Contractors and Consumers: New Protections from Lead-based Paint Take Effect April 22
Public Info Session held in Portland, Maine on Friday, March 26
(Boston, Mass. – March 23, 2010) – The federal deadline to make lead safety the standard of care for renovations and painting projects in pre-1978 housing is April 22, 2010.
The new EPA rule, announced in 2008 and in development for years before that, sets in place more protective work practices to limit children’s potential exposure to lead dust due to painting, repair or renovation work in older houses and buildings. Anyone receiving compensation for renovating, repairing and painting work in residences built before 1978 that disturbs painted surfaces is subject to the new Renovation, Repair and Painting Rule (RRP). Also affected by the RRP are those performing similar work on facilities occupied by children less than six years of age, such as schools and day-care centers built prior to 1978.
EPA, along with federal and state partners, is holding a public information session on the new RRP rule on Friday, March 26, 2010 in Portland, Maine, between 1:00 – 4:00 p.m. The session is free and open to the public. However, space is limited so registration is required to ensure your spot. Registration can be done on-line or in person the day of the session. The meeting will be held at Holiday Inn by the Bay, (http://innbythebay.com/) 88 Spring Street, Portland, Maine 04101 (207) 775 -2311, in the Cumberland and the Kennebec Rooms. Register online (at www.epa.gov/region1/topics/pollutants/lead.html .)
Beginning April 22, 2010, no paid job can disturb painted surfaces in pre-1978 homes or child care facilities unless (1) the firm is certified by the EPA or a state and (2) the renovator has completed training and is a certified renovator. The requirements under the rule apply to maintenance, renovation or repair activities where six square feet (about the size of a poster) or more of a painted surface is disturbed inside, or where 20 square feet or more of painted surface (about the size of a door) is disturbed on the exterior. Window replacement is also covered by the rule. The only exceptions are where paint is proven lead free or the job is smaller than six square feet.
Lead hazards created by renovation and painting projects cause one in three known lead poisoning cases in Maine. Using safe work practices before, during, and after such work prevents the spread of dangerous lead dust and paint chips. These practices include posting a warning sign, spreading plastic to pick up debris, refraining from sanders or other machines without a filter to prevent the spread of dust, thorough clean-up, and checking the work area. A day of training is enough to prepare a renovator, painter, property manager, plumber, electrician, or handyman to use these practices, and federal law now requires it. Landlords who perform the work described above are also affected by the rule and bound by the same requirements.
“Because we have so much older housing stock here in New England, protecting kids from exposure to lead-based paint is one of the most important things we can do. Lead exposure is entirely preventable, and can cause permanent, serious, life-long problems,” said Curt Spalding, regional administrator for EPA’s New England region.
Lead, a toxic metal that was used for many years in products such as lead-based paint, may cause a range of health effects from behavioral problems and learning disabilities, to seizures and death. Children six years old and under are most at risk. In 1978 the sale and use of lead-based paint was banned for residential use.
Until the new rule takes effect, contractors should follow these three simple procedures: contain the work area; minimize dust; and cleanup thoroughly.
More information:
Register for the Portland ME informational meeting (March 26, 2010): (www.epa.gov/region1/topics/pollutants/lead.html)
Renovator & Trainers Lead-safe Tool Box: (www.epa.gov/lead/pubs/toolkits.htm)
Find a certified firm near you: (http://cfpub.epa.gov/flpp/searchrrp_firm.htm)
General info on lead: (www.epa.gov/lead)
National Lead Information Center at 1-800-424-LEAD (1-800-424-5323)
Renovation, Repair and Painting rule: (www.epa.gov/lead/pubs/renovation.htm)
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Monday, March 29, 2010
Chinese Drywall
From Mar. 18 New Orleans Times-Picayune
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Chinese drywall guidance offered by National Association of Home Builders By Rebecca Mowbray, The Times-Picayune March 18, 2010, 8:13PM
While the U.S. Consumer Product Safety Commission dallies on instructing people how to fix homes damaged by corrosive drywall, the National Association of Home Builders has become the first major player to advance its own set of "evolving solutions."
The guidance to builders nationwide comes as the national consolidated litigation over problem drywall in U.S. District Court in New Orleans proceeds swiftly toward figuring out how to repair homes. Federal efforts to find effective ways to fix homes, meanwhile, have been thorough but too slow for many impatient families living in homes where hydrogen sulfide gas is making them sick and corroding metal appliances, fixtures and wiring.
Remarkably, the repair procedures outlined by the home builders are similar to what the committee of plaintiffs attorneys has proposed in Judge Eldon Fallon's courtroom in New Orleans. Rather than some cheaper air-filtration and drywall treatments that others have suggested, the home builders association advocates ripping out drywall, plumbing and possibly wiring, paying for families to temporarily relocate, and allowing homes time to air out after being gutted.
"When I look at what the NAHB is recommending and what the plaintiffs steering committee is recommending in court, the differences are not substantial," said David Loeb, an attorney for the Home Builders Association of Greater New Orleans.
Report may serve as blueprint
David Jaffe, vice president of legal affairs at the trade association of 175,000 builders, said his group is not attempting to upstage the Safety Commission's quest for official "remediation protocols," but wanted to advise its members on the latest available science on corrosive drywall and the experience of large builders who have attempted to tackle the problem.
But others note that the formal assessment by the home builders, written by the risk management firm Marsh USA Inc., could effectively serve as a blueprint for the Safety Commission and help a diverse set of foreign manufacturers, builders, distributors, homeowners and their attorneys coalesce around a limited set of ideas.
Scott Wolfson, a spokesman for the safety commission, said his group has its own task force of experts and should release "remediation protocols" in 45 days. [snip]
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Full article at:
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Chinese drywall guidance offered by National Association of Home Builders By Rebecca Mowbray, The Times-Picayune March 18, 2010, 8:13PM
While the U.S. Consumer Product Safety Commission dallies on instructing people how to fix homes damaged by corrosive drywall, the National Association of Home Builders has become the first major player to advance its own set of "evolving solutions."
The guidance to builders nationwide comes as the national consolidated litigation over problem drywall in U.S. District Court in New Orleans proceeds swiftly toward figuring out how to repair homes. Federal efforts to find effective ways to fix homes, meanwhile, have been thorough but too slow for many impatient families living in homes where hydrogen sulfide gas is making them sick and corroding metal appliances, fixtures and wiring.
Remarkably, the repair procedures outlined by the home builders are similar to what the committee of plaintiffs attorneys has proposed in Judge Eldon Fallon's courtroom in New Orleans. Rather than some cheaper air-filtration and drywall treatments that others have suggested, the home builders association advocates ripping out drywall, plumbing and possibly wiring, paying for families to temporarily relocate, and allowing homes time to air out after being gutted.
"When I look at what the NAHB is recommending and what the plaintiffs steering committee is recommending in court, the differences are not substantial," said David Loeb, an attorney for the Home Builders Association of Greater New Orleans.
Report may serve as blueprint
David Jaffe, vice president of legal affairs at the trade association of 175,000 builders, said his group is not attempting to upstage the Safety Commission's quest for official "remediation protocols," but wanted to advise its members on the latest available science on corrosive drywall and the experience of large builders who have attempted to tackle the problem.
But others note that the formal assessment by the home builders, written by the risk management firm Marsh USA Inc., could effectively serve as a blueprint for the Safety Commission and help a diverse set of foreign manufacturers, builders, distributors, homeowners and their attorneys coalesce around a limited set of ideas.
