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SECTION 1. CHEMICAL IDENTIFICATION

CHEMINFO Record Number: 698
CCOHS Chemical Name: Benzo(a)pyrene

Synonyms:
3,4-Benz(a)pyrene
3,4-Benzopyrene
3,4-Benzpyrene
6,7-Benzopyrene
Benzo(d,e,f)chrysene
B(a)P
BP
Benzopyrene (non-specific name)

Chemical Name French: Benzo(a)pyrène
CAS Registry Number: 50-32-8
RTECS Number(s): DJ3675000
EU EINECS/ELINCS Number: 200-028-5
Chemical Family: Aromatic hydrocarbon / polycyclic aromatic hydrocarbon / PAH
Molecular Formula: C20-H12

SECTION 2. DESCRIPTION

Appearance and Odour:
Pale yellow crystals; yellow-green fluorescence in ultraviolet light (1,3,10); faint aromatic odour reported, but this may be due to contaminants.(17)

Odour Threshold:
Probably odourless (non-volatile)

Warning Properties:
POOR - Inadequate warning of exposure to carcinogenic PAHs

Composition/Purity:
Benzo(a)pyrene (B(a)P) is not produced commercially and does not occur as a pure substance, except as a research chemical (99% purity).(1) More commonly, B(a)P occurs naturally as a major component of complex mixtures of polycyclic aromatic hydrocarbons (PAHs), which are formed when organic substances such as oil, wood, coal, coal tar creosote, petroleum or petroleum products are burned, heated or pressurized. There are hundreds of different PAHs and they are almost always mixed with many other different products of combustion. This CHEMINFO record reviews the specific information which is available for pure B(a)P and is intended to be used to understand the potential hazards and control measures of the research chemical. The available information for B(a)P has been supplemented by general information for PAHs, with caution. This is because there is a wide variation in the toxicity of different PAHs. For example, some PAHs are potent carcinogens, while others are practically non- toxic. PAHs do, however, share certain physical properties, such as stability, low solubility in water and low vapour pressure.

Uses and Occurrences:
There is no commercial production or known use of this compound except as a research chemical. B(a)P and other PAHs are widely used in cancer research laboratories.
Benzo(a)pyrene is widely distributed in the environment as a by-product of the incomplete combustion and thermal decomposition (pyrolysis) of fossil fuels and organic matter. It is present in tobacco smoke, automobile and diesel exhaust, barbecue smoke, urban air, coal tar, crude oils, used lubricating oils, various edible oils and fats, fruits, vegetables and cereals and natural water, lake sediments and sewage sludge.(1,2)


SECTION 3. HAZARDS IDENTIFICATION

EMERGENCY OVERVIEW:
Pale yellow crystals, greenish-yellow fluorescence in ultraviolet light. Probably odourless. SUSPECT CANCER HAZARD - may cause cancer. SUSPECT REPRODUCTIVE HAZARD - may cause embryotoxic and teratogenic effects and may reduce fertility. MUTAGEN - may cause genetic damage. May cause photosensitization, an extreme sensitivity to sunlight.



POTENTIAL HEALTH EFFECTS

Effects of Short-Term (Acute) Exposure

Inhalation:
Pure benzo(a)pyrene (B(a)P) is a dust with an extremely low tendency to form a vapour. Health effects following short-term inhalation exposures have not been described in the literature.
The International Agency for Research on Cancer (IARC) has concluded that B(a)P is probably carcinogenic to humans (Group 2A). The development of cancer has been observed in animals even after relatively short-term exposures.(3)

Skin Contact:
Mild irritation has been reported for B(a)P in an animal test. There is no specific human information available.
Contact sensitization (an allergic skin reaction) has been reported in animals following short-term exposure to benzo(a)pyrene. Contact photosensitization (a condition in which the skin becomes extremely sensitive to sunlight or burns easily) has been reported in animals following contact with anthracene, a related PAH.(3,4)

Eye Contact:
Specific information is not available for B(a)P. Based on mild skin irritation observed in an animal test, eye irritation may also occur.

