Wood Warning Label
in English and Spanish
[see other information and links below]
Inorganic Arsenical Pressure-Treated Wood (including CCA, ACA, and ACZA)
Consumer Safety Information Sheet
For additional information, call toll-free at 1-800-282-0600 or see our website at www.ccasafetyinfo.com
This wood has been preserved by pressure-treatment with an EPA-registered pesticide containing inorganic arsenic to protect it from termite attack and decay. Wood treated with inorganic arsenic should be used only where such protection is important.
Inorganic arsenic penetrates deeply into and remains in the pressure-treated wood for a long time. However, some chemical may migrate from treated wood into surrounding soil over time and may also be dislodged from the wood surface upon contact with skin. Exposure to inorganic arsenic may present certain hazards. Therefore, the following precautions should be taken both when handling the treated wood and in determining where to use and dispose of the treated wood.
Use Site Precautions
All sawdust and construction debris should be cleaned up and disposed of after construction.
Do not use treated wood under circumstances where the preservative may become a component of food or animal feed. Examples of such sites would be use of mulch from recycled arsenic-treated wood, cutting boards, counter tops, animal bedding, and structures or containers for storing animal feed or human food.
Only treated wood that is visibly clean and free of surface residue should be used for patios, decks and walkways.
Do not use treated wood for construction of those portions of beehives which
may come into contact with honey. Treated wood should not be used where it may come into direct or indirect contact with drinking water, except for uses involving incidental contact such as docks or bridges.
Dispose of treated wood by ordinary trash collection. Treated wood should not be burned in open fires or in stoves, fireplaces, or residential boilers because toxic chemicals may be produced as part of the smoke and ashes. Treated wood from commercial or industrial use (e.g., construction sites) may be burned only in commercial or industrial incinerators or boilers in accordance with state and Federal regulations.
Avoid frequent or prolonged inhalation of sawdust from treated wood. When sawing, sanding, and machining treated wood, wear a dust mask. Whenever possible, these operations should be performed outdoors to avoid indoor accumulations or airborne sawdust from treated wood.
When power-sawing and machining, wear goggles to protect eyes from flying particles.
Wear gloves when working with the wood. After working with the wood, and before eating, drinking, toileting, and use of tobacco products, wash exposed areas thoroughly.
Because preservatives or sawdust may accumulate on clothes, they should be laundered before reuse. Wash work clothes separately from other household clothing.
Madera Tratada a Presión Con Arsenico Inorganico (incluye CCA, ACA y ACZA)
Hoja de información sobre seguridad para el consumidor
Para obtener información adicional, llame sin cargo al 1-800-282-0600 o visite nuestro sitio web en www.ccasafetyinfo.com
información para el consumidor
Esta madera ha sido preservada mediante un tratamiento a presión con un pesticida registrado ante la EPA (Agencia de Protección Ambiental) que contiene arsénico inorgánico para protegerla contra el ataque de los insectos y la descomposición. La madera tratada con arsénico inorgánico debe usarse solamente cuando dicha protección sea importante.
El arsénico inorgánico penetra profundamente en la madera tratada a presión y permanece allí por mucho tiempo. Sin embargo, ciertas sustancias químicas pueden migrar con el tiempo desde la madera tratada hacia el suelo circundante y también puede desprenderse de la superficie de la madera al contacto con la piel. La exposición al arsénico inorgánico puede presentar ciertos peligros. Deben tomarse las siguientes precauciones tanto al manipular la madera tratada como al determinar cuándo usarla o deshacerse de ella.
precauciones en el lugar de trabajo
Todo el aserrín y los residuos de la construcción deben limpiarse y desecharse después de la construcción.
No usar la madera tratada bajo circunstancias donde el conservante pueda pasar a ser un componente de alimentos para humanos o animales. Algunos ejemplos serían el uso de la madera tratada con arsénico reciclada y molida para cubrir vegetales, tablas para cortar, mesadas de cocina, lechos para animales y estructuras o contenedores donde se almacenen alimentos para consumo humano o animal.
Sólo la madera tratada que está visiblemente limpia y libre de residuos superficiales debe usarse para patios, cubiertas y pasarelas.
No usar la madera tratada para construir panales que pudieran entrar en contacto con la miel.
La madera tratada no debe usarse donde pueda entrar en contacto directo o indirecto con agua para beber, excepto en aquellos usos que impliquen contacto incidental, como muelles y puentes.
Precauciones en cuanto al manejo
Desechar la madera tratada siguiendo el método para recolección de basura habitual. La madera tratada no debe quemarse en fogatas ni estufas, ni tampoco en calderas residenciales ya que puede emanar sustancias químicas tóxicas como parte del humo y las cenizas. La madera tratada proveniente de usos comerciales o industriales (como de obras en construcción) puede quemarse sólo en incineradores o calderas industriales de conformidad con las reglamentaciones estatales y federales.
Evitar la inhalación frecuente o prolongada del aserrín de madera tratada. Cuando se serruche, lije o tornee, usar una máscara para polvo. Siempre que sea posible, estas actividades deben realizarse al aire libre para evitar la acumulación en espacios interiores y que vuele el aserrín desprendido de la madera tratada.
Cuando se usen sierras o tornos eléctricos, se deben usar anteojos protectores para proteger los ojos contra partículas voladoras.
