SRP: The scientific literature for the use of contact lenses in industry is conflicting. The benefit or detrimental effects of wearing contact lenses depend not only upon the substance, but also on factors including the form of the substance, characteristics and duration of the exposure, the uses of other eye protection equipment, and the hygiene of the lenses. However, there may be individual substances whose irritating or corrosive properties are such that the wearing of contact lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In any event, the usual eye protection equipment should be worn even when contact lenses are in place.|Precautions for safe handling: Avoid contact with skin and eyes. Avoid inhalation of vapour or mist. Keep away from sources of ignition - No smoking.Take measures to prevent the build up of electrostatic charge.|Appropriate engineering controls: Avoid contact with skin, eyes and clothing. Wash hands before breaks and immediately after handling the product.|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 3-METHYLPYRIDINE (6 total), please visit the HSDB record page.
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IDENTIFICATION AND USE: 3-Methylpyridine is a colorless liquid. It is used as a solvent; intermediate in dye and resins industries; in manufacture of insecticides, waterproofing agents, niacin and niacinamide. HUMAN EXPOSURE AND TOXICITY: 3-Methylpyridine caused eye irritation, gastro-intestinal disturbances and central nervous system (CNS) effects in one worker and may have produced liver abnormalities and facial skin eruptions in another. ANIMAL STUDIES: 3-Methylpyridine was a marked skin irritant in rabbits and guinea-pigs and has caused severe eye irritation in rabbits.. It has affected electrophysiological parameters in rats. Moderate acute oral, dermal and inhalation toxicity was demonstrated in laboratory animals, the principal site of toxic attack being the CNS. Repeated inhalation exposure resulted in increased liver weight in rats. 3-Methylpyridine was tested in three independent bacterial gene mutation studies; all studies gave negative results in S. typhimurium or E. coli tester strains, with and without exogenous metabolic activation. In vivo, no significant increases in the frequencies of micronucleated erythrocytes were observed in peripheral blood of male or female mice. In NTP cancerogenicity studies there was equivocal evidence of carcinogenic activity of 3-methylpyridine in male mice based on increased incidences of alveolar/ bronchiolar adenoma and alveolar/bronchiolar adenoma or carcinoma (combined). There was clear evidence of carcinogenic activity of 3-methylpyridine in female mice based on the increased incidences of alveolar/ bronchiolar adenoma or carcinoma (combined) in the lung and of hepatocellular carcinoma and hepatoblastoma in the liver. In the similar studies in rats there was no evidence of carcinogenic activity of 3-methylpyridine in male rats. There was some evidence of carcinogenic activity of 3-methylpyridine in female rats based on increased incidences of alveolar/bronchiolar adenoma and alveolar/bronchiolar adenoma or carcinoma (combined).
Male and female F344/N rats and B6C3F1/N mice were exposed to beta-picoline (greater than 96% pure) in drinking water for 3 months or 2 years. Genetic toxicology studies were conducted in Salmonella typhimurium, Escherichia coli, and mouse peripheral blood erythrocytes.|3-MONTH STUDY IN MICE Groups of 10 male and 10 female mice were exposed to 0, 78, 156, 312, 625, or 1,250 mg beta-picoline/L drinking water for 14 weeks (equivalent to average daily doses of approximately 10, 20, 37, 77, or 148 mg beta-picoline/kg body weight to males and 9, 18, 38, 72, or 134 mg/kg to females). All mice survived to the end of the study. Mean body weights and water consumption were generally similar among exposed and control groups of male and female mice. Lung weights of 1,250 mg/L females were significantly less than those of the controls. No histopathologic lesions were attributed to beta-picoline exposure.|3-MONTH STUDY IN RATS Groups of 10 male and 10 female core study rats were exposed to 0, 78, 156, 312, 625, or 1,250 mg beta-picoline/L drinking water for 14 weeks (equivalent to average daily doses of approximately 6, 11, 22, 38, or 70 mg beta-picoline/kg body weight to males and 6, 12, 23, 38, or 64 mg/kg to females). Special study groups of 10 male and 10 female rats were exposed to the same concentrations for 23 days for determinations of cytochrome P450 enzyme activity. All rats survived to the end of the study. Mean body weights of males and females exposed to 625 or 1,250 mg/L were significantly less than those of the controls. Water consumption by 625 and 1,250 mg/L males and females was less than that by the controls at weeks 1 and 13 due to poor palatability. On day 23, hepatic 7-pentoxyresorufin-O-dealkylase activity was significantly increased in 312 mg/L or greater males and in 156 mg/L or greater females compared to that in the controls. Absolute liver weights of 625 and 1,250 mg/L males and absolute and relative liver weights of 625 and 1,250 mg/L females were significantly less than those of the controls. The Markov transition matrix analyses of estrous cyclicity indicated female rats in the 312 and 625 mg/L groups had a significantly higher probability of extended estrus than the control females, suggesting a potential for beta-picoline to be a reproductive toxicant in female rats exposed to these concentrations. The severity of chronic progressive nephropathy was increased in 625 and 1,250 mg/L males and that of hyaline droplet accumulation in proximal renal tubules was increased in 1,250 mg/L males. The concentrations of renal a2u-globulin were significantly increased in 312 mg/L or greater males compared to the controls.|2-YEAR STUDY IN MICE Groups of 50 male and 50 female mice were exposed to 0, 312.5, 625, or 1,250 mg beta-picoline/L drinking water for 105 weeks (equivalent to average daily doses of approximately 26, 50, or 92 mg beta-picoline/kg body weight to males and 18, 37, or 68 mg/kg to females). Survival of all exposed groups was similar to that of the control groups. Mean body weights of 1,250 mg/L males were 10% less than those of the control group after week 57, and those of 1,250 mg/L females were generally 10% less after week 13. Water consumption by exposed groups of males and females was similar to that by con-trols during the first 13 weeks of the study; water consumption by 625 and 1,250 mg/L males and 1,250 mg/L females was less than that in the controls after week 13. In the liver of females, there were significantly increased incidences of hepatocellular adenoma in the 312.5 mg/L group and hepatocellular carcinoma in all exposed groups. The combined incidences of hepatocellular carcinoma or hepatoblastoma were significantly increased in all exposed females. In the lung, the incidence of alveolar/bronchiolar adenoma in 625 mg/L males was significantly increased. The incidences of alveolar/bronchiolar adenoma occurred with a positive trend in females. The incidences of alveolar/bronchiolar carcinoma were increased in all exposed groups of females. The incidence of alveolar/bronchiolar adenoma or carcinoma (combined) was significantly increased in 1,250 mg/L females. The incidence of alveolar epithelium hyperplasia was significantly increased in 1,250 mg/L females. In the nose, there were significantly increased incidences of olfactory epithelium respiratory metaplasia in 625 mg/L males and 1,250 mg/L males and females; the incidence of olfactory epithelium atrophy was significantly increased in 1,250 mg/L females.|For more National Toxicology Program Studies (Complete) data for 3-METHYLPYRIDINE (7 total), please visit the HSDB record page.
TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 115(SRC), determined from a structure estimation method(2), indicates that 3-methylpyridine is expected to have high mobility in soil(SRC). The pKa of 3-methylpyridine is 5.63(3), indicating that this compound will exist partially in cation form in the environment and cations generally adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(4). Soil studies with 2-methylpyridine(5), a compound expected to have similar sorption properties as 3-methylpryidine(SRC), demonstrated that Koc can vary with pH with lowest adsorption occurring in the non-ionized form(5). Volatilization of 3-methylpyridine from moist soil surfaces is expected to be an important fate process(SRC) given a Henry's Law constant of 7.73X10-6 atm-cu m/mole(6). 2-Methylpyridine is expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 6.05 mm Hg at 25 °C(7). 3-Methylpyridine is expected to biodegrade fairly rapidly in aerobic soil; however, under anaerobic conditions, this compound may be persistent(8,9). 3-Methylpyridine was added to aerobic Fincastle silt loam for a period of 32 days; 69.3% of the available nitrogen was released after this time(8). However, in an aerobic surface soil experiment, only 35% biodegradation was reported in 3 months while in anaerobic surface soil, under denitrifying and sulfidogenic conditions, 50 and 10 to 20% of the initially added 3-methylpyridine was biodegraded, respectively, in 3 months(9).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 115(SRC), determined from a structure estimation method(2), indicates that 3-methylpyridine is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is expected(3) based upon a Henry's Law constant of 7.73X10-6 atm-cu m/mole(4). Using this Henry's Law constant and an estimation method(3), volatilization half-lives for a model river and model lake are 5 and 37 days, respectively(SRC). According to a classification scheme(5), an estimated BCF of 3(SRC), from its log Kow of 1.20(6) and a regression-derived equation(2), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Low bioconcentration was reported for BCF tests using carp (Cyprinus carpio)(7). Rapid biodegradation under aerobic conditions is likely although 3-methylpyridine seems resistant to biodegradation under anaerobic conditions(8,9). 3-Methylpyridine was rapidly biodegraded in acclimated aerobic natural waters with complete removal within 2 to 4 days(8). However, in sulfidogenic estuarine sediments, 3-methylpyridine was not biodegraded over 200 days(9). 3-Methylpyridine is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(3). The UV absorption spectrum of 3-methylpyridine in aqueous solution shows no absorption >290 nm(10); therefore, 3-methylpyridine is not expected to be susceptible to direct photolysis by sunlight(SRC).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), 2-methylpyridine, which has a vapor pressure of 6.05 mm Hg at 25 °C(2), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase 3-methylpyridine is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 7 days(SRC), calculated from its rate constant of 2.30X10-12 cu cm/molecule-sec at 25 °C(3). The UV absorption spectrum of 3-methylpyridine in aqueous solution shows no absorption >290 nm(4); therefore, 3-methylpyridine is not expected to be susceptible to direct photolysis by sunlight(SRC).
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. If symptoms (such as wheezing, coughing, shortness of breath, or burning in the mouth, throat, or chest) develop, call a physician and be prepared to transport the victim to a hospital. 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: DO NOT INDUCE VOMITING. If the victim is conscious and not convulsing, give 1 or 2 glasses of water to dilute the chemical and IMMEDIATELY call a hospital or poison control center. Be prepared to transport the victim to a hospital if advised by a physician. If the victim is convulsing or unconscious, do not give anything by mouth, ensure 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. (NTP, )
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Fresh air, rest. Refer for medical attention.
Remove contaminated clothes. Rinse skin with plenty of water or shower. Refer for medical attention .
First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical attention.
/SRP:/ 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 as 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. /Aromatic hydrocarbons and related compounds/|/SRP:/ 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 necessary. 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 as 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. Administer activated charcoal ... . /Aromatic hydrocarbons and related compounds/|/SRP:/ Advanced treatment: Consider orortracheal 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 agonistic such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start an IV with D5W TKO /SRP: "To keep open", minimal flow rate/. 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 ... . /Aromatic hydrocarbons and related compounds/
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