Section 1 - CHEMICAL PRODUCT AND COMPANY IDENTIFICATION

PRODUCT NAME

WHITMIRE ULD BP-50

NFPA

PRODUCT USE

Contact insecticide.

Section 2 - HAZARDS IDENTIFICATION

CANADIAN WHMIS SYMBOLS

EMERGENCY OVERVIEW

RISK

HARMFUL - May cause lung damage if swallowed.
Repeated exposure may cause skin dryness and cracking.
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 damaging to the health of the individual.  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.  Considered an unlikely route of entry in commercial/industrial environments. The liquid may produce gastrointestinal discomfort and may be harmful if swallowed. Ingestion may result in nausea, pain and vomiting. Vomit entering the lungs by aspiration may cause potentially lethal chemical pneumonitis.  

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

  Repeated exposure may cause skin cracking, flaking or drying following normal handling and use.  Skin contact with the material may damage the health of the individual; systemic effects may result following absorption.  The material may accentuate any pre-existing dermatitis condition.  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.  

INHALED

  Inhalation may produce health damage*.  Inhalation of vapours may cause drowsiness and dizziness. This may be accompanied by narcosis, reduced alertness, loss of reflexes, lack of coordination and vertigo.  Inhalation of aerosols (mists, fumes), generated by the material during the course of normal handling, may be damaging to the health of the individual.  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 oil droplets/ aerosols may cause discomfort and may produce chemical pneumonitis.  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.  