Usar guantes cuando se trabaje con la madera. Después de trabajar con la madera y antes de comer, beber, ir al baño o fumar, deben lavarse a fondo las zonas expuestas.
Debido a que los conservantes y el aserrín se pueden acumular en la ropa, ésta debe lavarse antes de volver a usar. La ropa de trabajo debe lavarse aparte de la demás ropa de la casa.
1.0 What is CCA and is it harmful?
CCA, or Chromated Copper Arsenate, is a chemical wood preservative and pesticide formulation that is regulated by the Environmental Protection Agency (EPA) under FIFRA(1) . As its name suggests, CCA consists of three principal compounds – arsenic in the form of arsenic pentoxide, chromium, in the form of both hexavalent chromium and trivalent chromium, and copper in the form of copper oxide(2). Two of these chemical components (arsenic and hexavalent chromium) have a notorious reputation as toxins, carcinogens and teratogens, as this article will detail.
CCA originated in 1938 and has been manufactured in three formulations over the years, known as CCA-A, CCA-B and CCA-C respectively. CCA-C, the modern variant of the formula, is the most widely used today. All three formulas contain the same basic ingredients, just in different proportions.
The health hazards and toxicity of CCA are well known. The Minnesota Pollution Control Agency Web site states that "Chromated Copper Arsenate (CCA) is a restricted-use pesticide that is regulated …on the basis of the potential human health hazards associated with long-term, low-level exposure or chronic exposure.(3)"
The concern over CCA in pressure-treated wood products actually began a few years ago, when researchers discovered that the fly ash from incinerators contained high levels of arsenic, a known toxin and carcinogen. Further investigation revealed that CCA-treated wood scrap had been burned as fuel in these incinerators, which in turn released the deadly arsenic in the wood as arsine gas, as well as leaving behind arsenic and chromium in the ash. The levels of arsenic in CCA wood scrap are high enough that one tablespoon of arsenic-tainted CCA wood ash is considered lethal to humans.
To accurately discuss the hazards of CCA-treated wood and the CCA chemical compound itself, it is necessary to discuss CCA's component chemicals in detail, as both arsenic and hexavalent chromium are considered toxic, carcinogenic, and teratogenic(4). It is hoped that this "sum of the parts" discussion will provide for the reader a clearer picture of the inherent problems with CCA by reviewing much of the available medical and scientific literature.
First and foremost, we shall discuss the most infamous chemical in the CCA formula: arsenic.
2.0 The Health Hazards of Arsenic:
Arsenic is the most notorious of the chemicals contained in CCA. It is legendary as a poison - its use dating back thousands of years. Arsenic was known to Aristotle and Socrates, and used by Nero and other villains throughout history to poison their enemies. "Arsenic and Old Lace", a famous play by John Kesselring, easily comes to mind when one thinks about arsenic. Moreover, arsenic is also an element- it is atomic number 33 in our periodic table- and it is probably the most mysterious and multi-faceted element in the periodic chart. It is a metalloid element, but when refined, arsenic is tasteless, odorless and colorless.
Since arsenic is ubiquitous, it is important to differentiate between inorganic arsenic, the type of arsenic found in pesticides and CCA, which is quite toxic, and organic arsenic, which is generally less toxic. In fact, one form of organic arsenic, arsenobetaine, occurs naturally in marine organisms where it is sometimes referred to as "fish arsenic" and is considered "practically nontoxic"(5). Even well-trained toxicologists are known to err on this point, that fish arsenic is not considered toxic, as there have been no reports of long term ill effects from the consumption of seafood. However, its chemical cousins, the inorganic arsenicals, such as the arsenic contained in CCA, are of great concern to all.
The health hazards of arsenic are so wide and so varied that they take up hundreds of pages of text in public health service manuals published by the U.S. government (6). In addition, the California Environmental Protection Agency lists both forms of arsenic (arsenic trioxide and arsenic pentoxide) as carcinogens and developmental toxins under Proposition 65. To understand more about the human health hazards posed by arsenic, we shall review them in detail below. Please note that for brevity, hazards to plants, marine life and animals are omitted.
2.1 General and Systemic Effects of Arsenic Exposure:
Due to the unfortunate exposure of several population groups around the world to arsenic in their water supplies, the adverse health effects of long term arsenic exposure are well known and well documented. They include the following systemic effects:
2.1.1 Toxicological: As previously mentioned, arsenic is a human poison (toxin). Mild chronic poisoning can occur at doses as low as 0.15 mg daily. According to the Journal of Pesticide Reform, "the lethal dose of arsenic for an adult human is between 1 and 2.5 milligrams per kilogram (mg/kg) of body weight"(7). Thus, for a typical adult male weighing 165 pounds (75 kg), the fatal dose can be as little as 75 milligrams.
2.1.2 Dermatological: Skin cancers in the form of basal cell or squamous cell carcinomas, are one of the most serious long-term dermatological health hazards from continuous exposure to arsenic. Other serious dermatological hazards from chronic arsenic exposure can include pre-cancerous actinic keratosis (AK), darkening of the skin (hyperpigmentation), Mees' lines in the fingernails, or hair loss. Papillomas (warts or corns), as well as hyperkeratosis (lesions) of the palms and soles of the feet and torso have also been evidenced. However, less serious effects from arsenic exposure can be manifested as just a skin irritation or rash.