Scott Wolfson, a spokesman for the safety commission, said his group has its own task force of experts and should release "remediation protocols" in 45 days. [snip]
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Full article at:
Thursday, March 25, 2010
EPA Takes Action to Establish New Bug Bomb Labeling
Pesticide News Story: EPA Takes Action to Establish New Bug Bomb Labeling Requirements to Improve Safety and Reduce Risk
For Release: March 24, 2010
Today, EPA is taking action to improve residential safety and reduce risks associated with bug bombs, or total release foggers (TRFs). The Agency is calling for significant changes to their labeling to address the most common causes of exposure incidents associated with TRFs.
EPA is requiring manufacturers to make a number of labeling changes by September 30, 2011. Since the largest proportion of incidents is attributable to failure to follow label instructions, the changes are targeted at minimizing those incidents. To draw attention to critical information, future bug bomb labels must be written in plain language with clear headings. To further enhance clarity and risk understanding, the new labels will also incorporate pictograms, which can be more effective than text in communicating certain information, including explosion hazards and the amount of time that a residence must be vacated after releasing the fogger. The changes also strengthen instructions to vacate upon use and air out upon return by requiring greater label prominence. A new provision is that door hang-tags must be provided to inform others to stay out of treated areas.
In addition to these labeling improvements, EPA is continuing to work with registrants on developing non-labeling improvements, including transitioning to smaller foggers, time-delayed release, and nonflammable propellants.
The number of foggers used is estimated at roughly 50 million units per year. Although the available evidence suggests that bug bomb incidents are infrequent relative to use of the devices, incidents of serious injury have been reported. EPA’s new bug bomb labeling improvements are consistent with the recommendations of two 2008 state reports and are intended to address concerns raised by the New York City Department of Health.
EPA will continue to monitor these products closely to ensure that these new public health protections are effective and evaluate whether additional actions are needed.
For more information on the new labeling requirements, the petition, and EPA’s analysis and response, please see the fogger section of EPA’s pyrethroid and pyrethrins fact sheet.
For Release: March 24, 2010
Today, EPA is taking action to improve residential safety and reduce risks associated with bug bombs, or total release foggers (TRFs). The Agency is calling for significant changes to their labeling to address the most common causes of exposure incidents associated with TRFs.
EPA is requiring manufacturers to make a number of labeling changes by September 30, 2011. Since the largest proportion of incidents is attributable to failure to follow label instructions, the changes are targeted at minimizing those incidents. To draw attention to critical information, future bug bomb labels must be written in plain language with clear headings. To further enhance clarity and risk understanding, the new labels will also incorporate pictograms, which can be more effective than text in communicating certain information, including explosion hazards and the amount of time that a residence must be vacated after releasing the fogger. The changes also strengthen instructions to vacate upon use and air out upon return by requiring greater label prominence. A new provision is that door hang-tags must be provided to inform others to stay out of treated areas.
In addition to these labeling improvements, EPA is continuing to work with registrants on developing non-labeling improvements, including transitioning to smaller foggers, time-delayed release, and nonflammable propellants.
The number of foggers used is estimated at roughly 50 million units per year. Although the available evidence suggests that bug bomb incidents are infrequent relative to use of the devices, incidents of serious injury have been reported. EPA’s new bug bomb labeling improvements are consistent with the recommendations of two 2008 state reports and are intended to address concerns raised by the New York City Department of Health.
EPA will continue to monitor these products closely to ensure that these new public health protections are effective and evaluate whether additional actions are needed.
For more information on the new labeling requirements, the petition, and EPA’s analysis and response, please see the fogger section of EPA’s pyrethroid and pyrethrins fact sheet.
Wednesday, March 24, 2010
1,2-Dichloroethane
1,2-Dichloroethane (ethylene dichloride) is a clear, colorless, oily liquid with a chloroform-like odor and a boiling point of 83.5°C. Its vapor pressure ranges from 5.33 to 14.0 kPa over the temperature range 10 to 30°C. 1,2-Dichloroethane is miscible with most organic solvents and is appreciably soluble in water, with a solubility ranging from 8700 to 9200 mg/L over the temperature range 0 to 25°C. It has a log octanol-water partition coefficient of 1.48.1
1,2-Dichloroethane has been reported to be one of the most widely used chemicals in the world.2 Annual usage in the Great Lakes Basin has been estimated at 900 million kilograms.3 Canadian production in 1984 was 680 million kilograms, of which 180 million kilograms were exported and 500 million kilograms were consumed domestically.4
Almost all of the domestic 1,2-dichloroethane is used as a chemical intermediate in the preparation of vinyl chloride. About 1% is used as a solvent and as a lead scavenger in leaded gasoline formulations.4 This use has decreased over the past few years and will continue to decrease as the use of lead in fuels drops.5 1,2-Dichloroethane enters the environment through atmospheric emissions, waste effluents to waterways and land disposal of liquid and solid wastes.6 Because of its high volatility, 1,2-dichloroethane that is released to land and water can be expected to be transferred predominantly to the atmosphere. About 1 to 1.7% of total U.S. yearly production was estimated to be released to the environment as emissions.6
Exposure
1,2-Dichloroethane was detected frequently in treated drinking water and raw water samples taken from 30 treatment facilities across Canada in 1979.7 Mean concentrations in treated water were between 4 and 5 µg/L during August and September and less than 1 µg/L in November and December. The overall mean of 31 positive determinations was 3.2 µg/L. Maximum concentrations of 30 and 11 µg/L were found during August and September and during November and December, respectively. 1,2-Dichloroethane was detected at trace levels (0.34 to 0.38 µg/L) in one municipal water supply in Quebec during February 1986, but it was not detected in a later survey, during August 1986, of 18 Quebec municipalities.8 It was also undetected in 1985 and 1986 surveys of 40 municipalities in the four Maritime provinces,9,10 in a 1984 survey of seven municipalities in the Niagara River area11 and in the 1978 to 1985 surveys of 29 municipal water supplies in Alberta.12 The average daily intake* from drinking water containing 1,2-dichloroethane was estimated to be 0.069 µg/kg bw, based on the mean of 3.2 µg/L observed in the Otson study.7
Few data are available on concentrations of 1,2-dichloroethane in foods. Concentrations ranging from 2 to 23 µg/g were found in 11 of 17 different spice oleoresins that had been subjected to solvent extraction with 1,2-dichloroethane.13 Residues of 1,2-dichloroethane in grain products arising from its use as a grain fumigant are expected to be negligible, as this use was suspended in Canada in 1984. The human intake from food sources was estimated to be negligible.6
No Canadian data are available on ambient air concentrations of 1,2-dichloroethane. A review of recent reports revealed that U.S. ambient air concentrations ranged from 0.062 to 6.20 ppb (0.25 to 25 µg/m3) with an intermediate value of 0.62 ppb (2.5 µg/m3).6 Based on these concentrations, the estimated average daily human intake of 1,2-dichloroethane from ambient air is 0.71 µg/kg bw, with a range of 0.07 to 7.14 µg/kg bw*. Atmospheric concentrations near production facilities were in the order of 10 ppb (40 µg/m3), and those near end-use facilities ranged from 0.69 to 0.99 ppb (2.8 to 4.0 µg/m3).6
Inhalation would therefore appear to be the primary route of exposure to 1,2-dichloroethane, with 0.71 µg/kg bw or 91% of an estimated total daily intake of 0.78 µg/kg bw derived from this source. The contribution from food is negligible,6 and estimated intake from drinking water is 0.07 µg/kg bw or 9% of the total.
Analytical Methods and Treatment Technology
The analysis of 1,2-dichloroethane in water at concentrations as low as 0.10 µg/L is possible using the purge and trap method and gas/liquid chromatography instrumentation equipped with a halogen-specific detector.6 The practical quantitation limit (PQL) (based on the ability of laboratories to measure 1,2-dichloroethane within reasonable limits of precision and accuracy) is 5 µg/L.14
The removal efficiency of volatile organic compounds by packed tower aeration and granular activated carbon adsorption for chlorinated aliphatic hydrocarbons has been estimated to be 90 to 93%.14 It would appear that, using advanced technology, a reduction in the concentration of 1,2-dichloroethane in drinking water to less than 1 µg/L would be feasible.
