Course: WB 1519
CE Original Date: July 1, 2009
CE Renewal Date: July 1, 2011
CE Expiration Date: July 1, 2013
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Upon completion of this section, you will be able to
- describe typical signs and symptoms of patients with acute PAH exposure,
- describe typical signs and symptoms of patients with chronic PAH exposure,
- describe important elements of the exposure history,
- describe the focus of the physical examination, and
- describe tests used to assist in evaluation of patients exposed to PAHs.
Acute effects attributed to PAH exposure, such as headache, nausea, respiratory and dermal irritation, are probably caused by other agents.
Since PAHs have low acute toxicity, other more acutely toxic agents probably cause the acute symptoms attributed to PAHs. Hydrogen sulfide in roofing tars and sulfur dioxide in foundries are examples of concomitant, acutely toxic contaminants. Naphthalene, the most abundant constituent of coal tar, is a skin irritant, and its vapors may cause headache, nausea, vomiting, and diaphoresis [Rom 1998].
Effects reported from occupational exposure to PAHs include
- chronic bronchitis,
- chronic cough irritation,
- bronchogenic cancer,
- cutaneous photosensitization, and
- pilosebaceous reactions.
Reported health effects associated with chronic exposure to coal tar and its by-products (e.g., PAHs).
- Skin: erythema, burns, and warts on sun-exposed areas with progression to cancer. The toxic effects of coal tar are enhanced by exposure to ultraviolet light.
- Eyes: irritation and photosensitivity.
- Respiratory system: cough, bronchitis, and bronchogenic cancer.
- Gastrointestinal system: leukoplakia, buccal-pharyngeal cancer, and cancer of the lip.
- Hematopoietic system: leukemia (inconclusive) and lymphoma.
- Genitourinary system: hematuria and kidney and bladder cancers.
Exposure is most often determined based on the patient exposure history.
A relevant patient history might include the following information:
- occupational history,
- occupation of the spouse and other household members,
- use of medications, including coal tar-containing dermatologic preparations,
- diet, especially charbroiled meats,
- alcohol consumption; and
- smoking habits.
Hobbies and recreational activities might reveal additional evidence of exposure to PAH-containing mixtures.
In general, risk increases with total dose.
For more information on the exposure history, see the Taking an Exposure History CSEM at www.atsdr.cdc.gov/csem/exposure-history/cover-page.html
Physical examination is important.
Physical examination should include a review of all systems, with the knowledge that cancer is the most significant endpoint of chronic PAH toxicity. If PAH exposure is suspected, the clinician should be alert to malignant transformation of actinic skin lesions. The buccal mucosa and oropharynx should be inspected for malignant changes. Inspection of sun-exposed areas for evidence of hyperpigmentation in response to sunlight is advised.
Direct biologic measurement of PAHs is neither cost-effective nor clinically useful. Direct measurement refers to testing directly for the parent compound (or specific PAHs exposed to), not the metabolites.
Although researchers have examined PAHs directly in the blood and tissues of experimental animals, these methods have not been widely used for human samples. The high costs of testing and limited knowledge of the significance of background levels in humans limit the clinical usefulness of such tests.
The most common tests for determining exposure to PAHs involve examining tissues, blood, and urine for the presence of metabolites.
Pyrene is commonly found in PAH mixtures, and its urinary metabolite, 1-hydroxypyrene, has been used as an indicator of exposure to PAH chemicals [Becher and Bjorseth 1983; Granella and Clonfero 1993; Popp 1997; Santella et al. 1993, CDC 2005]. The ACGIH recommends measurement of 1-hydroxypyrene in the end-of-shift, end-of-work-week urine samples as a biological exposure index (BEI) for assessment of exposure to mixtures containing PAHs. This practice may help identify workplaces requiring improved industrial hygiene measures [ACGIH 2005; Heikkila et al. 1995].
In the Third National Report on Human Exposure to Environmental Chemicals, urinary levels of hydroxylated metabolites of PAHs were measured in a subsample of the National Health and Nutrition Examination Survey (NHANES) participants aged 6 years and older during 1999–2002. The geometric mean for 1-hydroxypyrene (ng/g of creatinine) for the U.S. population aged 6 years and older during 1999–2002 was 74.2, with a 95% confidence interval of (61.6–89.3).
Note that finding a measurable amount of one or more metabolites in the urine does not mean that the levels of the PAH metabolites cause an adverse health effect. Whether levels of PAH metabolites at the levels reported are cause for health concern is not known, and more research is needed. These data provide physicians with a reference range so that they can determine whether people have been exposed to higher levels of PAHs than are found in the general population. As well, the data help scientists plan and conduct research on exposure to PAHs and health effects.
Deoxyribonucleic acid (DNA) adducts may be used as an indicator of exposure in research settings and can be measured in a variety of biologic media [Popp 1997; Ross et al. 1991; Santella et al. 1993; Weyand and La Voie 1988]. For example, tissue in culture can be labeled with radioactive phosphorus and analyzed by thin-layer chromatography and scintillation to identify and quantify the DNA adducts formed. Also, an immunoassay technique, ELISA, has been developed to detect antibodies to the PAH-DNA adducts in blood. These tests aren’t readily available for routine clinical use.
PAH diol epoxides form adducts with hemoglobin in the red blood cells. These adducts can be quantified by use of fluorescence spectroscopy. This technique is limited in its potential usefulness, however, because of individual differences in PAH metabolism and the limited specificity of the technique itself.
In general, indirect biologic monitoring can be useful in determining whether exposure to PAHs has occurred. However, it is not clinically useful for evaluating individual patients because normal or toxic levels have not been determined. Arterial blood gases, a chest radiograph, and other monitoring might be indicated. Individual variability, confounding effects of drugs or cigarettes, and nonspecificity of techniques are likely to complicate the interpretation of the results, especially in low-level environmental exposures.
Employees exposed to CTPVs in the coke oven industry are covered by the coke oven emissions standardexternal icon. This OSHA standard includes elements of medical surveillance for workers exposed to coke oven emissions. It should be noted that OSHA recommended surveillance set at the time of the standard may not necessarily be consistent with current evidenced based medical practice.
- Acute effects attributed to PAH exposure are probably caused by other agents.
- Exposure is most often determined based on the patient exposure history.
- Pertinent exposure history should include past and current occupational, recreational, hobbies, dietary, and smoking assessments.
- Physical examination is important, including a review of all systems.
- Direct biologic measurement of PAHs is neither cost-effective nor clinically useful.
- A commonly measured urinary metabolite used to assess PAH exposure is 1-hydroxypyrene.
- DNA adducts may be used as an indicator of exposure in research settings and can be measured in a variety of biologic media.