Section 1 - CHEMICAL PRODUCT AND COMPANY IDENTIFICATION

PRODUCT NAME

LEAD DRIER

NFPA

PRODUCT USE

Paint and varnish drier, wood preservative, insecticide, catalyst for reaction between
unsaturated fatty acids and air. Regeant

SYNONYMS

C7-H12-O2.xPb, octoate, "lead 2-ethylhexoate", "lead 2-ethylhexoate", "lead ethylhexoate",
"lead naphthenate", "lead neodeconate", "ilead sononanate", "cyclohexanecarboxylic acid,
lead salt", "lead terebine", "naphthenic acid, lead salt"

Section 2 - HAZARDS IDENTIFICATION

CANADIAN WHMIS SYMBOLS

EMERGENCY OVERVIEW

RISK

Danger of cumulative effects.
Irritating to skin.
May cause harm to the unborn child.
Possible risk of impaired fertility.
HARMFUL - May cause lung damage if swallowed.
Harmful: danger of serious damage to health by prolonged exposure through
inhalation, in contact with skin and if swallowed.
Harmful by inhalation and if swallowed.
Flammable.
Vapors may cause dizziness or suffocation.
Very toxic to aquatic organisms, may cause long- term adverse effects in the
aquatic environment.

POTENTIAL HEALTH EFFECTS

ACUTE HEALTH EFFECTS

SWALLOWED

  Accidental ingestion of the material may be harmful; animal experiments indicate that ingestion of less than 150 gram may be fatal or may produce serious damage to the health of the individual.  Swallowing of the liquid may cause aspiration into the lungs with the risk of chemical pneumonitis; serious consequences may result. (ICSC13733).  The LD50s of naphthenic acids (a mixture of isomers of dimethylcyclohexanecarboxylic acid) in mice and rats were 1770 and 1750 mg/kg, respectively. Cumulative properties of naphthenic acids were mild. The oral LD50 in male mice of commercial sodium salts of naphthenic acids was found to be 3550 mg/kg body weight. Symptoms included central nervous system depression, convulsions and respiratory arrest. For rats the oral LD50 value for commercial naphthenic acids was 3000 mg/kg, while for mixtures of dicyclohexane (a specific naphthenic acid), the oral LD50 was 1750 mg/kg.  Exposure of Wistar rats to single or repeated oral doses of naphthenic acids produced a number of treatment-related effects, particularly in the highest dose groups. Marked reduction in food consumption was observed immediately following dosing in the high-dose group of the acute toxicity study. A similar decrease in food consumption was observed in the subchronic study, but in both cases the effect was short-lived. Appetite suppression was probably not due to direct irritation of the gastrointestinal lining, since repeated exposure did not sustain the effect in the subchronic study. In addition, there was no histopathological evidence of gastrointestinal irritation in either study. The mechanism of toxicant-induced anorexia has yet to be determined.  The results of the acute toxicity test suggested exposure to naphthenic acids at levels of 300 mg/kg in rats had both cardiovascular and hepatic effects. A single oral dose of 300 mg/kg produced significant cerebral hemorrhage in male rats. Vasoactive effects of naphthenic acids were also noted study by following intramuscular injection with 150 mg/kg cyclopentane naphthenic acid for 10 days; increased vascular permeability of cerebral capillaries was seen. Such an effect could be linked to the cerebral hemorrhaging or periarteriolar necrosis/fibrosis in the heart that was apparent following acute exposure to naphthenic acids. It is unclear why the cerebral hemorrhage was more prevalent in male than in female rats. It is unknown whether the effects of acute naphthenic acid dosing on cardiac tissue (periarteriolar necrosis/fibrosis) are attributable to parent naphthenic acids or their metabolites.  The clearest demonstration of a target organ in the acute toxicity test was the liver, where the inflammation of tissues around the bile duct (pericholangitis) was consistent between sexes and highly dose-dependent.  Central nervous system (CNS) depression may include general discomfort, symptoms of giddiness, headache, dizziness, nausea, anaesthetic effects, slowed reaction time, slurred speech and may progress to unconsciousness. Serious poisonings may result in respiratory depression and may be fatal.  Ingestion of petroleum hydrocarbons can irritate the pharynx, esophagus, stomach and small intestine, and cause swellings and ulcers of the mucous. Symptoms include a burning mouth and throat; larger amounts can cause nausea and vomiting, narcosis, weakness, dizziness, slow and shallow breathing, abdominal swelling, unconsciousness and convulsions. Damage to the heart muscle can produce heart beat irregularities, ventricular fibrillation (fatal) and ECG changes. The central nervous system can be depressed. Light species can cause a sharp tingling of the tongue and cause loss of sensation there. Aspiration can cause cough, gagging, pneumonia with swelling and bleeding.  