Ingestion:
An animal study has shown low short-term oral toxicity for B(a)P. There is no human information available. Ingestion is not a typical route of occupational exposure.

Effects of Long-Term (Chronic) Exposure

There is no relevant human information available for B(a)P. Based on animal studies, cancer appears to be the key health effect following long-term exposure to B(a)P. Other long-term exposure studies of animals to PAH mixtures have been reported to cause minor effects on the liver, kidneys, lungs, blood, and/or lymph system.(4,15)
Studies of workers in a rubber processing factory have associated B(a)P with impaired lung function.(26,27) No conclusions can be drawn from these studies due to worker exposure to other potentially hazardous materials at the same time.
Human population studies have associated PAH exposure with cardiovascular disease. These studies are limited due to the complexity of the exposures and other factors.(39,40) No specific conclusions can be drawn for B(a)P, as it is not possible to evaluate the contribution of any one PAH to the overall effects of these mixtures.

SKIN CONTACT: A 1% solution of B(a)P in benzene was applied daily to small areas of the skin of 26 patients with various pre-existing skin disorders. Within 4 months, the following redness, pigmentation, scaling and benign skin tumours developed. The changes reversed completely within 2 to 3 months after the treatment was stopped.(16) Unfortunately, no control group for the solvent, benzene, was used in the study. Therefore, it is not known if the exposure to B(a)P, benzene or both materials at the same time caused the observed effects. Similar cases of skin changes in men accidentally exposed to B(a)P have also been reported.(3) Occupational exposure to products containing PAHs has resulted in dermatitis (red, thick, cracked and itchy skin).(4)
Photoallergy (increased sensitivity to sunlight) has been attributed to occupational exposure to complex mixtures of PAHs present in coal tars and coal tar pitch volatiles.(3) Contact sensitization has been reported in two animal studies following exposure to B(a)P, but there are insufficient details to draw conclusions.

Carcinogenicity:

B(a)P is a moderately potent carcinogen in many animal species by inhalation, dermal and oral exposure. However, little specific information is available on the carcinogenicity of B(a)P to humans.
Skin cancer developed in a man exposed to B(a)P for three weeks while carrying out animal experiments.(10) In addition, exposure to occupational and environmental contaminants containing B(a)P (for example, tobacco smoke, coal tar pitch, coke oven emissions, chimney soot, or products containing PAHs, such as shale oil) has been associated with increased incidence of lung, skin and scrotal cancer in humans.(1,3,4,10) These cancers are related to exposure to complex mixtures of PAHs, and it is not possible to evaluate the contribution of any particular PAH to the carcinogenicity observed. Nevertheless, when these studies are considered in light of the animal information available, it can be concluded that B(a)P is probably carcinogenic in humans.

The International Agency for Research on Cancer (IARC) has concluded that this chemical is probably carcinogenic to humans (Group 2A).

The American Conference of Governmental Industrial Hygienists (ACGIH) has designated this chemical as a suspected human carcinogen (A2).

The US National Toxicology Program (NTP) has listed this chemical as reasonably anticipated to be a human carcinogen.

Teratogenicity and Embryotoxicity:
There is no human information available. B(a)P is embryotoxic and teratogenic in mice and rats.(1,3,12,13)

Reproductive Toxicity:
There is no human information available. Studies in mice have shown that B(a)P reduces fertility in a dose-dependent fashion.(13,14)

Mutagenicity:
B(a)P has produced mutations in cultured human cells (point and forward mutations, micronuclei and sister chromatid exchanges).(31,32,33) Recent studies have attempted to correlate PAH exposure with mutagenic effects (DNA adducts in placentas or in white blood cells) as a biological indicator of human exposure.(3) B(a)P has produced positive results in numerous short-term in-vitro assays using bacteria, fruit flies and cultured mammalian cells and in in-vivo tests in mammals.(1,3,8)

Toxicologically Synergistic Materials:
Numerous studies with carcinogenic PAHs such as B(a)P show that the incidence of tumours can be increased or decreased by factors such as diet, exposure to other PAHs, and treatment with chemicals which affect the metabolism of PAHs. The interactions are extremely complex.(3,15)