CHRONIC HEALTH EFFECTS

  There has been some concern that this material can cause cancer or mutations but there is not enough data to make an assessment.  Limited evidence suggests that repeated or long-term occupational exposure may produce cumulative health effects involving organs or biochemical systems.  There is some evidence that inhaling this product is more likely to cause a sensitization reaction in some persons compared to the general population.  There is some evidence to provide a presumption that human exposure to the material may result in impaired fertility on the basis of: some evidence in animal studies of impaired fertility in the absence of toxic effects, or evidence of impaired fertility occurring at around the same dose levels as other toxic effects but which is not a secondary non-  specific consequence of other toxic effects.  Based on experience with animal studies, there is a possibility that exposure to the material may result in toxic effects to the development of the fetus, at levels which do not cause significant toxic effects to the mother.  Chronic poisoning by natural pyrethrins may result in convulsion, tetanic paralysis, rapid and uneven heart beat, liver and kidney damage, or death.  The natural pyrethrins may produce hypersensitivity, especially following previous sensitising exposure. In general, repeated exposures over 2 or 3 years are required to elicit a response and involve exposure to pyrethrum rather than its individual components (including pyrethrins). The sesquiterpene lactone (pyrethrosin) and the pyrethrum glycoproteins account for the immediate and delayed hypersensitivity seen in guinea pigs following a single injection of ground chrysanthemum in Freud's adjuvant. Mild erythematic vesicular dermatitis (with papules), pruritus, localized oedema (particularly of the face, lips and eyelids), rhinitis, tachycardia, pallor and sweating are the most common syndromes. An initial skin sensitisation can progress to marked dermal oedema and skin cracking. Pyrethrum dermatitis appears to increase in hot weather or under conditions were heavy perspiration is produced. The active ingredients of pyrethrum (except pyrethrin II) are inactive in patch tests. Those patients allergic to ragweed pollen are particularly sensitive to pyrethrin.  Rats fed on a diet of pyrethrins for 5000 ppm for 2 years showed some signs of tissue damage including liver lesions, bile duct proliferation and focal necrosis of the liver cells. A no-effect level of 1000 ppm found in animal experiments correspond to a daily dose of 3600 mg/man.  The primary effect of long-term exposure to methylenedioxyphenol insect synergists such as the piperonyls (such as piperonyl butoxide - PBO) in animals is an increase in liver and thyroid weight, liver and kidney damage, and a decrease in body weight. These symptoms were observed in a diet of 52.8 mg/kg or more a day in a chronic study with dogs.PBO is a possible human carcinogen. Currently there is no data from accidental exposure available regarding its carcinogenicity in humans; the only information is from animal studies. Several studies have shown that PBO treatment in rats causes an increase in liver cancer at high doses. The incidence of hepatocellular carcinoma, in male and female rats given 2.4% piperonyl butoxide was 80.0% and 57.7% respectively. Preneoplastic hepatic lesions such as nodular hyperplasia, cholangiofibrosis, and modular hyperplasia were also seen.Some studies have shown that PBO treatment in rats corresponds with a very slight increase in thyroid cancer.Rats fed diets containing from 0.6 to 2.4% piperonyl butoxide for approximately two years showed dose-related decreases in body weight. Roughened hair, lethargy, epistaxis, abdominal swelling, and decreased food consumption were observed at 2.4%. All dose rates induced skin tumours after about 1 year. Cumulative mortality varied from around 15 to 50%. Caecal haemorrhage was the cause of death. Dead rats with hepatic tumours were seen from week 74, but caecal haemorrhage or possible leukaemia was the cause of death. At necroscopy in rats surviving to the end of the study,  hepatocellular adenomas and carcinomas occurred in both sexes in a dose-related manner. A dose-related increase in thrombocythemia was seen in male rats. The authors * of this study concluded that the primary feature of chronic piperonyl-butoxide toxicity is hepatocarcinogenicity. It is generally accepted that PBO does not demonstrate any significant potential for mutagenicity (genetic damage) but debate still existsPBO weakens the immune system by inhibiting lymphocyte response. Lymphocytes are a class of white blood cells that consume potentially dangerous pathogens and release antibodies. Inhibiting lymphocyte response weakens the body's ability to defend against foreign invaders. Preventing the breakdown of toxic chemicals, may exacerbate potentially toxic effects.PBO has been shown to adversely affect a variety of reproductive functions. Two-generational laboratory studies on rats show that litter weight and size are less for mothers exposed to high concentrations of PBO, and there is an increase in birth defects and fetal death. In one study the difference in the average weight of PBO-exposed offspring immediately after birth is negligible, but 7-14 days post-natal is significantly greater for those mothers that are exposed to PBO than for those that are not. The U.S. EPA maintains that results for teratogenicity (the ability to produce birth defects) in animals have been mixed, and while some studies suggest some teratogenicity, most do not. PBO may also interfere with sexual development because the enzymes it inhibits are responsible not only for the breakdown of toxic chemicals but also for the metabolism of other compounds such as steroids, which include the sex hormones. Rats exposed to PBO over the course of two years experience an atrophy of the testes a decrease in weight of the seminal vesicles (sperm producing structures), and an increase in ovarian weights. There is no evidence that PBO affects fertility.Data has shown that PBO alone interferes with enzymes that maintain homeostasis of sodium and calcium in the brain and nervous system, possibly affecting neural response. Additionally, it increases the neurotoxicity of other compounds. Despite this data, EPA believes that these neurotoxic effects are slight and maintains that PBO poses no neurological risk.Behavioral changes have been noted with PBO as well. In a laboratory experiment, exposed rats experience more trouble navigating a maze than unexposed rats. The exposed rats travel longer distances and turned more frequently in the maze. PBO also induces changes in olfactory behavior of the offspring of exposed mothers. Offspring of exposed mothers are less likely to enter a compartment that smells like home than unexposed mothers. Exploratory behavior in mice increases as the dose of PBO they were treated with increased. This data shows that PBO has the ability to affect behaviors in mammals.Research on rats has found that PBO can cause intestinal ulcers and bleeding. Liver damage is common in studies,and kidney damage has been found as well. Long-term ingestion of PBO causes anemia, a decrease in the amount of hemoglobin (oxygen-transporting molecules) in blood, and increases the blood cholesterol level in rats. PBO can also damage the larynx, and there have been reports that it can cause labored breathing, an accumulation of fluid in the lungs, nasal bleeding, abdominal swelling, and loss of the ability to coordinate muscle movement. There has been a fair amount of investigation into the effects of dermal contact with PBO since it is used as a topical agent for lice, but there has been no evidence of it causing any local or systemic toxicity, and the amount of PBO absorbed from skin contact is characterized by some researchers as low.ChemicalWatch Fact SheetTakahashi, O.,S. et al: Fundamental and Applied Toxicology: Vol 22., pp 293-303, Feb 1994.