Health Effects
Animal studies with 1,2-dichloroethane have shown that it is rapidly and extensively absorbed via the lungs.15 Uptake from the gastrointestinal tract was efficient and rapid,15 although both the rate and extent were vehicle-dependent,16 peak values for the blood levels being 5 times higher for solutions in water than for solutions in oil. Dermal absorption was shown to be significant in rats, with an absorption rate of 479 nmol/min per square centimetre.17
1,2-Dichloroethane was rapidly distributed to all body tissues.15 As expected from its properties as a general anaesthetic in man, it readily crossed the blood-brain barrier. It was also efficiently transferred to the foetus of the rat.18
There was good evidence to show that the metabolism of 1,2-dichloroethane proceeded via two principal pathways. One involved a saturable microsomal (P-450-mediated) oxidation, leading to the formation of 2-chloroacetaldehyde, the putative 1-chloroso-2-chloroethane and, ultimately, glutathione conjugates. A second pathway involved a cytosolic glutathione-dependent pathway leading to glutathione conjugates, such as S-(2-chloroethyl glutathione).19,20 These metabolites were believed to be involved in covalent binding with DNA, although other metabolites, conjugates and intermediates were also formed.19,20
The elimination of 1,2-dichloroethane followed a two- or three-compartment mathematical model after administration by various routes and was dose-dependent.15,16,21 Material balance studies, following oral and inhalation dosing, have shown that metabolism was the primary elimination mechanism.15 After the administration of an oral dose of 150 mg/kg bw to rats, 29% was excreted unchanged in exhaled air, 5% was metabolized to carbon dioxide and 60% appeared in the urine as metabolites. After an inhalation exposure to 150 ppm (600 mg/m3) for six hours, rats were estimated to have received a total dose of 50 mg/kg bw. Of this dose, 2% was excreted unchanged in air, 7% was metabolized to carbon dioxide and more than 84% was recovered as urinary metabolites.
No epidemiological studies on human health effects induced by 1,2-dichloroethane have been published. The characteristic symptoms of poisoning by chlorinated aliphatic hydrocarbons have been reported in acute and chronic occupational exposures to inhaled 1,2-dichloroethane. Nausea, headache, gastrointestinal disturbances, vomiting, rapid and weak pulse, progressive cyanosis, dyspnoea, loss of consciousness and, ultimately, death have been documented.6 Deaths have also been reported after ingestion of 1,2-dichloroethane, and the acute lethal dose in humans has been estimated to be between 8 and 200 mL (143 to 3571 mg/kg bw).6
Acute exposure studies in animals showed that the severity of effects was dependent on the duration and level of exposure to 1,2-dichloroethane. For rats exposed for five to eight hours via inhalation, adverse effects were not elicited at 200 ppm (800 mg/m3). The first signs of intoxication appeared at a concentration of 300 ppm (1200 mg/m3) and mortality at about 600 ppm (2400 mg/m3).22,23 The acute lethal oral dose in rats was reported to be 680 mg/kg bw.24 In male and female CD-1 mice, the acute lethal oral doses were 489 and 413 mg/kg bw, respectively.25 The LD50 for skin exposures in rabbits was estimated to be between 2.8 and 4.9 g/kg bw.6
In a subchronic study, 15 rats of each sex, eight guinea pigs of each sex, one female and two male rabbits and two male monkeys were exposed to 1,2-dichloroethane vapour at concentrations of 400 and 100 ppm (1600 and 400 mg/m3) for 7 h/d, five days per week for six months. In addition, a further 15 rats of each sex and eight guinea pigs of each sex were exposed to 200 ppm (800 mg/m3) for 30 and 36 weeks, respectively.22 No adverse effects were observed in any of the four species exposed to 100 ppm. At the 200 ppm level, no adverse effects were seen in rats, but slight parenchymatous degeneration of the liver, with some vacuolization, was seen in guinea pigs. Severe effects, including hepatotoxicity and death, were observed in rats and guinea pigs exposed at the 400 ppm level.
Chronic studies with 1,2-dichloroethane in animals have been limited to those that were primarily designed as cancer bioassays. There have been two principal studies, one in which both sexes of rats and mice were dosed by gavage with solutions in corn oil26 and the other in which the same species were exposed by the inhalation route.27
In the National Cancer Institute study,28 the maximum tolerated dose (MTD) and one-half the MTD, determined from preliminary studies, were administered by gavage on five consecutive days per week to 50 Osborne-Mendel rats of each sex, beginning at eight weeks of age, and to 50 B6C3F1 mice, starting at five weeks of age. In addition, 20 animals were given no treatment, and 20 animals were dosed with the vehicle alone for each dose and sex group. Early signs of toxicity in both species indicated that the selected MTDs were inappropriate and necessitated several changes in the administered dosages during the 78 weeks of the study. Thus, the time-weighted average doses received by the male and female rats were 97 and 47 mg/kg bw (MTD and one-half the MTD). For male mice, the doses were 195 and 97 mg/kg bw, and for female mice, 299 and 149 mg/kg bw.
Multiple tumors were induced in both species. A statistically significant increase (P < 0.05) in the incidence of squamous cell carcinomas of the fore-stomach, hemangiosarcomas of the circulatory system and fibromas of the subcutaneous tissue occurred in male rats. There was also a statistically significant increase in the incidence of adenocarcinomas of the mammary gland and hemangiosarcomas of the circulatory system in female rats. Tumours were also observed at other sites, including the spleen, liver, adrenal glands, pancreas, large intestine, subcutaneous tissue and abdominal cavity.
In B6C3F1 mice, there was a statistically significant increase in incidences of hepatocellular carcinomas and alveolar/bronchiolar adenomas in male mice. In female mice, there was a statistically significant increase in incidences of alveolar/bronchiolar adenomas, mammary carcinomas and endometrial tumours.
Supportive evidence for the National Cancer Institute study was available from a pulmonary tumor bioassay29 in which mice were dosed intraperitoneally with 1,2-dichloroethane in tricaprylin and from a skin application study in mice.30 Both of these studies showed that 1,2-dichloroethane could induce a significant increase in tumors at sites (e.g., lung and stomach) remote from the point of application.
No evidence of carcinogenicity was found in a recent lifetime inhalation study in which Sprague-Dawley rats and Swiss mice were exposed to concentrations of 1,2-dichloroethane that ranged from 5 to 150 ppm (20 to 600 mg/m3).27 Nor was there any evidence of carcinogenicity from an earlier subchronic study in which Wistar rats were exposed to 200 ppm (800 mg/m3) 7 h/d, five days per week for six months.22 The apparent discrepancies between inhalation and other routes of exposure in oncogenicity studies have led to considerable discussion.15,31 Among other factors it was considered that the delivered dose in the inhalation studies was lower than that received by the animals in the oral dosing study and was probably too low to elicit a statistically significant tumor response in the number of animals used.
A recent review has concluded that 1,2-dichloroethane causes gene mutations in bacteria, plants, Drosophila and Chinese hamster ovary cells.32 The results of reproductive and teratogenicity testing have indicated that 1,2-dichloroethane has little potential for producing adverse reproductive effects or for adversely affecting the developing foetus unless the exposure is high enough to produce maternal toxicity.6,33
* This estimate was based on a 70-kg man breathing 20 m3 of air per day.