Potential for Accumulation:
B(a)P is readily absorbed by inhalation, oral and dermal routes of exposure in rats. B(a)P is absorbed through the skin in humans. There are no direct studies regarding the absorption of PAHs in humans following inhalation exposure. B(a)P derived from industrial pollution is often inhaled attached to larger dust particles, and it may take longer to absorb B(a)P from these; the rate of uptake depends on particle size and composition.(8) Indirect evidence suggests that B(a)P present in broiled meat may not be readily absorbed following ingestion in humans. In general, PAH absorption following the ingestion of contaminated food or drinking water depends on the compound's vehicle of administration. PAH absorption is enhanced when they are solubilized in a vehicle that is readily absorbed, such as certain oils, e.g. corn oil. Absorbed B(a)P is distributed rapidly and widely in the body, then metabolized and eliminated. The chief site of metabolism is the liver and bile system (hepatobiliary).(3,8,10) B(a)P requires metabolic activation to exert its mutagenic and carcinogenic effects. The main route of elimination for B(a)P and its metabolites is the feces, with smaller amounts excreted in the urine.(1,3,10,15)


SECTION 4. FIRST AID MEASURES

Inhalation:
This material is a suspect carcinogen and reproductive hazard. Take proper precautions to protect your own health before attempting rescue (e.g., wear appropriate protective equipment). Remove source of contamination or move victim to fresh air. Obtain medical attention immediately.

Skin Contact:
Avoid direct contact. Wear chemical protective gloves, if necessary. Quickly and gently blot or brush away excess chemical. Wash gently and thoroughly with water and non-abrasive soap for 5 minutes or until chemical is removed. Under running water, remove contaminated clothing, shoes and leather goods (e.g. watchbands, belts). If irritation persists, repeat flushing. Obtain medical attention immediately. Discard contaminated clothing, shoes and leather goods. DO NOT launder or re- use.

Eye Contact:
Avoid direct contact. Wear chemical protective gloves, if necessary. Quickly and gently blot or brush away excess chemical. Immediately flush the contaminated eye(s) with lukewarm, gently flowing water for 5 minutes, or until the chemical is removed, while holding the eyelid(s) open. If dust or solid particle(s) go(es) into eye(s), do not allow victim to rub eye(s). Let the eye(s) water naturally for a few minutes. Have victim look right and left, and then up and down. If particle/dust does not dislodge, flush with lukewarm, gently flowing water for 5 minutes or until particle/dust is removed, while holding eyelid(s) open. DO NOT attempt manually to remove anything stuck to the eye. If irritation persists, obtain medical attention immediately.

Ingestion:
NEVER give anything by mouth if victim is rapidly losing consciousness, is unconscious or is convulsing. Have victim rinse mouth thoroughly with water. DO NOT INDUCE VOMITING. Have victim drink 240 to 300 mL (8 to 10 oz.) of water to dilute material in stomach. If vomiting occurs naturally, rinse mouth and repeat administration of water. Obtain medical attention immediately.

First Aid Comments:
Provide general supportive measures (comfort, warmth, rest). Consult a doctor and/or the nearest Poison Control Centre for all exposures except minor instances of inhalation or skin contact. All first aid procedures should be periodically reviewed by a doctor familiar with the material and its conditions of use in the workplace.



SECTION 5. FIRE FIGHTING MEASURES

Flash Point:
Not available.

Lower Flammable (Explosive) Limit (LFL/LEL):
Not available

Upper Flammable (Explosive) Limit (UFL/UEL):
Not available

Autoignition (Ignition) Temperature:
Not available

Sensitivity to Mechanical Impact:
Probably not sensitive. Normally stable material.

Sensitivity to Static Charge:
Will not accumulate static charge. Under certain conditions, airborne B(a)P dust can probably explode when ignited by an electrostatic spark or other ignition source.