2.1.3 Cardiovascular, Hepatic and Hematological: Cardiovascular side effects affecting the heart and arteries from chronic arsenic exposure include high blood pressure, irregular heartbeat, premature hardening of the arteries (arteriosclerosis), vascular lesions, diabetes mellitus, abnormal heart function and even myocardia. Hazards to the liver (hepatic effects) include cirrhosis, abnormal liver function, as well as symptoms such as "jaundice or simply an enlarged and tender liver"(8). Long term arsenic exposure can produces serious hematological (blood) problems ranging from anemia to more life-threatening ailments such as assorted forms of cytopenia, aplastic anemia and even acute leukemia in rare instances. Blackfoot's disease, a severe vascular disorder that causes a black discoloration of the feet and can lead to gangrene and limb amputation, is a well known complication of long term arsenic exposure, as seen in studies done in Bangladesh and Taiwan.
2.1.4 Respiratory: Continuous arsenic exposure can cause irritation and damage to the mucous membranes in nasal passages and airways, including pharyngitis and rhinitis, and can also aggravate symptoms of asthma. However, the greatest and most prevalent risk of prolonged arsenic exposure via inhalation is lung cancer. (see Carcinogenic effects below).
2.1.5 Gastrointestinal and Renal: The EPA's "Hazard Summary for Arsenic and its Compounds" states that "inhalation exposure to inorganic arsenic has resulted in gastrointestinal effects (nausea, diarrhea, and abdominal pain)"(9). Irritation of the digestive tract has also been common in the case of oral exposure(10). Other symptoms of oral or inhalational arsenic exposure can include dry mouth, severe nausea and vomiting, abdominal pain and cramps, internal bleeding and diarrhea. "Chronic low-dose arsenic ingestion…may produce a mild esophagitis, gastritis, or colitis with respective upper and lower abdominal discomfort. Anorexia, malabsorption and weight loss may be present."(8) The kidneys are also easily damaged by any oral exposure to arsenic, as they serve to excrete the arsenic and therefore tend to accumulate arsenic. This can result in a range of kidney-related problems, from oliguria to complete renal failure.
2.1.6 Neurological: The two most commonly-reported neurological effects of severe or chronic arsenic exposure are "pins and needles" feeling in the hands and feet, and partial paralysis of the limbs. In severe cases, degeneration of the peripheral nervous system has been noted. Elimination of the source of arsenic exposure has in some cases led to improvement over time of some, but not all, of the neurological symptoms. Some permanent damage is not uncommon. Other noted neurological side effects include hearing loss, memory loss, headaches, depression, anxiety attacks, and muscle and joint pain.
2.1.7 Carcinogenic: Chronic oral, dermal or inhalational arsenic exposure can lead to several kinds of cancer. The most common are skin cancer, bladder cancer, and lung cancer, the latter being most prevalent in cases of inhalational exposure. Skin cancer can result from dermal or oral exposure, and patients with arsenic-related skin cancer are more prone to other internal cancers. "More recent epidemiological studies in Taiwan have reported tumors of the lung, liver, bladder and kidney associated with arsenic-induced skin cancers."(11) Other cancers attributed to arsenic exposure include prostrate cancer, hepatic angiosarcoma, nasal cavity cancer, and colon cancer.(12) Because of the numerous and extensive carcinogenic risks posed by arsenic exposure, the Environmental Protection Agency (EPA) has ranked it as an Group A carcinogen.
2.1.8 Reproductive/Developmental: There are serious concerns with arsenic exposure and its potential to cause birth defects in both laboratory animals and humans. New information now suggests that arsenic is also an endocrine disruptor.
Numerous studies have been published since the early 1940s that show that both arsenic and chromium can cause a variety of birth defects in laboratory animals. The few available human studies show similar results. In fact, both arsenic and chromium are listed as known teratogens in the reference manual, "Catalog of Teratogenic Agents, 9th edition" by Thomas Shephard, M.D. In addition, arsenic is listed as a "developmental toxin" by the California Environmental Protection Agency.
One comprehensive study article on arsenic’s potential for reproductive toxicity, "The Role of Arsenic as a reproductive toxin with particular attention to neural tube defects", published in 1996, serves as a comprehensive review of many of the available studies and reaches the conclusion that "arsenic should be considered a probable human reproductive toxin"(13). Moreover, it has also been shown that "humans have been found to be more sensitive to arsenic that most laboratory animals"(14), by a factor of as much as 300 times. This heightened human sensitivity to arsenic's toxicity is likely to also be true from a teratogenic standpoint.
A review of the published scientific studies indicates that laboratory animals exposed to arsenic produced offspring with many different kinds of malformations, including cleft lip, cleft palate, open eye, limb defects, ear deformities, exencephaly, and protruding organs. This was true for several different species of laboratory animals, and the resultant malformations were dependant on both dosage and timing. Here are some excerpts from those studies:
A. In a study entitled "Malformations Induced by Sodium Arsenate" by Ferm and Carpenter, published in 1968 (15), their findings revealed that "administration of intravenous sodium arsenate on day 8 of gestation resulted in exencephaly in fetuses of the golden hamster." [Note: exencephaly is a neural tube disorder in which the brain of the fetus is located outside of the skull. It is generally fatal.]
