Section 1 - CHEMICAL PRODUCT AND COMPANY IDENTIFICATION

PRODUCT NAME

WHITMIRE 565 PLUS XLO PRESSURIZED CONTACT INSECTICIDE

NFPA

PRODUCT USE

Application is by spray atomization from a hand held aerosol pack. Contact insecticide.

Section 2 - HAZARDS IDENTIFICATION

CANADIAN WHMIS SYMBOLS

EMERGENCY OVERVIEW

RISK

Extremely flammable.
Harmful to aquatic organisms, may cause long- term adverse effects in the
aquatic environment.
Risk of explosion if heated under confinement.

POTENTIAL HEALTH EFFECTS

ACUTE HEALTH EFFECTS

SWALLOWED

  Accidental ingestion of the material may be damaging to the health of the individual.  Not normally a hazard due to physical form of product.  Considered an unlikely route of entry in commercial/industrial environments.  

EYE

  There is some evidence to suggest that this material can causeeye irritation and damage in some persons.  Not considered to be a risk because of the extreme volatility of the gas.  

SKIN

  There is some evidence to suggest that this material can cause inflammation of the skin on contact in some persons.  Spray mist may produce discomfort.  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

  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.  WARNING: Intentional misuse by concentrating/inhaling contents may be lethal.  Spray mist may produce discomfort.  

CHRONIC HEALTH EFFECTS

  There is limited evidence that, skin contact with 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.  There is some evidence that human exposure to the material may result in developmental toxicity. This evidence is based on animal studies where effects have been observed in the absence of marked maternal toxicity, or at around the same dose levels as other toxic effects but which are not secondary non-specific consequences of the other toxic effects.  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.