Combustion and Thermal Decomposition Products:
Carbon dioxide, carbon monoxide

Fire Hazard Summary:
Fires involving PAHs may produce toxic, irritating fumes and gases. Small amounts of B(a)P may be produced in fires involving other organic materials, by incomplete combustion. Under certain conditions, a cloud of PAH dust can probably explode when ignited by a spark or flame. Explosions of PAH dusts have occurred in industry.(20) B(a)P dust is unlikely to be an explosion hazard because it is used only in very small amounts. The fire hazard of solid B(a)P is probably low when exposed to heat or flame. It probably must be preheated before ignition can occur.

Extinguishing Media:
SMALL FIRES - Water spray, dry chemical powder, carbon dioxide, alcohol foam or polymer foam. LARGE FIRES - Water spray, fog, foam. (DOT recommendations for naphthalene).

Fire Fighting Instructions:
Evacuate area and fight fire from a safe distance or a protected location. Approach fire from upwind to avoid B(a)P.
If possible, isolate materials not involved in the fire, if this can be done without risk, and protect personnel. Avoid generating dust to minimize risk of explosion. Water or foam may cause frothing. The frothing may be violent and could endanger personnel close to the fire. However, a water spray or fog that is carefully applied to the surface of the material, preferably with a fine spray or fog nozzle, will cause frothing that will blanket and extinguish the fire. In addition, water can be used in the form of spray or fog to prevent dust formation, keep fire-exposed containers cool and absorb heat to help prevent rupture. Water spray may also be used to knock down irritating/toxic combustion products which may be produced in a fire. Apply water from as far a distance as possible.
B(a)P is a suspected human carcinogen and reproductive toxin. Do not enter without wearing specialized protective equipment for the situation. Firefighter's normal protective equipment (Bunker gear) will not provide adequate protection. A full-body encapsulating chemical resistant suit with positive pressure self-contained breathing apparatus (MSHA/NIOSH approved or equivalent) may be necessary.



NATIONAL FIRE PROTECTION ASSOCIATION (NFPA) HAZARD IDENTIFICATION

NFPA - Comments:
NFPA has no listing for this chemical in Codes 49 or 325.


SECTION 9. PHYSICAL AND CHEMICAL PROPERTIES

Molecular Weight: 252.32

Conversion Factor:
Not applicable

Physical State: Solid
Melting Point: 179-179.3 deg C (354-355 deg F) (3,15,17)
Boiling Point: 310-312 deg C (590-594 deg F) at 10 mm Hg; 495 deg C (923 deg F) at 760 mm Hg (1,3)
Relative Density (Specific Gravity): 1.351 (water = 1) (3,17)
Solubility in Water: Practically insoluble (3.8 x 10(-6) g/L) (1,3,10)
Solubility in Other Liquids: Soluble in benzene, toluene, xylene, cyclohexane, acetone, ether, dimethyl sulfoxide, dimethylformamide; sparingly soluble in ethanol, methanol.(1,3,18)
Coefficient of Oil/Water Distribution (Partition Coefficient): Log P(oct) = 6.06 (3,17)
pH Value: Not applicable
Vapour Density: Not applicable
Vapour Pressure: Practically zero (5.6 x 10(-9) mm Hg at 25 deg C) (3)
Saturation Vapour Concentration: Not applicable
Evaporation Rate: Not applicable
Critical Temperature: Not available

SECTION 10. STABILITY AND REACTIVITY

Stability:
Normally stable. B(a)P decomposes in light and air. Solutions of B(a)P in organic solvents darken and slowly oxidize in the presence of air and light.(10,17)

Hazardous Polymerization:
Probably cannot occur

Incompatibility - Materials to Avoid:

NOTE: Chemical reactions that could result in a hazardous situation (e.g. generation of flammable or toxic chemicals, fire or detonation) are listed here. Many of these reactions can be done safely if specific control measures (e.g. cooling of the reaction) are in place. Although not intended to be complete, an overview of important reactions involving common chemicals is provided to assist in the development of safe work practices.


OXIDIZING AGENTS - May react violently or produce toxic/irritating fumes.(17).
STRONG ACIDS (e.g. sulfuric acid and nitric acids) - Decompose PAHs.

Hazardous Decomposition Products:
Not available

Conditions to Avoid:
Static charge, sparks, light and air.

