Health and Environment
Health and Environmental Impacts
Human Health Effects
Human exposure to PCE can occur from occupational practices, environmental contamination or use of consumer products that contain PCE. PCE levels in the environment tend to be higher in urban and industrial areas. The most prevalent route of exposure to PCE is by inhalation and it is readily absorbed into blood through the lungs.
Another potential exposure route of concern is oral, via drinking water or contaminated food. General dermal exposure is not considered a major route of exposure but direct skin exposure to PCE in the liquid form can result in irritation and blistering. The primary organs targeted by PCE are the central nervous system (CNS) and the liver.
Some studies suggest that long term frequent over-exposure to organic solvents such as PCE may cause lasting and possibly permanent CNS effects. Fatigue, lack of muscle coordination, loss of concentration as well as short term memory loss, and personality changes exhibited as nervousness, anxiety or irritability are some of the potential permanent long-term effects of chronic and frequent exposure. In addition, PCE inhaled by pregnant women can cross the placenta causing exposure of the developing fetus. PCE has also been found in breast milk of mothers exposed to the chemical.
Concentrations of 200 ppm or more have been associated with dizziness, confusion, headache, nausea, and irritation of the eyes and mucous tissue. Exposure to extremely high levels of PCE (>1,500 ppm) may lead to unconsciousness and, in extreme cases, death from respiratory depression. Nausea and vomiting may follow from inhalation of large amounts of PCE. The immediately dangerous to life or health air concentration value (IDLH) used by the National Institute for Occupational Safety and Health (NIOSH) as respirator selection criteria for PCE has been set at 150 ppm.
Symptoms of exposure to skin can include redness, itching, and pain. Prolonged exposure can result in the removal of natural protective oils from skin resulting in irritation, dryness, cracking and dermatitis. Likewise, extended dermal contact can result in second- and third-degree chemical burns. Contact of PCE vapors above 75 ppm with the eyes will result in irritation, redness, and pain.
Long term exposure to PCE may cause liver, kidney or CNS damage. Furthermore, the exposure can aggravate pre-existing conditions. For example, persons with pre-existing skin disorders, eye problems or impaired liver or kidney function may be more susceptible to the effects of the substance. PCE can affect your brain and CNS as a whole; in a similar way as the consumption of alcohol does. Therefore the consumption of alcoholic beverages within a short time period of exposure to PCE enhances the toxic effects from PCE and alcohol. The two would have an additive effect on the CNS.
Overexposure may result in cumulative liver and CNS damage or narcosis. Overall, PCE can affect the liver, kidneys, eyes, skin, respiratory system, and CNS.
Several agencies have investigated PCE's association with cancer. The US National Toxicology Program classifies PCE as "Reasonably anticipated to be human carcinogen". IARC lists PCE as Group 2A, "Probably carcinogenic to humans." EPA is currently reassessing PCE's carcinogenicity classification and ACGIH designates it as an A3, confirmed animal carcinogen. A recent Massachusetts-based research project on Cape Cod looked at PCE exposure through contaminated drinking water and found an association between PCE exposure and cancer rates.
There are conflicting data on the status of PCE as a reproductive or developmental toxin in either humans or animals. Some studies have reported adverse reproductive effects of PCE, including spontaneous abortions, menstrual disorders, altered sperm structure and reduced fertility. These studies were limited and are not generally considered to be conclusive.
Studies also show conflicting evidence of birth defects in animals, with some finding increased incidences in liver tumors and leukemia while others find no teratogenic effects. What is widely agreed upon is that PCE is able to transport across the placenta to the fetuses of pregnant women who have been highly exposed. In addition, PCE has been found in the breast milk of nursing mothers.
The OSHA PELs for PCE are 100 ppm for an 8 hour day and a maximum exposure level of 200 ppm for 5 minutes in any 3-hour period. California's OSHA program has set the PCE permissible exposure level at 25 ppm. ACGIH has established a threshold limit value of 25 ppm, and a short term exposure limit of 100 ppm. Recent studies in California and Massachusetts have highlighted concerns over the exposure of workers (especially in automotive repair facilities) using aerosol PCE products for cleaning and repair work.
PCE most often enters the environment via fugitive emissions from dry cleaning and metal degreasing industries and by spills or accidental releases to air, soil and water. When released to soil, PCE will evaporate fairly rapidly into the atmosphere due to its high vapor pressure and low rate of adsorption in soil. PCE can leach rapidly through sandy soil and therefore may reach groundwater. PCE is reported to be the chemical most widely found in groundwater contamination at Superfund Sites.
When PCE is released in water, the primary loss is by evaporation. Chemical and biological degradation are expected to be very slow. PCE is not expected to accumulate in aquatic organisms or to adsorb onto sediment; however it is toxic to aquatic organisms.
When released to the atmosphere, PCE is expected to remain in the vapor phase. Photo-oxidation of PCE will form chlorine atoms. PCE can degrade in the atmosphere in two ways, through reaction with photochemical produced hydroxyl radicals or by reacting with the chlorine produced by its own photo-oxidation.
(For section references, see endnote #1)