B. Dr. Ronald Hood published several studies on the teratogenic effects of arsenic. One study published in 1972 entitled "The Teratogenic Effects of Sodium Arsenate in Mice" (16), stated that, "administration of a barely sublethal dose of sodium arsenate to pregnant mice on days 6 to 11 of gestation produced a variety of malformations in the surviving fetuses." (The percentage of grossly malformed mice ranged as high as 63%, depending on the day of treatment.) The malformations included exencephaly, trunk and limb defects, protuding internal organs, and cleft palate and cleft lip.
C. A second 1972 study by Dr. Hood, entitled "Effects of Sodium Arsenite on Fetal Development"(16), stated that "The most common defects associated with arsenite treatment were exencephaly, micrognathia, and open eye… arsenite exposure was also associated with skeletal anomalies." The study also found that "Arsenite is effective [as a teratogenic agent] at a much lower dose level that is arsenate (10 vs. 45 mg/kg)." In a 1978 study, Dr. Hood was also able to generate similar fetal malformations in mice, including open eye, exencephaly, and cleft palate, by administering oral and injected doses of sodium arsenate (16).
D. In a paper published by UCLA’s Center for Environmental Risk Reduction (17), the statement is made that, "In addition to its toxic and carcinogenic effects on the adult population, investigators suspect that arsenic may cause neural tube defects (NTDs) in human embryos exposed in utero; arsenic is a known teratogen in rodents producing NTDs and a variety of other fetal malformations, as well as inducing embryolethality. The few human studies reported have all found associations between high environmental arsenic levels and adverse outcomes of pregnancies."
E. A series of studies were published in 1978 and 1979 by Nordstrom, Beckman and Nordenson (18) that documented the reproductive hazards of arsenic by studying women who worked in a copper smelter in Sweden and were exposed to arsenic dust. These studies showed that due to their exposure, "babies born to women exposed to arsenic dust had a higher than expected incidence of congenital malformations", including lower-than-normal birth weights and spontaneous abortions.
F. In addition, there have been recent studies that detail the concerns about arsenic as an endocrine disruptor. One new study, published this year in the journal Environmental Health Perspectives (19), details how arsenic affects the glucocortoid receptors within the nucleus of the cell itself. It states that "very low levels of arsenic-equivalent to about 10 parts per billion" can cause effects inside the cell that "alter hormonal function in the glucocortoid system".
G. The Florida Center for Solid and Hazardous Waste Management, whose groundbreaking work on how CCA leaches from pressure-treated wood has helped to bring the hazards of CCA-treated lumber to the foreground, is also planning further research testing this year on CCA as a endocrine disruptor using hormonally active chemical assays.
The studies listed above are just a sample of some of the many studies published worldwide that detail the reproductive hazards of arsenic exposure both to animals and humans. However, in spite of this wealth of laboratory data, many scientists and doctors remain skeptical that exposure to arsenic can cause birth defects in human populations. There are even a few recent studies (published by Dr. DeSossa of Mitretek Systems) that refute most, if not all ,of the known studies on the teratogenic hazards of inorganic arsenic compounds(20). However, it should also be noted that the sponsor of these studies is ATOFINA Chemicals, Inc., formerly known as Elf Atochem, a manufacturer of arsenic chemical products.
So, skeptics need only look to the recent class action lawsuit filed by the citizens of Bryan, Texas, who claimed numerous injuries due to their exposure to arsenic that was allegedly released from the Elf Atochem plant. The plant manufactured arsenic trioxide (a cotton defoliant) and pentavalent arsenic acid, an ingredient used in CCA wood preservative. The lawsuit, Lillian Hayden et. al. vs. Elf Atochem North American, claimed that nearby residents who were exposed to arsenic suffered personal injuries and illnesses, including cancers, central nervous system impairment, and assorted birth defects. A cluster of 13 children, born between 1990 and 1993 to families who lived close to the plant, suffered from arsenic-related birth defects such as anencephaly, microencephaly, holoprosencephaly, spina bifida, micro-phthalmia, anophthalmia, renal agenesis, myelomeningocele and coarctation of the aorta. Several of the children died.
Elf Atochem recently settled this lawsuit for $41.4 million. As part of the terms of the settlement, Elf Atochem has agreed "not to produce, use, or handle arsenic or arsenic-containing materials, organophosphates, pesticides, fungicides, herbicides, insecticides and rodenticides at the Bryan Plant, except as necessary for remediation activities" (21).
2.1.9 Mutagenic: The effects of arsenic on the genes, reads like a microcosm of its effects on the entire body as a whole. The deleterious effects noted in studies include "DNA damage and a wide variety of genetic alterations, which can range from simple gene mutations (DNA base pair changes) to grossly visible changes in chromosome structure or number (clastogenesis). Some of these changes may cause genetic damage transmissible to subsequent generations…"(8). Further studies indicate that arsenic may cause genetic damage by interfering with the mechanism by which DNA repairs itself.
3.0 General and Systemic Effects of Chromium Exposure:
Arsenic often gets the most attention in any discussion of the hazards of CCA and pressure-treated wood. However, the hazards of chromium, in particular hexavalent chromium, which is known to be present in CCA-treated wood at levels as high as 50% of the total chromium (22), and is proven to leach from CCA-treated wood, have in many cases gone unmentioned. However, hexavalent chromium is as insidious as its partner arsenic. It is also a known teratogen and is classified as a Group A carcinogen by the EPA. (Note: hexavalent chromium and its related compounds are known by many chemical names: chromium VI, Cr(VI), chromium trioxide, chromic acid, sodium dichromate, and potassium dichromate.)