Corrosivity to Metals:
Probably not corrosive

Stability and Reactivity Comments:
PAHs are relatively unreactive, but can be attacked readily by reactive chemicals such as nitric acid, sulfuric acid and chlorine. See reference 18 for some of the chemical reactions and biological degradation techniques of PAHs.


SECTION 11. TOXICOLOGICAL INFORMATION

Standard animal toxicity values (e.g. LD50s) are not available.
However, benzo(a)pyrene (B(a)P) has shown low oral and dermal toxicity in experimental animals following short-term exposure.(4)

Skin Irritation:

Application of 14 ug (0.014 mg) caused mild irritation to mice in a standard Draize test.(5,6)

Effects of Short-Term (Acute) Exposure:

Skin Contact:
Application of 0.05 mL of a 1% B(a)P solution in acetone to the skin of hairless mice caused changes in surface skin cell growth. In a number of studies, dermal application of 0.02 mL of B(a)P twice daily to the shaved backs of Swiss mice for about 4 days, suppressed and even destroyed sebaceous glands in mouse skin. These studies were limited due to the fact that control groups were not used.(3) B(a)P caused thickening of the skin of mice (hyperplasia), which may be related to the initiating or tumour promoting actions of B(a)P.(7)

Ingestion:
Small amounts of B(a)P in the diets of mice and rats caused no visible symptoms of short-term toxicity. A diet containing 0.1% (1000 ppm) B(a)P caused some slowing of growth.(8)

Effects of Long-Term (Chronic) Exposure:

Inhalation:
Rats were exposed nose-only to less than 1 ppm B(a)P for 2 hours/day for 4 weeks. There were no treatment related effects in the kidneys, lungs or nasal cavities observed.(28)

Skin Contact:
Repeated dermal application of B(a)P to mice for 29 weeks produced a pronounced inflammatory response, excess cell growth and thickening of the skin. This reaction was considered to be tumour promoting activity.(3,41)

Ingestion:
B(a)P (120 mg/kg/day) was administered in the diet to different strains of mice (which differed at a particular gene site) for up to 6 months. Strains that could not metabolize B(a)P showed considerable weight loss, depression of the bone marrow (aplastic anemia and pancytopenia) and death within 4 weeks, while other strains showed no effects. Death appeared to be caused by bone marrow depression which led to bleeding and infection.(3,9)

Skin Sensitization:
Dermal application of B(a)P has produced contact sensitization in mice and guinea pigs.(35,42) There are insufficient details available in these studies to conclude that B(a)P is a skin sensitizer (for example, the number of animals with positive reactions is not provided).

Carcinogenicity:
In numerous studies, B(a)P has been shown to cause cancer in mice, rats, hamsters, guinea pigs, rabbits and monkeys, by all relevant routes of exposure (inhalation, skin, oral) and by injection and transplacental exposure. Cancer occurred both locally and at sites other than the point of administration at doses as low as 9.5 mg/m3 (inhalation), 1.7 ug (0.0017 mg)/day (skin), and 5.2 mg/kg/day (oral).(1,3,10) The skin and lungs appear to be the main target organs, while liver and kidney tumours are seldom caused by B(a)P.(3,8) B(a)P is a moderately potent skin carcinogen and it is often used as a positive control in the bioassay of other agents. It has produced skin tumours in rats, rabbits and guinea pigs, but mice appear to be the most sensitive species.(3) B(a)P was consistently found to produce more skin tumours in mice in a shorter period of time than any other PAH, with the possible exception of dibenzo(a,h)anthracene.(10) B(a)P is considered a "complete carcinogen", in that it is both an initiator and promoter of cancer.(3,8) B(a)P is one of the few materials which is known to be carcinogenic in single- dose experiments and following prenatal exposure.(10) The carcinogenic potential of B(a)P is enhanced by co-administration of particulate matter or some gases.(1,3) The International Agency for Research on Cancer (IARC) has determined that there is sufficient evidence for the carcinogenicity of B(a)P in experimental animals.(1,11)

