care. If advice from a physician is not readily available and the victim is conscious and not convulsing, give the victim a glass of activated charcoal slurry in water or, if this is not available, a glass of milk, or beaten egg whites and IMMEDIATELY transport victim to a hospital. If the victim is convulsing or unconscious, do not give anything by mouth, assure that the victim's airway is open and lay the victim on his/her side with the head lower than the body. DO NOT INDUCE VOMITING. IMMEDIATELY transport the victim to a hospital. OTHER: Since this chemical is a known or suspected carcinogen you should contact a physician for advice regarding the possible long term health effects and potential recommendation for medical monitoring. Recommendations from the physician will depend upon the specific compound, its chemical, physical and toxicity properties, the exposure level, length of exposure, and the route of exposure. (NTP, 1992)

Fresh air, rest.

Rinse and then wash skin with water and soap.

Rinse with plenty of water (remove contact lenses if easily possible).

Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Poisons A and B/|Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/|Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag-valve-mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W TKO. Use 0.9% saline (NS) or lactated Ringer's (LR) if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam (Valium) or lorazepam (Ativan) ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/|Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Lead and Related Compounds/|For more Antidote and Emergency Treatment (Complete) data for LEAD CHROMATE (9 total), please visit the HSDB record page.

/SIGNS AND SYMPTOMS/ Food and Environmental Agents: Effect on Breast-Feeding: Reported Sign or Symptom in Infant or Effect on Lactation: Lead: Possible neurotoxicity. /from Table 7/|/CASE REPORTS/ A case of unique acute bone marrow toxicity and pancytopenia following subcutaneous exposure to lead chromate, xylene, and ethylbenzene in a previously healthy patient is reported. The patient sustained an extensive degloving injury to his lower extremity. The wound was contaminated with traffic paint containing lead chromate pigment along with a large volume of xylene and ethylbenzene solvent. Consequences of the patient's clinical course and management of degloving injuries are discussed.|/EPIDEMIOLOGY STUDIES/ Lung cancer mortality among workers at three English chromate pigment factories was investigated. Workers at factories 1 and 2 were exposed to both lead chromate and zinc chromate; those at factory 3 were exposed to lead chromate alone. A total of 152 workers made up the cohort of males completing at least 1 year of work by June 1975. Jobs were allocated to high, medium, and low exposure grades; total worker exposure was determined where possible. Observed deaths from respiratory cancers were compared to expected numbers of deaths taken from a national death rate schedule. Mortality from all causes except lung cancer showed a modest excess of deaths from nonmalignant respiratory diseases. For other respiratory cancers the ratio of observed to expected cases was 2.65. No lung cancer deaths had so far occurred among post 1967 work force entrants of any factory. At factory 1, among workers with high and medium exposure, the lung cancer mortality ratio was 2.22 among workers entering from 1932 to 1945 and 2.23 among 1946 to 1954 entrants. No excess was apparent among later entrants. At factory 2 the lung cancer mortality ratio among high and medium exposure workers entering service from 1948 to 1967 was 3.73. Two deaths occurred among all low exposure workers, compared with 1.03 expected. For factory 3, there were no excess deaths from lung cancer for any exposure groups at any time of entry. Examination of mortality data from factories 1 and 2 in 5 year followup intervals showed high and medium exposure worker lung cancer mortality significantly increased during the first 9 years after entry, with the excess most pronounced 10 and 24 years after entry, and diminishing thereafter. When high and medium exposure groups were examined separately results did not differ significantly. Occupational exposure to zinc chromate produces lung cancer among high and medium exposure workers after as little as 1 year, but no excess cancer was found in lead chromate workers.|/EPIDEMIOLOGY STUDIES/ A study of lung cancer mortality in chromate pigment manufacturing workers was conducted. The cohort consisted of 646 males employed for at least 1 year before 1968 at three chromate pigment factories (SIC-2816) in the United Kingdom. Two factories manufactured lead-chromate and zinc-chromate. The third manufactured only lead-chromate. Company personnel records were reviewed. The chromate exposures of the subjects were estimated on the basis of their job titles. Subjects employed in departments where pigments were ground, blended, and packed were classified as having high exposure. Subjects working in departments where precipitates were washed, pressed, and stove dried were considered to have medium exposure. Workers employed in laboratories, boiler stoking, painting, and bricklaying were classified as having low exposure. The vital status of the cohort was determined as of 1977 utilizing records maintained by the National Health Service Central Register. Death certificates were obtained for the deceased subjects. The observed lung cancer mortality was compared with that of the national rates for all males in England and Wales. No excess lung cancer mortality occurred in workers classified as having low exposure or in those exposed only to lead-chromate. A significant excess of lung cancer deaths occurred in workers classified as high or medium exposures to both zinc-chromate and lead-chromate. The latency periods of the deaths ranged from 5 to 25 years after first exposure. The author suggests that manufacturing zinc-chromate presents a risk of lung cancer. Although no evidence was found that lead-chromate causes lung cancer, it cannot be unequivocably stated that heavy exposures to lead-chromate do not present a cancer hazard.|For more Human Toxicity Excerpts (Complete) data for LEAD CHROMATE (17 total), please visit the HSDB record page.

lead chromate

The substance can be absorbed into the body by inhalation of dust and by ingestion.

Cough.

Redness.

Analytical reagent-grade lead chromate powder is available at a purity of > 98%.

Custom compounding of purchased resin|Chromic acid (H2CrO4), lead(2+) salt (1:1): ACTIVE|SP - indicates a substance that is identified in a proposed Significant New Use Rule.|LEAD CHROMATE-BASED INKS ARE USED FOR PRINTING COLORED PAGES OF SOME CHILDREN'S MAGAZINES (COMICS). THIS PAPER REPORTS INVESTIGATIONS OF 48 UNITED KINGDOM, 9 SPANISH, & 5 AUSTRIAN COMICS.|Chrome yellows (containing 52-98% lead chromate) are considered to be the most versatile of the inorganic pigments and are therefore found in many formulations designed for a wide spectrum of uses.|Considerable energy is released by the mixture /of lead chromate and aluminum dinitronaphthalene/ derived from chromate-catalyzed exothermic decomposition of the nitro compound, coupled with a thermite-type reaction of the aluminum and chromate. It is useful for cracking concrete.

Health Hazards -> Carcinogens