Furthermore, there are an equivalent number of laboratory studies that detail the health and reproductive hazards of exposures to hexavalent chromium. As done previously with arsenic, we shall review the details from these studies below.
3.1 General Effects:
In the "ToxFaqs for Chromium", the Agency for Toxic Substances and Disease Registry (ATSDR) details the following health hazards related to chromium exposure:
Very heavy exposure: damage to the nose, lungs, stomach and intestines, and possible asthma attacks.
High/moderate or chronic exposure: damage to the nose, (including nasal septal perforation, nasal ulcers/lesions, nasal bleeding, itching, or a constant runny nose), damage to the lungs, which can increase the risk of non-cancerous lung diseases, skin irritation, (including allergic contact dermatitis leading to severe redness and swelling), skin ulcers, changes in pulmonary function, kidney problems such as renal proteinuria, and asthma attacks, if the individual is allergic to chromium.
Very heavy ingestion: stomach upsets, ulcers, convulsions, kidney and liver damage or death.
According to the Journal for Pesticide Reform, additional health hazards from heavy chromium exposure include "diarrhea, blood loss into the digestive tract, and cardiovascular shock followed by liver and kidney necrosis"(7).
In the EPA's "Toxicological Review of Hexavalent Chromium", it is reported that in a study of 155 Chinese people exposed to hexavalent chromium in well water with an estimated dose rate of 0.57mg/kg-day, (Zhang and Li, 1987), "the reported effects at this dose included oral ulcers, diarrhea, abdominal pain, indigestion, vomiting, leukocytosis, and presence of immature neutrophils… Subjects were observed to have elevated white blood cell counts with respect to controls, as well as a higher per capita rate of cancers, including lung cancer and stomach cancer… The study suggests that gastrointestinal effects may occur in humans following exposures to hexavalent chromium at levels of 20 ppm in drinking water."(23).
For hexavalent chromium, the lethal dose is 50 mg/kg of body weight for humans. For a typical adult male weighing 165 pounds (75 kg), the fatal dose would be 3.75 grams.
Exposure to chromium has been known to cause lung cancer since the early 1930s. Numerous epidemiological studies since then have confirmed this fact. Based on extensive research on groups of workers in the chrome plating, tanning and welding industries, it is now known that exposure to hexavalent chromium in the workplace increases the risk of lung cancer in exposed persons by a factor of as much as 1500. As mentioned earlier, the EPA has classified hexavalent chromium as a Group A carcinogen.
There have been numerous studies performed on laboratory animals using both chromium and hexavalent chromium that demonstrate teratogenic effects that parallel those found in tests with arsenic. Here are excerpts from some of those studies:
A. A landmark study published in 1978 by Dr. T.F. Gale (24), "The Embryotoxic Effects of Chromium Trioxide in Hamsters", stated that "the present paper demonstrates that intravenously administered hexavalent chromium trioxide is embryolethal and produces some teratogenic effects in surviving hamster fetuses, including cleft palate and skeletal defects." In this study, Dr. Gale was able to produce cleft palates in 85% of the hamster fetuses with a dose of 7.5 mg/kg of chromium trioxide. Other defects were also elicited, including exencephaly, micrognathia, skeletal defects including unossified vertebrae, abnormal limbs, and internal defects, such as enlarged heart. The study continues by stating that, "Chromium… produces general [teratogenic] effects, i.e. edema and retardation, as well as site-specific damage to the developing secondary palate. …The cause may be related to the fact that chromium delays the overall maturation of some fetuses. In conclusion, chromium trioxide has been demonstrated to be both embryolethal and teratogenic when administered [intravenously] on the 8th day of gestation in hamsters." [Note: the 8th day of gestation for a hamster equates to days 24-28 of gestation in humans.]
B. Dr. Gale also produced other studies(25) on the teratogenic effects of chromium trioxide, including "The effect of time of administration of chromium trioxide on the embryotoxic response in hamsters", published in 1979. In this study, chromium trioxide was injected into pregnant hamsters on days 7,8,9, 10 or 11 of gestation in order to determine the effect of altering the time of treatment on embryotoxicity. The study noted that "cleft palate [was] the major malformation detected…". The study also "suggests a delay in growth as a major factor in chromium-induced cleft palate."
C. In a study published in 1979 by the University of Tokyo(26), "Embryotoxic and fetotoxic effects of chromium trioxide in mice", reported that, "In the group [of mice] treated with 20 mg/kg of CrO3 [chromium trioxide] on day 8 of gestation, external malformations were observed at the highest rate (about 30%, which included a high proportion of cleft palate)." The study concluded that "these results imply that CrO3 has some teratogenic and embryocidal actions as well as effects on the growth of the mouse fetus."
Newer studies have also shown that oral doses of hexavalent chromium compounds cause malformations in laboratory animals, including rats and mice.
D. In a 1989 study by Dr. Trivedi et. al, published in Reproductive Toxicology, mice were given high oral doses of potassium dichromate, (a hexavalent chromium chemical compound), in daily doses of 250 ppm, 500 ppm and 1000 ppm, throughout their entire gestational period. Abnormalities reported by the study included "decreased fetal weight, increased resorptions, and increased abnormalities (tail kinking, delayed ossification of the cranium) in exposed mice… Additional effects included treatment-related increases in abnormalities in the tail, wrist forelimbs and subdermal hemorrhagic patches in the offspring." (27).