Teratogenicity, Embryotoxicity and/or Fetotoxicity:
Placental transfer of B(a)P has been shown in rats and mice following oral administration.(1,3) The results of two oral studies in mice and one in rats indicate that B(a)P is embryotoxic and teratogenic, in the absence of maternal toxicity. The severity of the observed effects is dependent on the strain of mice (genetically linked), since some strains metabolize B(a)P differently.(12) Oral administration of 10 mg/kg B(a)P to mice during days 7 to 16 of pregnancy, resulted in reduction of the mean pup weight and in dramatic alterations of gonadal development. There was also a significant decrease in testicular weight. Most of the female offspring had no ovaries or just remnants of ovarian tissue.(13) In other studies, oral administration of B(a)P resulted in increased incidence of stillbirths, resorptions and malformations in selected strains of mice and rats.(3,12) Maternal toxicity was either not observed or doses administered were low enough that maternal toxicity would not have been expected. B(a)P is a transplacental carcinogen in mice and rabbits (i.e. causes tumours in offspring). Applications of B(a)P to the skin of pregnant mice over four generations, resulted in increased sensitization of the offspring to the effects of B(a)P.(1) B(a)P exposure of pregnant mice produced alterations in fetal blood forming tissues, including severe degeneration of the thymus.(36)

Reproductive Toxicity:
B(a)P has produced adverse reproductive effects in rodents following oral administration.(3,38) B(a)P reduced fertility in mice in a dose-dependent fashion (progressively lower number of pups were produced and the interval between births was increased). Other effects included decreased frequency of ovulation and decreased reproductive life-span.(14) In a modified two-generation oral study in mice, doses of 10, 40 or 160 mg/kg/day were administered during days 7-16 of pregnancy. A reduction in fertility and reproductive capacity occurred in both male and female offspring at 10 mg/kg/day, while 40 mg/kg/day caused almost complete sterility in the offspring of both sexes.(13)

Mutagenicity:
B(a)P has been used extensively as a positive control in a variety of short-term mutation tests. It was active in assays for DNA repair and mutation in bacterial cells; mutation in fruit flies; DNA binding, DNA repair, sister chromatid exchange (SCE), chromosomal aberrations, point mutation and transformation in mammalian cells in culture; and in in-vivo tests in mammals, including DNA binding, sister chromatid exchange, chromosomal aberrations, sperm abnormality and the somatic specific locus (spot) test.(1,3,8) Rats exposed to B(a)P during pregnancy or just after birth showed a higher frequency of sister chromatid exchanges (SCE) than controls when re- exposed as adults.(30) The International Agency for Research on Cancer (IARC) has determined that there is sufficient evidence that B(a)P is active in short-term tests.(1)

IMMUNOTOXICITY: There are reports that B(a)P suppressed the immune system following intraperitoneal and subcutaneous injection of mice. These routes of exposure are not considered relevant to occupational exposures. There is no information available concerning the immunotoxicity of B(a)P following inhalation, dermal or oral exposure.(3)


