**INCIDENT REPORT ASSOCIATED**

**INORGANIC ARSENICAL WOOD PRESERVATIVES**

February 2, 2004

Jonathan Chen, Ph.D.

U.S. Environmental Protection Agency

Office of Pesticide Programs

**Antimicrobials Division**

**TABLE OF CONTENTS**

**0.0 INTRODUCTION [3]{.underline}**

**1.0 INCIDENT REPORT DATA ASSOCIATED WITH HEALTH EFFECTS OF CCA
EXPOSURE [3]{.underline}**

**1.1 OPP's Incident Data System (IDS) [4]{.underline}**

**1.2 Poison Control Center (PCC) Data - 1993 through 1996
[5]{.underline}**

**1.3 California Data - 1982 through 1996 [5]{.underline}**

**1.4 Incident Reports Published in Scientific Literature.
[7]{.underline}**

**2.0 REFERENCES [9]{.underline}**

**0.0 INTRODUCTION**

The purpose of this chapter is to review the evidence of health effects
in humans resulting from exposure to chromated copper arsenate (CCA). In
particular, the acute and chronic toxicity, teratogenic/ reproductive
effects, and carcinogenicity are discussed.

A critical evaluation of the health effects of CCA is made difficult by
the fact that few studies have been conducted wherein the specific
exposure of interest was the mixture of chromated copper arsenate . For
a substance that has been widely used for many years by a large number
of people in many geographical areas, it is reasonable to expect that
much information would be written about the substance. Indeed, ample
information is available on physical and chemical properties and on
usage of materials treated with CCA. However, there is a true paucity of
structured studies with credible exposure assessments and appropriate
controls available for review. A few reports are available on
populations exposed to multiple wood preservatives, including CCA. In
contrast, a large body of literature exists on the health effects (acute
and chronic) in humans of exposure to the components in CCA, most
particularly arsenic and to a lesser degree, chromium and copper.
Nevertheless, considerable attention was given to presenting the
information collected during the review in as logical a format as
possible. In this section the potential acute health effects of CCA in
humans, reported as incident reports from different sources, are
summarized.

**1.0 INCIDENT REPORT DATA ASSOCIATED WITH HEALTH EFFECTS OF CCA
EXPOSURE**

4.1 TOXICITY ASSESSMENT OF NONCARCINOGENIC EFFECTSThere are many
incident report data associated with the individual components of CCA.
However, in view of evaluating the health effects of CCA exposure, in
this section, only incidents associated with direct CCA or CCA-treated
wood exposure are evaluated. The following data bases have been
consulted:

1.  **[OPP Incident Data System (IDS)]{.underline}** - The Incident Data
    System of The Office of Pesticide Programs (OPP) of the
    Environmental Protection Agency (EPA) contains reports of incidents
    from various sources, including registrants, other federal and state
    health and environmental agencies, and individual consumers,
    submitted to OPP since 1992. Reports submitted to the Incident Data
    System represent anecdotal reports or allegations only, unless
    otherwise stated. Typically no conclusions can be drawn implicating
    the pesticide as a cause of any of the reported health effects.
    Nevertheless, sometimes with enough cases and/or enough
    documentation risk mitigation measures may be suggested.

2.  **[Poison Control Centers]{.underline}** - as the result of a data
    purchase by EPA, OPP received Poison Control Center data covering
    the years 1993 through 1996 for all pesticides. Most of the national
    Poison Control Centers (PCCs) participate in a national data
    collection system, the Toxic Exposure Surveillance System which
    obtains data from about 65-70 centers at hospitals and universities.
    PCCs provide telephone consultation for individuals and health care
    providers on suspected poisonings involving drugs, household
    products, pesticides, etc.

