Phenylmercuric Chloride

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.

0.1 [mg/m3], as Hg

8 hr Time Weighted Avg (TWA): 0.1 mg/cu m, skin /Mercury, aryl cmpds, as Hg/

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. /Mercury, aryl cmpds, as Hg/

Mercury mainly affects the nervous system. Exposure to high levels of metallic, inorganic, or organic mercury can permanently damage the brain, kidneys, and developing fetus. Effects on brain functioning may result in irritability, shyness, tremors, changes in vision or hearing, and memory problems. Acrodynia, a type of mercury poisoning in children, is characterized by pain and pink discoloration of the hands and feet. Mercury poisoning can also cause Hunter-Russell syndrome and Minamata disease. (L7)

High-affinity binding of the divalent mercuric ion to thiol or sulfhydryl groups of proteins is believed to be the major mechanism for the activity of mercury. Through alterations in intracellular thiol status, mercury can promote oxidative stress, lipid peroxidation, mitochondrial dysfunction, and changes in heme metabolism. Mercury is known to bind to microsomal and mitochondrial enzymes, resulting in cell injury and death. For example, mercury is known to inhibit aquaporins, halting water flow across the cell membrane. It also inhibits the protein LCK, which causes decreased T-cell signalling and immune system depression. Mercury is also believed to inhibit neuronal excitability by acting on the postsynaptic neuronal membrane. It also affects the nervous system by inhibiting protein kinase C and alkaline phosphatase, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Organic mercury exerts developmental effects by binding to tubulin, preventing microtubule assembly and causing mitotic inhibition. Mercury also produces an autoimmune response, likely by modification of major histocompatibility complex (MHC) class II molecules, self peptides, T-cell receptors, or cell-surface adhesion molecules. (L7, A8, A25, A26)

... A large fraction of the /phenylmercury/ spray residue was found in the soil 30-50 days after application; the rest of the Hg was lost by vaporization (either as the organic cmpd or after conversion to Hg metal) or by migration to lower soil horizons since water containing organic cmpd from decomposing vegetable matter can leach adsorbed Hg. /Phenylmercury spray/

Phenylmercuric chloride was applied in three doses (5 ppm, 30 ppm Hg, and 30 ppm Hg + 4 ppm Se) via the food for 60 days. The effect of Hg with and without Se was studied histologically and the data of a shortened spermatogram were evaluated. Treatment with 30 ppm Hg resulted in hypospermia, occurrence of abnormally maturing spermatozoa, reduction of the volume of semen, and decrease in the number of spermatozoa. The dose of 5 ppm Hg only resulted in the appearance of abnormally developing cells and decreased sperm motility. The addition of Se maintained spermatogenesis and the values of semen on the control level.

The seed mordants Agronal Super, which contains the organic mercury (5.4% phenylmercury chloride), has appeared to induce poisoning and even death of many people and animals. Minimal single embryotoxic doses of Agronal Super were estimated in 24-day old chick embryos using the CHEST method and compared with the minimal embryotoxic doses of other 8 seed mordants without mercury. Minimal embryotoxic doses (the beginning of the embryotoxicity range) of Agronal Super were between 0.1-1.0 ug/embryo. The seed mordants without mercury appeared to be less toxic: The minimal embryotoxic doses of Baytan Combi, Baytan Universal, Fundasol, Quinolate and Wolfen Thiuram were between 1-10 ug/embryo. Novozir and Sibutol had minimal embryotoxic doses within the range 10-100 ug/embryo. The least dangerous appeared the seed mordant Vincit, which produced no embryotoxic effect, even after administration of the highest doses (100 ug/embryo). Our results demonstrated the difference of several orders of magnitude between embryotoxic doses of Agronal Super and other 8 seed mordants. Replacement of seed mordants containing organic mercury (e.g. Agronal Super) by new ones with minimal or no embryotoxic effect (e.g. Vincit) is advisable.

The effect of phenyl mercury with and without selenium on the egg production of laying hens and on the fertility, hatchability and properties of eggs was studied. Mercury was administered via the feed at dosages of 5 ppm, 30 ppm, and 30 ppm Hg + 4 ppm Se, for 56 days. After two months, egg production decreased by 8.18% and 7.74% in hens fed 30 ppm Hg, and 30 ppm Hg + 4 ppm Se, respectively. Egg weight decreased in all experimental groups. In comparison to the controls, these results were highly significant (P < 0.01) in hens fed 30 ppm Hg and 30 ppm Hg + 4 ppm Se and significant (P < 0.05) between hens fed 5 ppm Hg and 30 ppm Hg. Fertility rate and hatchability were not affected. Mercury exposure did not affect egg shape, egg-white height, egg-shell hardness or yolk colour. Both egg-shell thickness and weight decreased in all experimental groups. In the group supplemented with selenium there was a nonsignificant improvement in egg production, hatchability and all qualitative properties of eggs in comparison with the group without selenium supplementation. Residual mercury levels in egg yolk greatly surpassed the level found in the egg white: the highest values were measured in the group fed 30 ppm Hg. The addition of selenium had a protective effect upon residual Hg deposits in the yolk, but not in the egg-white.

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. Phenylmercuric chloride is included on this list.

Used formerly as antimycotic, antisyphilitic, diuretic, agricultural fungicide, antiseptic, and germicide; Not currently registered with the EPA for use in the US; [HSDB]

Use in paints as a biocide was discontinued in 1991 in the US; [HSDB]

Using Disinfectants or Biocides [Category: Clean]

For Phenylmercuric Chloride (USEPA/OPP PC Code: 066007) there are 0 labels match. /SRP: Not registered for current use in the U.S./

Antimycotic /Former use/

Used as antisyphilitic and diuretic ... use for this purpose has been restricted or stopped because of ... numerous side effects and toxicity /Former use/