SECTION 16. OTHER INFORMATION

Selected Bibliography:
(1) IARC Monographs on the evaluation of the carcinogenic risk of chemicals to humans : polynuclear aromatic compounds, Part 1, chemical, environmental and experimental data. Vol. 32. IARC, 1983. P. 33-91, 211-217
(2) Lunn, G., et al. Destruction of hazardous chemicals in the laboratory. John Wiley & Sons, 1990
(3) Toxicological profile for polycyclic aromatic hydrocarbons (PAH's). U.S. Department of Health and Human Services, August, 1995.
(4) Cavender, F. Aromatic hydrocarbons. In: Patty's Industrial Hygiene and Toxicology. 4th ed. Vol. 2B. John Wiley & Sons, 1994. p. 1380-1381, 1390- 1391
(5) Brune, K., et al. Inflammatory, tumor initiating and promoting activities of polycyclic aromatic hydrocarbons and diterpene esters in mouse skin as compared with their prostaglandin releasing potency in vitro. Cancer Letters. Vol. 4 (1978). p. 333-342
(6) RTECS record for benzo(a)pyrene. Date of last update 9610.
(7) Bresnick, E., et al. Epidermal hyperplasia after topical application of benzo(a)pyrene, benzo(a)pyrene diol epoxides, and other metabolites. Cancer Research. Vol. 37 (April 1977). p. 984-990
(8) Osborne, M.R., et al. Benzopyrenes. Cambridge University Press, 1987
(9) Robinson, J.R., et al. Relationship between "aromatic hydrocarbon responsiveness" and the survival times in mice treated with various drugs and environmental compounds. Molecular Pharmacology. Vol. 11, no. 6 (1975). p. 850-865
(10) IARC Monographs on the evaluation of the carcinogenic risk of chemicals to man: certain polycyclic aromatic hydrocarbons and heterocyclic compounds. Vol. 3. IARC, 1972. p. 91-116
(11) IARC Monographs on the evaluation of carcinogenic risks to humans. Supplement 7. IARC, 1987. p. 58
(12) Legraverend, C., et al. Importance of the route of administration for genetic differences in benzo(a)pyrene-induced in utero toxicity and teratogenicity. Teratology. Vol. 29 (1984). p. 35-47
(13) Mackenzie, K.M., et al. Infertility in mice exposed in utero to benzo(a)pyrene. Biology of Reproduction. Vol. 24 (1981). p. 183-191
(14) Mattison, D.R., et al. The effect of smoking on reproductive ability and reproductive life-span. In: Smoking and reproductive health, edited by M.J. Rosenberg. PSG Publishing Company, Inc., 1987. p. 47-54
(15) Health impacts of polynuclear aromatic hydrocarbons. Noyes Data Corporation, 1981
(16) Cottini, G.B., et al. The effects of 3:4-benzpyrene on human skin. American Journal of Cancer. Vol. 37 (1939). p. 186-195
(17) HSDB record for benzo(a)pyrene. Last revision date 96/06/19.
(18) Laboratory decontamination and destruction of carcinogens in laboratory wastes : some polycyclic aromatic hydrocarbons. (IARC Scientific Publications No. 49). IARC, 1983
(19) Armour, M.A. Hazardous laboratory chemicals disposal guide. CRC Press, 1991. p. 52-53
(20) Field, P. Explosibility assessment of industrial powders and dusts. Her Majesty's Stationery Office, 1983
(21) Fire protection guide to hazardous materials. 10th ed. National Fire Protection Association, 1991
(22) NIOSH pocket guide to chemical hazards. NIOSH, June 1994. p. 74-75
(23) Report on Carcinogens. 11th ed. US Department of Health and Human Services, Public Health Service, National Toxicology Program
(24) Forsberg, K., et al. Quick selection guide to chemical protective clothing. 3rd edition. Van Nostrand Reinhold, 1997
(25) European Communities (EC). Commission Directive 2004/73/EC. Apr. 29, 2004
(26) Gupta, P., et al. Prevalence of impaired lung function in rubber manufacturing factory workers exposed to benzo(a)pyrene and respirable particulate matter. Indoor Environment. Vol. 2, No. 1. (1993). p. 26-31
(27) Gupta, P., et al. Effect of pollutants on airway resistance in rubber factory workers. Indoor Environment. Vol. 2, No. 2 (1993). p. 105-110