3.  **[California Department of Pesticide Regulation]{.underline}** -
    California has collected uniform data on suspected pesticide
    poisonings since 1982. Physicians are required, by statute, to
    report to their local health officer all occurrences of illness
    suspected of being related to exposure to pesticides. The majority
    of the incidents involve workers. Information on exposure (worker
    activity), type of illness (systemic, eye, skin, eye/skin and
    respiratory), likelihood of a causal relationship, and number of
    days off work and in the hospital are provided.

4.  **[Literature Published Incident Report]{.underline}**s - Some
    incident reports associated with CCA related human health hazard are
    published in the scientific literature.

**1.1** **OPP's Incident Data System (IDS)**

Please note that the following cases from the IDS do not have
documentation confirming exposure or health effects. . Registrants are
not required to report incidents involving exposure to previously
treated wood, only direct exposure to CCA itself. Therefore, it is
possible that serious adverse effects involving exposures to treated
wood have been missed by this review. Legal claims of severe damage to
eyes and skin including infections requiring amputation have been
reported but only in a cursory way and without enough documentation to
be included in this review.

**[Incident \# I001618-001]{.underline}**

In an incident report received 8/1/91, a Florida man handling arsenic
treated lumber, which was not properly marked with warnings, reported
severe injury. He experienced itching, burning rashes, neurological
symptoms, and breathing problems.

**[Incident \# I002606-001]{.underline}**

In an incident report received 9/10/95, a woman and her child were
exposed to treated wood in their condominium stairs. The child developed
a film on their teeth and the woman developed dermatitis. Reported as a
potential source of inhalation and dermal exposure was sap draining from
the wood.

**[Incident \# I003604-010]{.underline}**

In Virginia, multiple chlorine and wood preservative spills result in
high numbers of fish-kills reported 4/15/92.

**[Incident# I006508-001]{.underline}**

In a report dated 1/1/94, a construction supervisor reported "ruined"
nerves in feet and legs. Believes saw dust and fumes from cutting and
routing much CCA-treated lumber are responsible.

**[Incident #I007587-033]{.underline}**

Washington State Department of Health 1997 annual report includes 219
incidents involving CCA that were investigated by the Washington
Department of Agriculture and the Washington State Departments of Labor
and Health in 1996.

**[Incident#I002365-001]{.underline}**

On 01/01/91 an incident was reported in which pressurized timber was
used as a wall around a vegetable garden. Persons who ate the vegetables
became ill. Arsenic was detected in soil and potato samples.

**[Incident I007824-001]{.underline}**

In an incident report dated 01/01/95, pressure treated wood caused a
chronic rash that persisted for three years. The rash was subsiding
when, in 9/98, the person cut some pieces of CCA-treated wood and the
rash returned.

**[Incident I008468-001]{.underline}**

On 5/16/95 a person received a splinter from CCA-treated wood which then
developed into a severe infection requiring surgery. Dorsal cellulitis,
ascending limphangitis, and acute tenosynovitis were reported.

**1.2** **Poison Control Center (PCC) Data - 1993 through 1996**

No information available.

**1.3** **California Data - 1982 through 1996**

Detailed descriptions of nine cases submitted to the California
Pesticide Illness Surveillance Program (1982-1996) were reviewed. A
brief summary of each of these reported incidences are listed below.
**Table 4-1** presents the types of illnesses reported by year. The
first four number of the incident Case ID is the year the incident was
happened.

**Incident #1987-866.**

Sawdust from CCA-treated wood blew into a clerk's eye. The eye became
swollen and irritated. The report indicated that the clerk had
previously been sawing the wood and had worn safety goggles.

**Incident# 1987-1009.**

Two workers were exposed while working with CCA-treated wood. Dust masks
were worn. Symptoms reported included headache, nausea, shakiness, and
thirst.

**Incident \# 1987-1576**

A worker not wearing protective gloves was handling CCA-treated wood and
wiped his eye with his contaminated hand. Eye swelling and redness was
reported.

**Incident# 1989-1496**

A lumber yard worker scraped his back on a pile of wood. It was unknown
if the wood was treated with CCA. He was wearing proper clothing but
developed a large rash around the initial scratch. Diagnosis of contact
dermatitis was made.