Classification and Assessment
1,2-Dichloroethane is classified in Group II --probably carcinogenic to man (sufficient evidence in animals, inadequate evidence in man) -- on the basis that it has been shown to be carcinogenic in both sexes of two animal species. Incorporating a surface area correction and using the robust linear extrapolation model, one can calculate the unit lifetime risk associated with the ingestion of 1 µg/L 1,2-dichloroethane in drinking water to be 1.6 x 10-6 (based on hemangiosarcomas in the circulatory system of male Osborne-Mendel rats)*.26 These tumors were selected because they represented the most sensitive response and occurred at locations remote from the site of contact with the agent. The estimated concentrations in drinking water corresponding to lifetime risks of 10-5, 10-6 and 10-7 for the same tumor type based on the model described above are 6.2, 0.62 and 0.062 µg/L.
* Average adult body weight = 70 kg; average daily intake of drinking water = 1.5 L.
Rationale
Because 1,2-dichloroethane is classified as a probable human carcinogen in Group II, the maximum acceptable concentration (MAC) is derived based on consideration of available practicable treatment technology and estimated lifetime cancer risks. Because the MAC must also be measurable by available analytical methods, the PQL is also taken into consideration in its derivation.
An interim MAC (IMAC) of 0.005 mg/L (5 µg/L) for 1,2-dichloroethane was established, therefore, on the basis of the following considerations:
(1) The estimated unit lifetime risk associated with the ingestion of 1 µg/L 1,2-dichloroethane in drinking water is 1.6x 10-6 (based on hemangiosarcomas in male rats). Therefore, the estimated lifetime risk associated with the ingestion of drinking water containing 5 µg/L 1,2-dichloroethane is 8x 10-6. The MAC is considered interim because intake in drinking water is approximately 9% of the total intake, and the estimated total risk from all sources therefore will exceed 1 x 10-5, which is above the maximum value in the range considered "essentially negligible."
(2) It is unlikely that 1,2-dichloroethane concentrations are reduced significantly during conventional water treatment processes. However, it is possible to achieve concentrations below 1µg/L using packed tower aeration or granular activated carbon adsorption.
(3) The PQL (based on the ability of laboratories to measure 1,2-dichloroethane within reasonable limits of precision and accuracy) is 5 µg/L.
References
1. Valvani, S.C., Yalnowsky, S.H. and Roseman, T.J. Solubility and partitioning. IV. Aqueous solubility and octanol-water partition coefficients of liquid non-electrolytes. J. Pharm. Sci., 70: 502 (1981).
2. International Agency for Research on Cancer. ARC Monogr. Eval. Carcinog. Risk Chem. Man, 20: 429 (1979).
3. International Joint Commission. 1981 annual report, Committee on Human Health Effects of Great Lakes Water Quality (1981).
4. Corpus Information Services. CPI product profiles: ethylene dichloride (ECD). Toronto (1985).
5. Senes Consultants Ltd. Drinking water criteria reviews for 1,2-dichloroethane, 1,1,1-trichloroethane and 1,1,2,2-tetrachloroethane. Contract for the Ontario Ministry of the Environment (1985).
6. U.S. Environmental Protection Agency. Health assessment document for 1,2-dichloroethane (ethylene dichloride). EPA/600/8-84/006F, Office of Health and Environmental Assessment, Washington, DC (1985).
7. Otson, R., Williams, D.T. and Bothwell, P.D. Volatile organic compounds at thirty potable water treatment facilities. J. Assoc. Off. Anal. Chem., 65: 1370 (1982).
8. Ayotte, P. Micropollutants organiques, campagnes d'échantillonnage 1986. Direction des eaux souterraines et de consommation, Ministère de l'environnement, Gouvernement du Québec (1987).
9. Lebel, G.L. Volatile organic compounds in Atlantic area drinking water sources. Unpublished report, Monitoring and Criteria Division, Environmental Health Directorate, Department of National Health and Welfare (1987).
10. Environment Canada. Data summary reports; federal-provincial drinking water sources, toxic chemical survey, 1985-1986, Newfoundland, Nova Scotia, New Brunswick, Prince Edward Island. Water Quality Branch, Atlantic Region, Moncton (1987).
11. Ontario Ministry of the Environment. Survey of Niagara area and selected Lake Ontario municipal drinking water supplies. Toronto (1984).
12. Alberta Environment. Drinking water survey, 1978-1985. Municipal Engineering Branch, Pollution Control Division, Edmonton (1985).
13. Page, B.D. and Kennedy, P.P.C. Determination of methylene chloride, ethylene dichloride and trichloroethylene as solvent residues in spice oleoresins, using vacuum distillation and electron capture detection. J. Assoc. Off. Anal. Chem., 60: 710 (1975).
14. U.S. Environmental Protection Agency. National primary drinking water regulations; volatile synthetic organic chemicals. Fed. Regist., 50(219): 46902 (1985).
15. Reitz, R.H., Fox, T.R., Ramsey, J.C., Quast, J.F., Langvardt, P.W. and Watanabe, P.G. Pharmacokinetic and macromolecular interactions of ethylene dichloride in rats after inhalation or gavage. Toxicol. Appl. Pharmacol., 62: 190 (1982).
16. Withey, J.R., Collins, B.T. and Collins, P.G. Effect of vehicle on the pharmacokinetics and uptake of four halogenated hydrocarbons from the gastrointestinal tract of the rat. J. Appl. Toxicol., 3: 249 (1983).
17. Tsuruta, H. Percutaneous absorption of organic solvents. II. A method for measuring the penetration rate of chlorinated solvents through excised rat skin. Ind. Health, 15: 131 (1977).
18. Withey, J.R. and Karpinski, K. The fetal distribution of some aliphatic chlorinated hydrocarbons in the rat after vapor phase exposure. Biol. Res. Pregnancy, 6: 79 (1985).
19. Guengerich, F.P., Crawford, W.M., Domradizki, J.Y., McDonald, T.L. and Watanabe, P.G. In vitro activation of 1,2-dichloroethane by microsomal and cytosolic enzymes. Toxicol. Appl. Pharmacol., 55: 303 (1980).
20. Anders, M.W. and Livesey, J.C. Metabolism of 1,2-dichloroethanes. In: Ethylene dichloride: a potential health risk? B.N. Ames, P. Infante and R. Reitz (eds.). Cold Spring Harbor Laboratory, Cold Spring Harbor, NY. p. 331 (1980).
21. Withey, J.R. and Collins, B.T. Chlorinated aliphatic hydrocarbons used in the foods industry: the comparative pharmacokinetics of methylene chloride, 1,2-dichloroethane, chloroform and trichloro-ethylene after i.v. administration in the rat. J. Environ. Pathol. Toxicol., 3: 313 (1980).
22. Spencer, H.C., Rowe, V.K., Adams, E.M., McCollister, D.D. and Irish, D.D. Vapor toxicity of ethylene dichloride determined by experiments on laboratory animals. Ind. Hyg. Occup. Med., 4: 482 (1951).
23. Heppel, L.A., Neal, P.A., Perrin, T.L., Endicott, K.M. and Porterfield, V.T. Toxicology of 1,2-dichloroethane. III. Its acute toxicity and the effect of protective agents. J. Exp. Pharmacol. Ther., 83: 53 (1945).
24. McCollister, D.D., Hollingsworth, R.L., Oyen, F. and Rowe, V.K. Comparative inhalation toxicity of fumigant mixtures. Arch. Ind. Health, 13: 1 (1956).
25. Munson, A.E., Sanders, W.M., Douglas, K.A., Sain, L.E., Kaufmann, B.M. and White, K.L. In vivo assessment of immunotoxicity. Environ. Health Perspect., 43: 41 (1982).
26. National Cancer Institute. Bioassay of 1,2-dichloroethane for possible carcinogenicity. Department of Health, Education and Welfare Publication No. (NIH) 78-1361 (NCI Carcinogenesis Technical Report Series No. 55), Washington, DC (1978).