(28) Wolff, R., et al. Effects of repeated inhalation exposures to 1- nitropyrene, benzo(a)pyrene, Ga2O3 particles, and SO2 alone and in combinations on particle clearance, bronchoalveolar lavage fluid composition, and histopathology. Journal of Toxicology and Environmental Health. Vol. 27 (1989). p. 123-138
(29) Higginbotham, S., et al. Tumor-initiating activity and carcinogenicity of dibenzo(a,l)pyrene versus 7,12-dimethylbenz(a)anthracene and benzo(a)pyrene at low doses in mouse skin. Carcinogenesis. Vol. 14, No. 5 (1993). p. 875- 878
(30) Igaz, P., et al. Long-lasting persistence of elevated sister-chromatid exchange frequencies induced by perinatal benzo(a)pyrene treatment in rat bone- marrow cell. Experientia. Vol. 51, No. 6 (1995). p. 612-615
(31) Lafleur, A., et al. Bacterial and human cell mutagenicity study of some C18H10 cyclopenta-fused polycyclic aromatic hydrocarbons associated with fossil fuels combustion. Environmental Health Perspectives. Vol. 101, No. 2 (1993). p. 146-153
(32) Warshawsky, D., et al. Induction of micronuclei and sister chromatid exchanges by polycyclic and N-heterocyclic aromatic hydrocarbons in cultured human lymphocytes. Environmental and molecular mutagenesis. Vol. 26 (1995). p. 109-118
(33) Busby, W., et al. Mutagenicity of benzo(a)pyrene and dibenzopyrenes in the Salmonella Typhimurium TM677 and the MCL-5 human cell forward mutation assays. Mutation Research. Vol. 342 (1995). p. 9-16
(34) Cavalieri, E., et al. Comparative dose-response tumorigenicity studies of dibenzo(a,l)pyrene versus 7,12-dimethylbenz(a)anthracene, benzo(a)pyrene and two dibenzo(a,l)pyrene dihydrodiols in mouse skin and rat mammary gland. Carcinogenesis. Vol. 12, No. 10 (1991). p. 1939-1944
(35) Klemme, J.C., et al. Induction of contact hypersensitivity to dimethylbenz(a)anthracene and benzo(a)pyrene in C3H/HeN mice. Cancer Research. Vol. 47, no. 22 (Nov. 5, 1987). p. 6074-6078
(36) Holladay, S., et al. Fetal hematopoietic alterations after maternal exposure to benzo(a)pyrene: A cytometric evaluation. Journal of Toxicology and Environmental Health. Vol. 42 (1994). p. 259-273
(37) LaVoie, E., et al. Exceptional tumor-initiating activity of 4- fluorobenzo(j)fluoranthene on mouse skin: comparison with benzo(j)fluoranthene, 10-fluoro-benzo(j)fluoranthene, benzo(a)pyrene, dibenzo(a,l)pyrene and 7,12-dimethylbenz(a)anthracene. Cancer Letter. Vol. 70 (1993). p. 7-14
(38) Kristensen, P., et al. Fertility in mice after prenatal exposure to benzo(a)pyrene and inorganic lead. Environmental Health Perspectives. Vol. 103, No. 6 (1995). p. 588-590
(39) Clavel, J., et al. Occupational exposure to polycyclic aromatic hydrocarbons and the risk of bladder cancer: A French case-control study. International Journal of Epidemiology. Vol. 23, No. 6 (1994). p. 1145-1153
(40) Strom, J., et al. Polycyclic aromatic hydrocarbons and cardiovascular disease - A review of the epidemiologic and toxicologic evidence for an etiologic relationship. Journal of Occupational Medicine and Toxicology. Vol. 2, No. 4 (1993). p. 311-334
(41) Albert, R., et al. Benzo(a)pyrene-induced skin damage and tumor promotion in the mouse. Carcinogenesis. Vol. 12, no. 7 (1991). p. 1273-1280
(42) Old, L.J., et al. Contact reactivity to carcinogenic polycyclic hydrocarbons. Nature. Vol. 198, no. 4886 (June 22, 1963). p. 1215-1216
(43) (Forsberg) Forsberg, K., et al. Quick selection guide to chemical protective clothing. 4th ed. Van Nostrand Reinhold, 2002

Information on chemicals reviewed in the CHEMINFO database is drawn from a number of publicly available sources. A list of general references used to compile CHEMINFO records is available in the database Help.


Review/Preparation Date: 1997-06-25

Revision Indicators:
TLV comments 1998-08-01
EU Safety 1999-12-01
Carcinogenicity 2002-12-18
PEL transitional comments 2003-12-19
PEL-TWA final 2003-12-19
TLV comments 2004-01-04
Resistance of materials for PPE 2004-04-13
EU classification 2004-11-29
EU risks 2004-11-29
EU comments 2004-11-29
Bibliography 2005-02-02



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