E. To further explore the teratogenic effects of hexavalent chromium, Dr. Junaid et al., published a study in Toxicology Letters in 1996, which involved exposing female mice during days 6-14 of their gestations (a critical developmental phase in the gestational period) to potassium dichromate in their drinking water in doses of 250, 500, and 750 ppm. The results were disturbing. The study's authors reported teratogenic effects and malformations which included "retarded fetal development and embryo- and fetotoxic effects including reduced fetal weight, reduced number of fetuses (live and dead) per dam, higher incidences of stillbirths and postimplantation loss in the 500 and 750 ppm dosed mothers… significantly reduced ossification in nasal, frontal, parietal, interparietal, caudal, and tarsal bones was observed in the high-dose group…" (28).
F. In that same year, (1996), a nearly identical study was conducted by Dr. Kanojia et. al and published in Toxicology Letters. This study, however, tested whether pre-gestational exposure to hexavalent chromium would prove to cause reproductive harm to the offspring of exposed female rats. The rats were exposed to doses of 250, 500 and 750 ppm for 20 days prior to fertilization. Chromium was detected in the blood, placenta, and fetuses of these test animals in proportion to the dosage they were given. Once again, severe malformations and birth defects were noted in the offspring of the test animals, including "a reduced number of implantations, retarded fetal development, and embryo- and fetotoxic effects including reduced number of fetuses (live and dead) per dam, and higher incidences of stillbirths and postimplantation loss in the 500 and 750 ppm dosed mothers. Significantly reduced parietal and interparietal ossification was observed in the high-dose group." (29) So, even exposure to hexavalent chromium compounds before gestation causes birth defects in laboratory animals, probably due to the bioacumulation of chromium in the mother and the fetus.
These findings clearly show the cause-and-effect relationship between exposure to hexavalent chromium compounds and birth defects during the time preceding fertilization and the critical early phases of fetal development. It is important to note that in the Junaid study, exposure to hexavalent chromium during the period of days 6-14 of the mice's gestational period produced extensive fetal malformations. This critical time period correlates to days 18-42 of the human gestational period (30).
One can easily extrapolate from these laboratory studies that peri-conceptual (pre-pregnant) and pregnant women run a similar risk of birth defects, if exposed to hexavalent chromium compounds, (such as those found in CCA-treated wood products), during this critical period in their fetus's development. Moreover, since the majority of women are not even aware that they are pregnant until the fetus is 4 weeks old, the risk of handling products that contain known teratogens increases for this group.
4.0 Summary of the Health Hazards of Arsenic, Chromium and CCA:
This article has detailed the general and specific health hazards of two of the chemical compounds, arsenic and chromium. Both are known carcinogens and teratogens. Both are toxic and can cause a wide variety of severe health problems.
The third compound found in CCA, copper (copper oxide) also can be toxic in large quantities and is known to have damaging effects to marine life, such as daphnia and algae, and other aquatic vertebrates. While it is nowhere near as toxic as its cousins, arsenic and chromium, it is by no means a healthful substance.
Thus, the chemical formula for CCA (chromated copper arsenate) is a toxic "witches brew", whose toxicity and carcinogenicity may well be synergistic. That is, the combination of known toxins and carcinogens into a single chemical formula may well result in an even stronger toxin, carcinogen and teratogen. A 1989 study by Drs. Mason and Edwards on the acute toxicity of combining the chemical compounds in CCA came to the same conclusion. It stated that " CCA may present a greater acute toxicity hazard than exposure of the constituent compounds separately." (31)
Still, billions of cubic feet of lumber treated with CCA are sold each year in the United States alone. And until this year, no warning labels or warning literature were available to the average consumer, so that an informed choice could be made.
How many new cancers will result from this "new" exposure? How many new birth defects? In the case of birth defects, it is likely that many have already occurred, but are not being properly attributed to CCA exposure, instead having their cause logged as "multi-factorial". The mothers in Bryan, Texas, who were unknowingly exposed to arsenic are one exception. However, the human studies of the teratogenic effects of these toxic compounds are few. Instead, the general population of "do-it-yourselfers" and construction workers have become the de facto guinea pigs in an uncontrolled, unregulated and unconsented "study".
The California Hazard Evaluation System and Information Service (HESIS) in their "HESIS Fact sheet: Wood Preservatives Containing Arsenic and Chromates" describe the reproductive hazards of CCA like this, "The effects of arsenicals and chromates on the reproductive system are not understood. Both have been shown to cause birth defects when directly injected into pregnant [laboratory] animals. However, it is not certain what these animal studies mean in terms of human risks. We do know that arsenic and chromates can cross the placenta in a pregnant woman to reach a fetus. Because of the effects of these chemicals in animals, and because there is evidence that they may be able to harm genetic material, we recommend that pregnant or nursing women minimize their exposure". They even go on to state a similar point about men's reproductive health, "Because of the possible effects on genetic material, men should also minimize their exposure." (32)
Yes, the wood treatment industry is well aware of the health hazards of CCA. They regularly attend seminars where data is presented on these topics(33). They are aware of the fact that CCA treated wood leaches both arsenic and chromium, and that the public, including children and pregnant women, are handling and being unknowingly exposed to these potentially hazardous compounds. Yet, they continue to drag their feet on solving the problem by switching to safer chemicals, such as ACQ, a CCA alternative. Meanwhile, more and more CCA product is sold, with an average life span of 15 years or more, guaranteeing that it will pose a problem for years to come.