27. Maltoni, C., Valgimigli, L. and Scarnato, C. Long-term carcinogenic bioassays on ethylene dichloride administered by inhalation to rats and mice. In: Ethylene dichloride: a potential health risk? B.N. Ames, P. Infante and R. Reitz (eds.). Cold Spring Harbor Laboratory, Cold Spring Harbor, NY. p. 3 (1980).
28. Weisburger, E. Carcinogenicity studies on halogenated hydrocarbons. Environ. Health Perspect., 21: 7 (1977).
29. Theiss, J., Stoner, G., Schimkin, M. and Weisberger, E.L. Test for carcinogenicity of organic contaminants of United States drinking water by pulmonary tumor response in strain A mice. Cancer Res., 37: 2717 (1977).
30. Van Duuren, B., Goldschmidt, B., Loewengart, G., Smith, A., Mechionne, S., Seldman, I. and Roth, D. Carcinogenicity of halogenated olefinic and aliphatic hydrocarbons in mice. J. Natl. Cancer Inst., 63: 1433 (1979).
31. Hooper, K., Gold, L. and Ames, B. The carcinogenicity potency of ethylene dichloride in two animal bioassays: a comparison of inhalation and gavage studies. In: Ethylene dichloride: a potential health risk? B.N. Ames, P. Infante and R. Reitz (eds.). Cold Spring Harbor Laboratory, Cold Spring Harbor, NY (1980).
32. Fishbein, L. Potential halogenated industrial carcinogenic and mutagenic chemicals. III. Alkane halides, alkanols and ethers. Sci. Total Environ., 2: 223 (1979).
33. Lane, R.W., Riddle, B.L. and Borzelleca, J.F. Effects of 1,2-dichloroethane and 1,1,1-trichloroethane in drinking water on reproduction and development in mice. Toxicol. Appl. Pharmacol., 63: 409 (1982).
1,2-Dichloroethane has been reported to be one of the most widely used chemicals in the world.2 Annual usage in the Great Lakes Basin has been estimated at 900 million kilograms.3 Canadian production in 1984 was 680 million kilograms, of which 180 million kilograms were exported and 500 million kilograms were consumed domestically.4
Almost all of the domestic 1,2-dichloroethane is used as a chemical intermediate in the preparation of vinyl chloride. About 1% is used as a solvent and as a lead scavenger in leaded gasoline formulations.4 This use has decreased over the past few years and will continue to decrease as the use of lead in fuels drops.5 1,2-Dichloroethane enters the environment through atmospheric emissions, waste effluents to waterways and land disposal of liquid and solid wastes.6 Because of its high volatility, 1,2-dichloroethane that is released to land and water can be expected to be transferred predominantly to the atmosphere. About 1 to 1.7% of total U.S. yearly production was estimated to be released to the environment as emissions.6
Exposure
1,2-Dichloroethane was detected frequently in treated drinking water and raw water samples taken from 30 treatment facilities across Canada in 1979.7 Mean concentrations in treated water were between 4 and 5 µg/L during August and September and less than 1 µg/L in November and December. The overall mean of 31 positive determinations was 3.2 µg/L. Maximum concentrations of 30 and 11 µg/L were found during August and September and during November and December, respectively. 1,2-Dichloroethane was detected at trace levels (0.34 to 0.38 µg/L) in one municipal water supply in Quebec during February 1986, but it was not detected in a later survey, during August 1986, of 18 Quebec municipalities.8 It was also undetected in 1985 and 1986 surveys of 40 municipalities in the four Maritime provinces,9,10 in a 1984 survey of seven municipalities in the Niagara River area11 and in the 1978 to 1985 surveys of 29 municipal water supplies in Alberta.12 The average daily intake* from drinking water containing 1,2-dichloroethane was estimated to be 0.069 µg/kg bw, based on the mean of 3.2 µg/L observed in the Otson study.7
Few data are available on concentrations of 1,2-dichloroethane in foods. Concentrations ranging from 2 to 23 µg/g were found in 11 of 17 different spice oleoresins that had been subjected to solvent extraction with 1,2-dichloroethane.13 Residues of 1,2-dichloroethane in grain products arising from its use as a grain fumigant are expected to be negligible, as this use was suspended in Canada in 1984. The human intake from food sources was estimated to be negligible.6
No Canadian data are available on ambient air concentrations of 1,2-dichloroethane. A review of recent reports revealed that U.S. ambient air concentrations ranged from 0.062 to 6.20 ppb (0.25 to 25 µg/m3) with an intermediate value of 0.62 ppb (2.5 µg/m3).6 Based on these concentrations, the estimated average daily human intake of 1,2-dichloroethane from ambient air is 0.71 µg/kg bw, with a range of 0.07 to 7.14 µg/kg bw*. Atmospheric concentrations near production facilities were in the order of 10 ppb (40 µg/m3), and those near end-use facilities ranged from 0.69 to 0.99 ppb (2.8 to 4.0 µg/m3).6
Inhalation would therefore appear to be the primary route of exposure to 1,2-dichloroethane, with 0.71 µg/kg bw or 91% of an estimated total daily intake of 0.78 µg/kg bw derived from this source. The contribution from food is negligible,6 and estimated intake from drinking water is 0.07 µg/kg bw or 9% of the total.
Analytical Methods and Treatment Technology
The analysis of 1,2-dichloroethane in water at concentrations as low as 0.10 µg/L is possible using the purge and trap method and gas/liquid chromatography instrumentation equipped with a halogen-specific detector.6 The practical quantitation limit (PQL) (based on the ability of laboratories to measure 1,2-dichloroethane within reasonable limits of precision and accuracy) is 5 µg/L.14
The removal efficiency of volatile organic compounds by packed tower aeration and granular activated carbon adsorption for chlorinated aliphatic hydrocarbons has been estimated to be 90 to 93%.14 It would appear that, using advanced technology, a reduction in the concentration of 1,2-dichloroethane in drinking water to less than 1 µg/L would be feasible.
Health Effects
Animal studies with 1,2-dichloroethane have shown that it is rapidly and extensively absorbed via the lungs.15 Uptake from the gastrointestinal tract was efficient and rapid,15 although both the rate and extent were vehicle-dependent,16 peak values for the blood levels being 5 times higher for solutions in water than for solutions in oil. Dermal absorption was shown to be significant in rats, with an absorption rate of 479 nmol/min per square centimetre.17
1,2-Dichloroethane was rapidly distributed to all body tissues.15 As expected from its properties as a general anaesthetic in man, it readily crossed the blood-brain barrier. It was also efficiently transferred to the foetus of the rat.18
There was good evidence to show that the metabolism of 1,2-dichloroethane proceeded via two principal pathways. One involved a saturable microsomal (P-450-mediated) oxidation, leading to the formation of 2-chloroacetaldehyde, the putative 1-chloroso-2-chloroethane and, ultimately, glutathione conjugates. A second pathway involved a cytosolic glutathione-dependent pathway leading to glutathione conjugates, such as S-(2-chloroethyl glutathione).19,20 These metabolites were believed to be involved in covalent binding with DNA, although other metabolites, conjugates and intermediates were also formed.19,20
The elimination of 1,2-dichloroethane followed a two- or three-compartment mathematical model after administration by various routes and was dose-dependent.15,16,21 Material balance studies, following oral and inhalation dosing, have shown that metabolism was the primary elimination mechanism.15 After the administration of an oral dose of 150 mg/kg bw to rats, 29% was excreted unchanged in exhaled air, 5% was metabolized to carbon dioxide and 60% appeared in the urine as metabolites. After an inhalation exposure to 150 ppm (600 mg/m3) for six hours, rats were estimated to have received a total dose of 50 mg/kg bw. Of this dose, 2% was excreted unchanged in air, 7% was metabolized to carbon dioxide and more than 84% was recovered as urinary metabolites.
