Nickeldiiodid

SRP: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.

8 hr Time Weighted Avg (TWA) 0.1 mg/cu m (inhalable fraction). /Nickel, soluble inorganic compounds (NOS), as Ni/

Excursion Limit Recommendation: Excursions in worker exposure levels may exceed 3 times the TLV-TWA for no more than a total of 30 minutes during a work day, and under no circumstances should they exceed 5 times the TLV-TWA, provided that the TLV-TWA is not exceeded. /Nickel, soluble inorganic compounds (NOS), as Ni/

A4: Not classifiable as a human carcinogen. /Nickel, soluble inorganic compounds (NOS), as Ni/

The most common harmful health effect of nickel in humans is an allergic reaction. This usually manifests as a skin rash, although some people experience asthma attacks. Long term inhahation of nickel causes chronic bronchitis and reduced lung function, as well as damage to the naval cavity. Ingestion of excess nickel results in damage to the stomach, blood, liver, kidneys, and immune system, as well as having adverse effects on reproduction and development. (L41)

Nickel is known to substitute for other essential elements in certain enzmes, such as calcineurin. It is genotoxic, and some nickel compounds have been shown to promote cell proliferation. Nickel has a high affinity for chromatin proteins, particularly histones and protamines. The complexing of nickel ions with heterochromatin results in a number of alterations including condensation, DNA hypermethylation, gene silencing, and inhibition of histone acetylation, which have been shown to disturb gene expression. Nickel has also been shown to alter several transcription factors, including hypoxia-inducible transcription factor, activating transcription factor, and NF-KB transcription factor. There is also evidence that nickel ions inhibit DNA repair, either by directly inhibiting DNA repair enzymes or competing with zinc ions for binding to zinc-finger DNA binding proteins, resulting in structural changes in DNA that prevent repair enzymes from binding. Nickel ions can also complex with a number of cellular ligands including amino acids, peptides, and proteins resulting in the generation of oxygen radicals, which induce base damage, DNA strand breaks, and DNA protein crosslinks. (L41, A40)

Biological monitoring and hygienic monitoring complement each other in assessing occupational exposure to nickel. Biological monitoring is mainly directed to following the exposure of individual workers. In order to estimate exposure from data on biological monitoring, the exposing agent, ie, the chemical species of nickel involved must be known. Comparisons between exposures are most reliable when made under similar exposure conditions. In particular, when urine is monitored, contamination of the sample from the dust in the air, workers' clothes, and hands, is a major porblem. The sampling time must be standardized. At present, no clear cut preference can be given to plasma rather than urine or vice versa. With the exception of nickel carbonyl poisoning, no health risk estimation can be performed based on the resultsof biological monitoring.

A4: Not classifiable as a human carcinogen. /Nickel, soluble inorganic compounds (NOS), as Ni/

Evaluation: There is sufficient evidence in humans for the carcinogenicity of nickel sulfate, and of the combinations of nickel sulfides and oxides encountered in the nickel refining industry. There is inadequate evidence in humans for the carcinogenicity of metallic nickel and nickel alloys. There is sufficient evidence in experimental animals for the carcinogenicity of metallic nickel, nickel monoxides, nickel hydroxides and crystalline nickel sulfides. There is limited evidence in experimental animals for the carcinogenicity of nickel alloys, nickelocene, nickel carbonyl, nickel salts, nickel arsenides, nickel antimonide, nickel selenides and nickel telluride. There is inadequate evidence in experimental animals for the carcinogenicity of nickel trioxide, amorphous nickel sulfide and nickel titanate. The Working Group made the overall evaluation on nickel compounds as a group on the basis of the combined results of epidemiological studies, carcinogenicity studies in experimental animals, and several types of other relevant data, supported by the underlying concept that nickel compounds can generate nickel ions at critical sites in their target cells. Overall evaluation: Nickel compounds are carcinogenic to humans (Group 1). Metallic nickel is possibly carcinogenic to humans (Group 2B). /Nickel compounds/

Basic treatment: Establish a patent airway. Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilation if necessary. Administer oxygen by nonrebreather mask at 10 t0 15 L/min. Monitor for shock and treat if necessary ... . Monitor for pulmonary edema and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with normal saline 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 ... . /Nickel and related compounds/

Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious. Positive pressure ventilation techniques with a bag valve mask device may be beneficial. Monitor cardiac rhythm and treat arrhythmias if necessary ... . Consider drug therapy for pulmonary edema ... . Start an IV with D5W /SRP: "To keep open", minimal flow rate/. Use lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Consider vasopressors for hypotension with a normal fluid volume. Watch for signs of fluid overload ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Nickel and related compounds/

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. Nickel iodide is included on this list.

(CA) CALIFORNIA 100 ug/L /Nickel/

(CT) CONNECTICUT 100 ug/l /Nickel/

(DE) DELAWARE 100 ug/l /Nickel/

(FL) FLORIDA 100 ug/L /Nickel/

(WI) WISCONSIN 100 ug/L /Nickel/

(AZ) ARIZONA 150 ug/l /Nickel/

(MA) MASSACHUSETTS 100 ug/l /Nickel/

(ME) MAINE 140 ug/l /Nickel/

(MN) MINNESOTA 100 ug/l /Nickel/