CCA treated wood will undoubtedly go the way of asbestos. It has already been banned by some city, county and state governments. Warning labels now appear on new CCA lumber. Lumber retailers and treated wood manufacturers are coming under increasing pressure and scrutiny. Class action lawsuits have already been filed against the product's manufacturers, and more are likely to occur in the future. Now, more than ever, the time for a ban on CCA is here.
5.0 Notes and references:
(1) FIFRA: Federal Insecticide Fungicide, and Rodenticide Act. See EPA Web site: www.epa.gov/pesticides/fifra.htm .
(2) Osmose Wood Products. (1999, June), Osmose Material Safety Data Sheet (MSDS).
(3) Complete text available online: www.pca.state.mn.us/waste/pubs/lm-cca.pdf
(4) Teratogenic (Def.): Of, relating to, or causing developmental malformations. Webster's Collegiate Dictionary, 10th Edition.
(5) Yamauchi, H., Fowler, B. (1994), "Toxicity and Metabolism of Inorganic and Methylated Arsenicals", Arsenic in the Environment, Part II: Human Health and Ecosystem Effects, Jerome Nriagu, editor, John Wiley & Sons, Inc., pp. 44-45.
(6) U.S Agency for Toxic Substance and Disease Registry (ATDSR). (2000),"Toxocological Profile For Arsenic".
(7) Cox, Carolyn, editor. (1991), "Chromated Copper Arsenate", Journal of Pesticide Reform, Vol. 11 No. 1, pp. 2-6. Complete text available online at this address: http://www.pesticide.org/chromated.pdf .
(8)"Morton, E., Dunnette, D. (1994), "Health Effects of Environmental Arsenic", Arsenic in the Environment, Part II: Human Health and Ecosystem Effects" Jerome Nriagu, editor, John Wiley & Sons, Inc., pp. 20-25.
(9)U.S. Environmental Protection Agency (EPA). (2001, May 17), "Hazard Summary for Arsenic and its Compounds", EPA Web site. Complete text available online: http://www.epa.gov/ttn/uatw/hlthef/arsenic.html .
(10) Agency for Toxic Substances and Disease Registry(ATDSR). (1989, Mar.), "Arsenic - ATDSR Public Health Statement", Available online: http://www.atdsr.cdc.gov/ToxProfiles/phs8802.html .
(11) Naqvi, S., Vaishnavi, C., Singh, H. (1994), "Toxicity and Metabolism of Arsenic in Vertebrates", "Arsenic in the Environment, Part II: Human Health and Ecosystem Effects" , Jerome Nriagu, editor, John Wiley & Sons, Inc., pp. 72-74.
(12) Chen, C., Lin, L. (1994), "Human Carcinogenicity and Artherogenicity induced by Chronic Exposure to Inorganic Arsenic","Arsenic in the Environment, Part II: Human Health and Ecosystem Effects", Jerome Nriagu, editor, John Wiley & Sons, Inc., pp. 109-131.
(13) Shalat, Walker and Finnel. (1996), "The Role of Arsenic as a reproductive toxin with particular attention to neural tube defects", The Department of Veterinary Anatomy and Public Health, Texas A&M University.
(14) Townsend, Solo-Gabrielle, et. al. (2001), "New Lines of CCA-Treated Wood Research: In-Service and Disposal Issues", Florida Center for Solid and Hazardous Waste Management.
(15) Ferm, Carpenter. (1968), "Malformations Induced by Sodium Arsenate", Journal of Reproductive Fertility, Vol. 17.
(16) Hood, R., Bishop, S. (1972, Jan.), "The Teratogenic Effects of Sodium Arsenate in Mice", Archives of Environmental Health, Vol 24, pp. 62-65. Hood, R. (1972), "Effects of Sodium Arsenite on Fetal Development", Bulletin of Environmental Contamination & Toxicology, Vol. 7 NO. 4, pp. 216-222. Hood, R., et. al. (1978), "Prenatal Effects of Oral versus Intrapertoneal Sodium Arsenate in Mice", Journal of Environmental Pathology and Toxicology, Vol. 1., pp.857-864.
(17) UCLA Center for Environmental Risk Reduction. (1997), "Arsenic-Induced Embryopathy: A Mechanistic Approach", available online: http://www.cerr.ucla.edu/arsenic.htm .
(18) Nordstrom, Beckman, Nordenson. (1978), "Occupational and environmental risks in and around a smelter in northern Sweden, Part I. Variations in birth weight.", Hereditas Vol. 88 pp. 43-46. Nordstrom, Beckman, Nordenson. (1978), "Occupational and environmental risks in and around a smelter in northern Sweden, Part II. Frequencies of spontaneous abortion", Hereditas Vol. 88 pp. 51-54. Nordstrom, Beckman, Nordenson. (1979), "Occupational and environmental risks in and around a smelter in northern Sweden, Part VI. Congenital malformations", Hereditas Vol. 90 pp. 291-296.
(19) Kaltreider, R.C., A.M. Davis, J.P. Lariviere and J.W. Hamilton. (2001). "Arsenic Alters the Function of Glucocorticoid Receptor as a Transcription Factor", Environmental Health Perspectives, Vol. 109, pp. 254-251. Available online: http://www.ourstolenfuture.org/NewScience/oncompounds/2001kaltreideretal.htm .