No epidemiological studies on human health effects induced by 1,2-dichloroethane have been published. The characteristic symptoms of poisoning by chlorinated aliphatic hydrocarbons have been reported in acute and chronic occupational exposures to inhaled 1,2-dichloroethane. Nausea, headache, gastrointestinal disturbances, vomiting, rapid and weak pulse, progressive cyanosis, dyspnoea, loss of consciousness and, ultimately, death have been documented.6 Deaths have also been reported after ingestion of 1,2-dichloroethane, and the acute lethal dose in humans has been estimated to be between 8 and 200 mL (143 to 3571 mg/kg bw).6
Acute exposure studies in animals showed that the severity of effects was dependent on the duration and level of exposure to 1,2-dichloroethane. For rats exposed for five to eight hours via inhalation, adverse effects were not elicited at 200 ppm (800 mg/m3). The first signs of intoxication appeared at a concentration of 300 ppm (1200 mg/m3) and mortality at about 600 ppm (2400 mg/m3).22,23 The acute lethal oral dose in rats was reported to be 680 mg/kg bw.24 In male and female CD-1 mice, the acute lethal oral doses were 489 and 413 mg/kg bw, respectively.25 The LD50 for skin exposures in rabbits was estimated to be between 2.8 and 4.9 g/kg bw.6
In a subchronic study, 15 rats of each sex, eight guinea pigs of each sex, one female and two male rabbits and two male monkeys were exposed to 1,2-dichloroethane vapour at concentrations of 400 and 100 ppm (1600 and 400 mg/m3) for 7 h/d, five days per week for six months. In addition, a further 15 rats of each sex and eight guinea pigs of each sex were exposed to 200 ppm (800 mg/m3) for 30 and 36 weeks, respectively.22 No adverse effects were observed in any of the four species exposed to 100 ppm. At the 200 ppm level, no adverse effects were seen in rats, but slight parenchymatous degeneration of the liver, with some vacuolization, was seen in guinea pigs. Severe effects, including hepatotoxicity and death, were observed in rats and guinea pigs exposed at the 400 ppm level.
Chronic studies with 1,2-dichloroethane in animals have been limited to those that were primarily designed as cancer bioassays. There have been two principal studies, one in which both sexes of rats and mice were dosed by gavage with solutions in corn oil26 and the other in which the same species were exposed by the inhalation route.27
In the National Cancer Institute study,28 the maximum tolerated dose (MTD) and one-half the MTD, determined from preliminary studies, were administered by gavage on five consecutive days per week to 50 Osborne-Mendel rats of each sex, beginning at eight weeks of age, and to 50 B6C3F1 mice, starting at five weeks of age. In addition, 20 animals were given no treatment, and 20 animals were dosed with the vehicle alone for each dose and sex group. Early signs of toxicity in both species indicated that the selected MTDs were inappropriate and necessitated several changes in the administered dosages during the 78 weeks of the study. Thus, the time-weighted average doses received by the male and female rats were 97 and 47 mg/kg bw (MTD and one-half the MTD). For male mice, the doses were 195 and 97 mg/kg bw, and for female mice, 299 and 149 mg/kg bw.
Multiple tumors were induced in both species. A statistically significant increase (P < 0.05) in the incidence of squamous cell carcinomas of the fore-stomach, hemangiosarcomas of the circulatory system and fibromas of the subcutaneous tissue occurred in male rats. There was also a statistically significant increase in the incidence of adenocarcinomas of the mammary gland and hemangiosarcomas of the circulatory system in female rats. Tumours were also observed at other sites, including the spleen, liver, adrenal glands, pancreas, large intestine, subcutaneous tissue and abdominal cavity.
In B6C3F1 mice, there was a statistically significant increase in incidences of hepatocellular carcinomas and alveolar/bronchiolar adenomas in male mice. In female mice, there was a statistically significant increase in incidences of alveolar/bronchiolar adenomas, mammary carcinomas and endometrial tumours.
Supportive evidence for the National Cancer Institute study was available from a pulmonary tumor bioassay29 in which mice were dosed intraperitoneally with 1,2-dichloroethane in tricaprylin and from a skin application study in mice.30 Both of these studies showed that 1,2-dichloroethane could induce a significant increase in tumors at sites (e.g., lung and stomach) remote from the point of application.
No evidence of carcinogenicity was found in a recent lifetime inhalation study in which Sprague-Dawley rats and Swiss mice were exposed to concentrations of 1,2-dichloroethane that ranged from 5 to 150 ppm (20 to 600 mg/m3).27 Nor was there any evidence of carcinogenicity from an earlier subchronic study in which Wistar rats were exposed to 200 ppm (800 mg/m3) 7 h/d, five days per week for six months.22 The apparent discrepancies between inhalation and other routes of exposure in oncogenicity studies have led to considerable discussion.15,31 Among other factors it was considered that the delivered dose in the inhalation studies was lower than that received by the animals in the oral dosing study and was probably too low to elicit a statistically significant tumor response in the number of animals used.
A recent review has concluded that 1,2-dichloroethane causes gene mutations in bacteria, plants, Drosophila and Chinese hamster ovary cells.32 The results of reproductive and teratogenicity testing have indicated that 1,2-dichloroethane has little potential for producing adverse reproductive effects or for adversely affecting the developing foetus unless the exposure is high enough to produce maternal toxicity.6,33
* This estimate was based on a 70-kg man breathing 20 m3 of air per day.
Classification and Assessment
1,2-Dichloroethane is classified in Group II --probably carcinogenic to man (sufficient evidence in animals, inadequate evidence in man) -- on the basis that it has been shown to be carcinogenic in both sexes of two animal species. Incorporating a surface area correction and using the robust linear extrapolation model, one can calculate the unit lifetime risk associated with the ingestion of 1 µg/L 1,2-dichloroethane in drinking water to be 1.6 x 10-6 (based on hemangiosarcomas in the circulatory system of male Osborne-Mendel rats)*.26 These tumors were selected because they represented the most sensitive response and occurred at locations remote from the site of contact with the agent. The estimated concentrations in drinking water corresponding to lifetime risks of 10-5, 10-6 and 10-7 for the same tumor type based on the model described above are 6.2, 0.62 and 0.062 µg/L.
* Average adult body weight = 70 kg; average daily intake of drinking water = 1.5 L.
Rationale
Because 1,2-dichloroethane is classified as a probable human carcinogen in Group II, the maximum acceptable concentration (MAC) is derived based on consideration of available practicable treatment technology and estimated lifetime cancer risks. Because the MAC must also be measurable by available analytical methods, the PQL is also taken into consideration in its derivation.
An interim MAC (IMAC) of 0.005 mg/L (5 µg/L) for 1,2-dichloroethane was established, therefore, on the basis of the following considerations:
(1) The estimated unit lifetime risk associated with the ingestion of 1 µg/L 1,2-dichloroethane in drinking water is 1.6x 10-6 (based on hemangiosarcomas in male rats). Therefore, the estimated lifetime risk associated with the ingestion of drinking water containing 5 µg/L 1,2-dichloroethane is 8x 10-6. The MAC is considered interim because intake in drinking water is approximately 9% of the total intake, and the estimated total risk from all sources therefore will exceed 1 x 10-5, which is above the maximum value in the range considered "essentially negligible."
(2) It is unlikely that 1,2-dichloroethane concentrations are reduced significantly during conventional water treatment processes. However, it is possible to achieve concentrations below 1µg/L using packed tower aeration or granular activated carbon adsorption.
(3) The PQL (based on the ability of laboratories to measure 1,2-dichloroethane within reasonable limits of precision and accuracy) is 5 µg/L.