**Incident# 1991-3071**

A worker developed a rash on both forearms after handling CCA-treated
lumber. No gloves or arm protection was worn.

**Incident# 1992-1484**

A lumber yard worker developed contact dermatitis on both palms and
fingers after handling CCA-treated wood.

**Incident#1995-1057**

A lumber mill worker reported nausea and headache radiating down to
shoulders after boring holes in wood to check penetration of CCA
treatment.

**Incident#1996-301**

A wood treatment facility worker experienced eye irritation after CCA
from freshly-treated lumber splashed into his eye.

**Table 4- 1. Cases Due to CCA Exposure in California Reported by Type
of Illness and Year, 1982-1996**

  --------------------------------------------------------------------------
  Year                Illness Type                          
  ------------------- ------------- ----------- ----------- ----------------
                      Systemic^a^   Eye         Skin        Total

  1987                2             2           \-          4

  1989                \-            \-          1           1

  1991                \-            \-          1           1

  1992-96             1             1           1           3

  Total               4             3           3           9
  --------------------------------------------------------------------------

^a^ Category includes cases where skin, eye, or respiratory effects were
also reported.

**1.4** **Incident Reports Published in Scientific Literature.**

As reported by Hay, et al (2000), a 33-year-old man attempted suicide by
ingesting an unknown liquid, later identified as a CCA preservative, 75
minutes before his arrival in the emergency department. He was in severe
respiratory distress, drooling, tachycardia, and hypotensive. There was
an orange color on the palms of both hands. Severe green colored burns
of the buccal mucosa were observed. The larynx was edematous. Blood
tests revealed partially compensated metabolic acidosis. The patient
deteriorated rapidly; the systolic blood pressure dropped to 70 mmHg,
and he passed bloody diarrhea. The patient died 2.5 hours after his
arrival to the hospital.

According to Geschke, et al. (1996) a middle-age man, his wife, and his
father experienced severe abdominal pain, vomiting, and diarrhea one to
two hours after a barbeque. A dog present at the barbeque also seemed
unwell. The man's vomiting and diarrhea subsided after two days but was
followed by tingling of the fingers, facial numbness, and cramps down
the left side of his torso. Within the same week he experienced
exfoliation of the skin on both hands. The fuel for the barbeque was
timber offcuts from a nearby construction site. 3 days following the
incident urinary arsenic levels was 4.9 μmol/L. Food poisoning was ruled
out.

All eight members of a rural Wisconsin family experienced a three-year
period of sensory hyperesthesias, muscle cramps, recurrent pruitic
conjunctivitis, earaches, and otis media, sinusitus, bronchitis,
pneumonia, nose bleeds, easy bruising, and seasonal alopecia ranging
from thinning hair to complete baldness. A four-week old neonate with
recurring viral pneumonia and respiratory exacerbations was treated with
a permanent tracheotomy. All children exhibited recurrent "measle-like"
rashes. The children who went barefoot experienced reddened, thickened
skin on the soles of the feet and babies who crawled on the floor showed
rashes on the legs, arms, and diaper and stomach area which later became
desquamated. The youngest child developed a thrombosed penile artery.
All family members experienced malaise, easy fatigue, and lack of
sensation in the arms, hands, feet, and legs. Severe muscle cramps were
reported in the evening hours. Frequent headaches developed and the two
parents reported "black-outs" sometimes lasting for two hours in
duration. The two youngest children had multiple grand mal seizures from
birth to one year of age. One child was diagnosed by a physician as
having idopathic thrombocytopenic pupua. The mother's fifth pregnancy
resulted in a premature birth with placenta previa or abruptio placenta.
It was determined that the cause of the disorders was due to the use of
CCA-treated marine wood and plywood scraps in a wood stove used inside
the home for heating in winter months. Reported exposure occurred
through ingestion, inhalation, and direct contact with ashes, vapors,
and unburned wood (Peters, et al., 1984).