EYE

  There is some evidence to suggest that this material can causeeye irritation and damage in some persons.  Direct eye contact with petroleum hydrocarbons can be painful, and the corneal epithelium may be temporarily damaged. Aromatic species can cause irritation and excessive tear secretion.  

SKIN

  This material can cause inflammation of the skin oncontact in some persons.  The material may accentuate any pre-existing dermatitis condition.  Skin contact with the material may damage the health of the individual; systemic effects may result following absorption.  The liquid may be miscible with fats or oils and may degrease the skin, producing a skin reaction described as non-allergic contact dermatitis. The material is unlikely to produce an irritant dermatitis as described in EC Directives .  Entry into the blood-stream, through, for example, cuts, abrasions or lesions, may produce systemic injury with harmful effects. Examine the skin prior to the use of the material and ensure that any external damage is suitably protected.  Aromatic hydrocarbons may produce sensitivity and redness of the skin. They are not likely to be absorbed into the body through the skin but branched species are more likely to.  

INHALED

  Inhalation of aerosols (mists, fumes), generated by the material during the course of normal handling, may be harmful.  Inhalation of vapours may cause drowsiness and dizziness. This may be accompanied by narcosis, reduced alertness, loss of reflexes, lack of coordination and vertigo.  There is some evidence to suggest that the material can cause respiratory irritation in some persons. The body's response to such irritation can cause further lung damage.  Inhalation hazard is increased at higher temperatures.  Inhalation of high concentrations of gas/vapor causes lung irritation with coughing and nausea, central nervous depression with headache and dizziness, slowing of reflexes, fatigue and inco-ordination.  If exposure to highly concentrated solvent atmosphere is prolonged this may lead to narcosis, unconsciousness, even coma and possible death.  Lead fume is toxic and acts as a cumulative poison. Regular blood testing should be considered for workers who are regularly exposed.  Exposure to white spirit, in a controlled inhalation study using volunteers either at rest or during exercise, (1000 or 2500 mg/m3 for 30 minutes) produced a linear relationship between alveolar and arterial concentrations of the individual solvent components. Pulmonary absorption of the aliphatics ranged from 46-59%, whilst that of aromatic ranged from 58-70%. Although systemic absorption was greater during exercise, the proportion of circulating aliphatic to aromatic components decreased with increased activity. Exposure to 2500 - 5000 mg/m3 produces nausea and vertigo.  

CHRONIC HEALTH EFFECTS

  Harmful: danger of serious damage to health by prolonged exposure through inhalation.  Harmful: danger of serious damage to health by prolonged exposure through inhalation.  This material can cause serious damage if one is exposed to it for long periods. It can be assumed that it contains a substance which can produce severe defects. This has been demonstrated via both short- and long-term experimentation.  Ample evidence exists that developmental disorders are directlycaused by human exposure to the material.  Ample evidence from experiments exists that there is a suspicionthis material directly reduces fertility.  In dogs and rabbits that received naphthenic acids (10 mg/kg, intravenously, and 5-15 mg/kg, intramuscularly, respectively), a notable effect was observed on haemopoiesis of both the red and white cells and a greater effect was observed on platelet formation.  In a one generation reproduction study naphthenic acid in a carrier oil was administered dermally to 12 proven male New Zealand White rabbits at 2 ml/animal for 6 hrs, 5 days each week over 10, weeks and observed for an additional 12 week post-exposure period. There were no significant differences between treated and control animals in the following: survival, body weights, testes weights, numbers of animals achieving 1 or 2 viable litters or pregnancies, numbers of implantations, pre- or post-implantation losses,  numbers of viable fetuses. There were no signs of toxicity either systemically or at the site of application and no macroscopic or microscopic pathological findings.  Lead can accumulate in the skeleton for a very long time.  Chronic solvent inhalation exposures may result in nervous system impairment and liver and blood changes. [PATTYS].  Repeated application to the skin of mice over 30 weeks is reported to have produced tumors. (Source: Genium)