References
1. Valvani, S.C., Yalnowsky, S.H. and Roseman, T.J. Solubility and partitioning. IV. Aqueous solubility and octanol-water partition coefficients of liquid non-electrolytes. J. Pharm. Sci., 70: 502 (1981).
2. International Agency for Research on Cancer. ARC Monogr. Eval. Carcinog. Risk Chem. Man, 20: 429 (1979).
3. International Joint Commission. 1981 annual report, Committee on Human Health Effects of Great Lakes Water Quality (1981).
4. Corpus Information Services. CPI product profiles: ethylene dichloride (ECD). Toronto (1985).
5. Senes Consultants Ltd. Drinking water criteria reviews for 1,2-dichloroethane, 1,1,1-trichloroethane and 1,1,2,2-tetrachloroethane. Contract for the Ontario Ministry of the Environment (1985).
6. U.S. Environmental Protection Agency. Health assessment document for 1,2-dichloroethane (ethylene dichloride). EPA/600/8-84/006F, Office of Health and Environmental Assessment, Washington, DC (1985).
7. Otson, R., Williams, D.T. and Bothwell, P.D. Volatile organic compounds at thirty potable water treatment facilities. J. Assoc. Off. Anal. Chem., 65: 1370 (1982).
8. Ayotte, P. Micropollutants organiques, campagnes d'échantillonnage 1986. Direction des eaux souterraines et de consommation, Ministère de l'environnement, Gouvernement du Québec (1987).
9. Lebel, G.L. Volatile organic compounds in Atlantic area drinking water sources. Unpublished report, Monitoring and Criteria Division, Environmental Health Directorate, Department of National Health and Welfare (1987).
10. Environment Canada. Data summary reports; federal-provincial drinking water sources, toxic chemical survey, 1985-1986, Newfoundland, Nova Scotia, New Brunswick, Prince Edward Island. Water Quality Branch, Atlantic Region, Moncton (1987).
11. Ontario Ministry of the Environment. Survey of Niagara area and selected Lake Ontario municipal drinking water supplies. Toronto (1984).
12. Alberta Environment. Drinking water survey, 1978-1985. Municipal Engineering Branch, Pollution Control Division, Edmonton (1985).
13. Page, B.D. and Kennedy, P.P.C. Determination of methylene chloride, ethylene dichloride and trichloroethylene as solvent residues in spice oleoresins, using vacuum distillation and electron capture detection. J. Assoc. Off. Anal. Chem., 60: 710 (1975).
14. U.S. Environmental Protection Agency. National primary drinking water regulations; volatile synthetic organic chemicals. Fed. Regist., 50(219): 46902 (1985).
15. Reitz, R.H., Fox, T.R., Ramsey, J.C., Quast, J.F., Langvardt, P.W. and Watanabe, P.G. Pharmacokinetic and macromolecular interactions of ethylene dichloride in rats after inhalation or gavage. Toxicol. Appl. Pharmacol., 62: 190 (1982).
16. Withey, J.R., Collins, B.T. and Collins, P.G. Effect of vehicle on the pharmacokinetics and uptake of four halogenated hydrocarbons from the gastrointestinal tract of the rat. J. Appl. Toxicol., 3: 249 (1983).
17. Tsuruta, H. Percutaneous absorption of organic solvents. II. A method for measuring the penetration rate of chlorinated solvents through excised rat skin. Ind. Health, 15: 131 (1977).
18. Withey, J.R. and Karpinski, K. The fetal distribution of some aliphatic chlorinated hydrocarbons in the rat after vapor phase exposure. Biol. Res. Pregnancy, 6: 79 (1985).
19. Guengerich, F.P., Crawford, W.M., Domradizki, J.Y., McDonald, T.L. and Watanabe, P.G. In vitro activation of 1,2-dichloroethane by microsomal and cytosolic enzymes. Toxicol. Appl. Pharmacol., 55: 303 (1980).
20. Anders, M.W. and Livesey, J.C. Metabolism of 1,2-dichloroethanes. In: Ethylene dichloride: a potential health risk? B.N. Ames, P. Infante and R. Reitz (eds.). Cold Spring Harbor Laboratory, Cold Spring Harbor, NY. p. 331 (1980).
21. Withey, J.R. and Collins, B.T. Chlorinated aliphatic hydrocarbons used in the foods industry: the comparative pharmacokinetics of methylene chloride, 1,2-dichloroethane, chloroform and trichloro-ethylene after i.v. administration in the rat. J. Environ. Pathol. Toxicol., 3: 313 (1980).
22. Spencer, H.C., Rowe, V.K., Adams, E.M., McCollister, D.D. and Irish, D.D. Vapor toxicity of ethylene dichloride determined by experiments on laboratory animals. Ind. Hyg. Occup. Med., 4: 482 (1951).
23. Heppel, L.A., Neal, P.A., Perrin, T.L., Endicott, K.M. and Porterfield, V.T. Toxicology of 1,2-dichloroethane. III. Its acute toxicity and the effect of protective agents. J. Exp. Pharmacol. Ther., 83: 53 (1945).
24. McCollister, D.D., Hollingsworth, R.L., Oyen, F. and Rowe, V.K. Comparative inhalation toxicity of fumigant mixtures. Arch. Ind. Health, 13: 1 (1956).
25. Munson, A.E., Sanders, W.M., Douglas, K.A., Sain, L.E., Kaufmann, B.M. and White, K.L. In vivo assessment of immunotoxicity. Environ. Health Perspect., 43: 41 (1982).
26. National Cancer Institute. Bioassay of 1,2-dichloroethane for possible carcinogenicity. Department of Health, Education and Welfare Publication No. (NIH) 78-1361 (NCI Carcinogenesis Technical Report Series No. 55), Washington, DC (1978).
27. Maltoni, C., Valgimigli, L. and Scarnato, C. Long-term carcinogenic bioassays on ethylene dichloride administered by inhalation to rats and mice. In: Ethylene dichloride: a potential health risk? B.N. Ames, P. Infante and R. Reitz (eds.). Cold Spring Harbor Laboratory, Cold Spring Harbor, NY. p. 3 (1980).
28. Weisburger, E. Carcinogenicity studies on halogenated hydrocarbons. Environ. Health Perspect., 21: 7 (1977).
29. Theiss, J., Stoner, G., Schimkin, M. and Weisberger, E.L. Test for carcinogenicity of organic contaminants of United States drinking water by pulmonary tumor response in strain A mice. Cancer Res., 37: 2717 (1977).
30. Van Duuren, B., Goldschmidt, B., Loewengart, G., Smith, A., Mechionne, S., Seldman, I. and Roth, D. Carcinogenicity of halogenated olefinic and aliphatic hydrocarbons in mice. J. Natl. Cancer Inst., 63: 1433 (1979).
31. Hooper, K., Gold, L. and Ames, B. The carcinogenicity potency of ethylene dichloride in two animal bioassays: a comparison of inhalation and gavage studies. In: Ethylene dichloride: a potential health risk? B.N. Ames, P. Infante and R. Reitz (eds.). Cold Spring Harbor Laboratory, Cold Spring Harbor, NY (1980).
32. Fishbein, L. Potential halogenated industrial carcinogenic and mutagenic chemicals. III. Alkane halides, alkanols and ethers. Sci. Total Environ., 2: 223 (1979).
33. Lane, R.W., Riddle, B.L. and Borzelleca, J.F. Effects of 1,2-dichloroethane and 1,1,1-trichloroethane in drinking water on reproduction and development in mice. Toxicol. Appl. Pharmacol., 63: 409 (1982).
Tuesday, March 16, 2010
RRP Certification
Lead Update – NEW: EPA Certified Renovator RRP
Everyone is familiar with the hazards of lead and understands the need to minimize the exposure to lead – especially to the young. The EPA recently changed its regulations regarding the disturbance of lead based paint. Below we have included some basic information on those changes to keep you up to date. We hope that you find this newsletter useful, and as always, we look forward to providing you with the quality service and information that has made Fuss & O'Neill EnviroScience successful.