In 1993, a 36-year-old construction worker with a history of peptic
ulcer disease was admitted to a hospital for severe abdominal pain
localized to the epigastric region, lower left quadrant, or sometimes
everywhere. The pain was accompanied with nausea but no vomiting. An
extensive laboratory work-up was negative for ulcers upon admission.
Additionally, the patient had a negative colonoscopy, nerve conduction
test, and electromylegram. The man received Demerol, Dilaudid, Darvocet,
Percocet, and a low-dose morphine pump but the abdominal pain was still
severe. A urinalysis performed showed urinary arsenic levels of 865
mcg/L (normal less than 100 mcg/L) and the patient was treated for
arsenic toxicity. The patient indicated a definite exposure to
CCA-treated wood for the past several years in his occupation
(Nakawatase and Nakatsuka, 1993).

In 1976 Aitken reported on a 35-year-old self-employed carpenter who was
admitted to a Health Center with reports of the skin of his whole body
feeling cold. He had been working with CCA-treated wood and for the past
four months had been using scraps of the wood as fuel for cooking food.
A urinalysis showed arsenic levels of 230 mcg/L (normal less than 100
mcg/L). He was treated for arsenic exposure.

In 1998, seven cows out of a herd of 37 became ill with diarrhea,
weakness, stumbling, and prostration. Four of the seven cows died within
48 hours of onset of symptoms. All cows in the herd were in otherwise
good health and feed and water was negative for any causative agent. A
burnsite in the pasture was found to contain ashes and incompletely
burned CCA-treated fence posts with an arsenic concentration of 1850
ppm. Upon autopsy the four deceased cows had multifocal abomasal
hemorrhage, severe hyperemia of the small intestine, and arsenic
concentrations in the liver, abomasal contents, and rumen contents of
4.2, 42, and 105 ppm, respectively (Hullinger, et al. 1998).

Reported in 1980, seven Californian construction workers developed
symptoms of arsenic poisoning while building a pier using woods treated
with a combination of ammonium, copper and arsenic (ACA). Workers
urinary arsenic levels were elevated. This incident led to a study
conducted at 3 Californian wood treatment plants with varying levels of
worker exposure. A study of the urinary arsenic levels of workers
illustrates a dose-response relationship with high exposure resulting in
high urinary arsenic levels (Rosenburg, et al. 1980).

**2.0 REFERENCES**

Aitken, I. Arsenic Poisoning Associated with the Burning of
Arsenic-Treated Timber*. Papua New Guinea Medical Journal* 1976
June;19(2):103-104.

Geschecke, A., Lynch, V., Rouch, G., and Golec, R. Arsenic Poisoning
After a Barbeque. *MJA* 1996 Sep;165:296.

Hay, E., Derazon, H., Eisenberg, Y. and Natalia, B. (2000) Suicide by
Ingestion of CCA Wood Preservative. Journal of Emergency Medicine, 19
(2) 159-163.

Hullinger, G., Sangster, L, Colvin, B., and Frazier, K. Bovine Arsenic
Toxicosis From Ingestion of Ashed Copper-Chrome-Arsenate Treated Timber.
*Vet Hum Toxicol* 1998 Jun;40(3):147-8.

Nakawatase, T. and Nakatsuka, C. Arsenic Toxicity in Hawaii: A Case
Report and Review. *Hawaii Medical Journal* 1993 Oct;52(10):258-260.

Rosenberg, M., Landrigan, P, and Crowley, S. Low-Level Arsenic Exposure
in Wood Processing Plants. *Am J Ind Med* 1980;1(1):99-107.

Peters, H., Croft, W., Woolson, E., Darcey, B., and Olson, M. Seasonal
Arsenic Exposure From Burning Chromium-Copper-Arsenate-Treated Wood.
*JAMA* 1984 May;215(18):2393-2396.