(20) Since the DeSossa studies were funded by grants from the chemical manufacturer, Elf Athochem, a conflict of interest is readily apparent, and these studies cannot be considered independent. However, the need for more studies, particularly human studies of the teratogenic effects of exposure to arsenic and CCA, are warranted.
(21) For details on the settlement for this class action lawsuit, see this Web page: http://www.bryantexasclassaction.com/RevAgreement.html .
(22) One study published in 1992 by the Annals of Occupational Hygiene entitled, "Occupational exposure to chromium, copper and arsenic during work with impregnated wood in joinery shops", stated the following: "Dust from commercially available [CCA] impregnated wood has been found to contain hexavalent chromium, which is regarded as a carcinogen."
(23) U.S. Environmental Protection Agency (EPA). (1998, Aug.), "Toxicological Review of Hexavalent Chromium", pg. 33.
(24) Gale, T.F. (1978, Jul.), "The Embryotoxic Effects of Chromium Trioxide in Hamsters", Environmental Research, Vol. 16 (1-3), pp.101-109.
(25) Gale, T.F., Bunch, J.D. (1979), "The effect of time of administration of chromium trioxide on the embryotoxic response in hamsters", Teratology Vol. 19 (1), pp. 81-86.
(26) Iijima, S., Shimizu, M., Matsumoto, N. (1979), "Embryotoxic and fetotoxic effects of chromium trioxide in mice", Teratology, Vol. 20, pg. 152.
(27) Trivedi, B; Sazena, RC; Murthy, RC; et al. (1989) "Embryotoxicity and fetotoxicity of orally administered hexavalent chromium in mice",. Reproductive Toxicology, Vol. 3, pp. 275-278.
(28) Junaid, M; Murthy, RC; Saxena, DK. (1996) "Embryotoxicity of orally administered chromium in mice: exposure during the period of organogenesis", Toxicology Letters Vol. 84, pp. 143-148.
(29) Kanojia, RK; Junaid, M; Murthy, RC. (1996) "Chromium induced teratogenicity in female rat", Toxicology Letters Vol. 89 pp. 207-213.
(30) Shephard, T. (1998), Catalog of Teratogenic Agents, 9th edition. John Hopkins University Press. Table of Comparative Time Periods of Embryonic and Fetal Development in Humans and Experimental Animals, inside cover flap.
(31) Mason, R., Edwards, I. (1989), "Acute Toxicity of Combinations of Sodium Dichromate, Sodium Arsenate, and Copper Sulphate in the Rat", Comparative Pharmacology and Toxicology, Vol. 93C, No. 1, pp. 121-125.
(32) California Hazard Evaluation System and Information Service (HESIS), (2001), "HESIS Fact sheet: Wood Preservatives Containing Arsenic and Chromates". Available online: www.dhs.cahwnet.gov/ohb/HESIS/arsen2.htm .
(33) Personal Notes from CCA Technical Advisory Group (TAG) Meeting, July 9, 2001, Nokomis, Florida.
source: http://www.bancca.org/Health_Hazards/cca_hlth_hzrds.htm 28jul02
Also see the Environmental Defense Fund's Chemical Scorecard, which summarizes information about health effects, hazard rankings, industrial and consumer product uses, environmental releases and transfers, risk assessment values and regulatory coverage.
EPA Phasing Out Arsenic Treated Wood
Treatment by Dec. 31, 2003
Pesticide Education Office, University of Nebraska-Lincoln
EPA Administrator Christie Whitman announced a voluntary decision by industry to move consumer use of treated lumber products away from a variety of pressure-treated wood that contains arsenic by Dec. 31, 2003, in favor of new alternative wood preservatives. This transition affects virtually all residential uses of wood treated with chromated copper arsenate, also known as CCA, including wood used in play-structures, decks, picnic tables, landscaping timbers, residential fencing, patios and walkways/boardwalks. By Jan. 2004, EPA will not allow CCA products for any of these residential uses.
"This action will result in a reduction of virtually all residential uses of CCA-treated wood within less than two years," said EPA Administrator Christie Whitman. "Today's announcement greatly accelerates the transition to new alternatives, responding to market place demands for wood products that do not contain CCA. This transition will substantially reduce the time it could have taken to go through the traditional regulatory process.""This is a responsible action by the industry," Whitman continued. "Today's action will ensure that future exposures to arsenic are minimized in residential settings. The companies deserve credit for coming forward in a voluntary way to undergo a conversion and retooling of their plants as quickly as possible. The transition to new alternatives will provide consumers with greater choice for their building needs."
The Time Line. The transition period will provide consumers with increasingly more non-CCA treated wood alternatives as the industry undergoes conversion and retooling of their industrial equipment and practices, while also allowing adequate time to convert treatment plants with minimal economic disruption for the industry's employees. Beginning immediately, and over the next 22 months, wood treatment plants will convert to new alternative wood preservatives that do not contain arsenic. In the current year, manufacturers expect a decline in production of CCA products for affected residential uses up to 25 percent, with a corresponding shift to alternatives. During 2003, the companies expect the transition away from CCA to continue and increase, with a decline in production of CCA products for affected residential uses up to 70 percent, with a corresponding shift to alternatives. New labeling will be required on all CCA products, specifying that no use of CCA will be allowed by the wood-treating industry for the affected residential uses after Dec. 31, 2003.
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