Renovation, Repair, and Painting Program (RRP) Details
A new EPA federal regulatory law
Affects contractors, property managers and others who disturb lead-based painted surfaces.
On April 22, 2010, the training, certification, and work practice requirements become effective.
Activities subject to the RRP program include
Remodeling, Repair, Maintenance, Electrical, Plumbing, Painting, Carpentry, Siding, Window
Companies/employees performing this work are required to be RRP certified and employees must be trained in lead safe work practices.
This requirement applies to renovation, repair, and painting work for compensation or wages in target buildings and child-occupied facilities.
Target buildings are those constructed prior to 1978.
A child-occupied facility is a building or portion of a building regularly visited by children under 6 years of age.
Child-occupied facilities may include daycare centers, preschools, and kindergarten classrooms. Common areas in these facilities (ex. bathrooms and cafeterias) regularly used by children under 6, are also included as part of a child-occupied portion in a building.
The new RRP rule also requires that property owners receive certain information before renovation occurs of six square feet or more of painted surfaces in a room for interior projects or more than twenty square feet of painted surfaces for exterior projects.
Fuss & O'Neill EnviroScience offers you EPA-required certification training classes for personnel who will be performing renovation work. Compliance with the new RRP Regulations is essential to prevent costly (up to $32,500) fines and to minimize worker exposure. Upon completion of the training, the participants will have fulfilled the regulatory training obligation and will have the practical knowledge to perform the necessary work safely and legally. Fuss & O'Neill EnviroScience has years of experience working with the lead regulations and how they affect schools and is offering this service to help you maintain or increase your regulatory compliance.
For training course details visit: www.fando.com/News_&_Resources/Releases/?NID=123
Everyone is familiar with the hazards of lead and understands the need to minimize the exposure to lead – especially to the young. The EPA recently changed its regulations regarding the disturbance of lead based paint. Below we have included some basic information on those changes to keep you up to date. We hope that you find this newsletter useful, and as always, we look forward to providing you with the quality service and information that has made Fuss & O'Neill EnviroScience successful.
Renovation, Repair, and Painting Program (RRP) Details
A new EPA federal regulatory law
Affects contractors, property managers and others who disturb lead-based painted surfaces.
On April 22, 2010, the training, certification, and work practice requirements become effective.
Activities subject to the RRP program include
Remodeling, Repair, Maintenance, Electrical, Plumbing, Painting, Carpentry, Siding, Window
Companies/employees performing this work are required to be RRP certified and employees must be trained in lead safe work practices.
This requirement applies to renovation, repair, and painting work for compensation or wages in target buildings and child-occupied facilities.
Target buildings are those constructed prior to 1978.
A child-occupied facility is a building or portion of a building regularly visited by children under 6 years of age.
Child-occupied facilities may include daycare centers, preschools, and kindergarten classrooms. Common areas in these facilities (ex. bathrooms and cafeterias) regularly used by children under 6, are also included as part of a child-occupied portion in a building.
The new RRP rule also requires that property owners receive certain information before renovation occurs of six square feet or more of painted surfaces in a room for interior projects or more than twenty square feet of painted surfaces for exterior projects.
Fuss & O'Neill EnviroScience offers you EPA-required certification training classes for personnel who will be performing renovation work. Compliance with the new RRP Regulations is essential to prevent costly (up to $32,500) fines and to minimize worker exposure. Upon completion of the training, the participants will have fulfilled the regulatory training obligation and will have the practical knowledge to perform the necessary work safely and legally. Fuss & O'Neill EnviroScience has years of experience working with the lead regulations and how they affect schools and is offering this service to help you maintain or increase your regulatory compliance.
For training course details visit: www.fando.com/News_&_Resources/Releases/?NID=123
Tuesday, March 9, 2010
PCBs (Polychlorinated Biphenyls) in Caulk
March 9, 2010
Welcome to the first in a series of regular newsletters that will provide updates and review topics relating to safety in industrial settings including indoor air quality, chemical safety, and environmental issues. The goal of these newsletters is to provide you with relevant and timely information.
This first issue covers a topic that has been on the minds of many of us the past few months – PCBs and caulk. Unfortunately, this has become a widespread issue that has many facilities managers scratching their heads and understandably worried about how to deal with this issue. In this newsletter, I have included some very basic information on how to proceed. I hope that you find this newsletter useful, and we look forward to supporting you with this difficult issue.
-------------------------------------------------------------------------------------
Basic information on how to manage PCBs in caulk:
Found in many buildings built between 1950 and 1978 (less likely outside these dates)
No visual differences between PCB and non-PCB caulk
PCB containing caulk is handled differently than asbestos containing caulk
Contact an expert to clarify the ramifications if planning to test caulk
If concerns about PCBs arise, air testing might be first test performed
If renovating or demolishing, caulk should be tested
Caulk known to contain ≥50 ppm PCBs must be removed
Adjacent material, if significantly contaminated, must also be removed
Remediation and disposal covered under current regulations (40 CFR part 761)
Cost depends on remediation strategy
EPA website: www.epa.gov/pcbsincaulk/
-------------------------------------------------------------------------------------
Fuss & O'Neill EnviroScience is a multi-disciplined industrial hygiene and environmental engineering firm that is positioned to provide a wide variety of environmental services – including PCB remediation. Our experts will work with your facility to ensure safe, timely, and legal removal of PCB contaminated materials. This process will include initial assessment, plan preparation and submission to government agencies, oversight of removal/remediation process, confirmation sampling, data management, and final report preparation. The goal of our service is to properly remediate the contaminated material and provide a working and living environment that is safe for the present and future.
For more information on seminar dates and times contact:
Kevin W. MIller, Ph.D.
kmiller@fando.com
March 9, 2010
Welcome to the first in a series of regular newsletters that will provide updates and review topics relating to safety in industrial settings including indoor air quality, chemical safety, and environmental issues. The goal of these newsletters is to provide you with relevant and timely information.
This first issue covers a topic that has been on the minds of many of us the past few months – PCBs and caulk. Unfortunately, this has become a widespread issue that has many facilities managers scratching their heads and understandably worried about how to deal with this issue. In this newsletter, I have included some very basic information on how to proceed. I hope that you find this newsletter useful, and we look forward to supporting you with this difficult issue.
-------------------------------------------------------------------------------------
Basic information on how to manage PCBs in caulk:
Found in many buildings built between 1950 and 1978 (less likely outside these dates)
No visual differences between PCB and non-PCB caulk
PCB containing caulk is handled differently than asbestos containing caulk
Contact an expert to clarify the ramifications if planning to test caulk
If concerns about PCBs arise, air testing might be first test performed
If renovating or demolishing, caulk should be tested
Caulk known to contain ≥50 ppm PCBs must be removed
Adjacent material, if significantly contaminated, must also be removed
Remediation and disposal covered under current regulations (40 CFR part 761)
Cost depends on remediation strategy
EPA website: www.epa.gov/pcbsincaulk/
-------------------------------------------------------------------------------------
Fuss & O'Neill EnviroScience is a multi-disciplined industrial hygiene and environmental engineering firm that is positioned to provide a wide variety of environmental services – including PCB remediation. Our experts will work with your facility to ensure safe, timely, and legal removal of PCB contaminated materials. This process will include initial assessment, plan preparation and submission to government agencies, oversight of removal/remediation process, confirmation sampling, data management, and final report preparation. The goal of our service is to properly remediate the contaminated material and provide a working and living environment that is safe for the present and future.
For more information on seminar dates and times contact:
Kevin W. MIller, Ph.D.
kmiller@fando.com
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