**INCIDENT REPORTS ASSOCIATED WITH**

Formaldehyde

(methanal, oxomethane, oxymethylene, methylene oxide,

formic aldehyde, methyl aldehyde)

PC Codes: 043001

January 30, 2008

U.S. Environmental Protection Agency

Office of Pesticide Programs

Antimicrobials Division

TABLE OF CONTENTS

[0.0 INTRODUCTION 1](#introduction)

[1.0 INCIDENT REPORT DATA ASSOCIATED WITH HEALTH EFFECTS
1](#incident-report-data-associated-with-health-effects)

[**1.1 OPP's Incident Data System (IDS)
2**](#opps-incident-data-system-ids)

[**1.2 Poison Control Center (1993 -- 2003)
2**](#__RefHeading___Toc189673198)

[**1.3 California Data - 1982 through 2004
3**](#__RefHeading___Toc189673199)

[**1.4 Incidents and Epidemiological Studies Published in Scientific
Literature
4**](#incidents-and-epidemiological-studies-published-in-scientific-literature)

[**Non-Carcinogenic - Dermal Exposure 4**](#__RefHeading___Toc189673201)

[**Non-Carcinogenic - Inhalation Exposure
5**](#__RefHeading___Toc189673202)

[**Non-Carcinogenic - Oral Exposure 9**](#__RefHeading___Toc189673203)

[**Mutagenic and Carcinogenic Effects
10**](#__RefHeading___Toc189673204)

[2.0 SUMMARY AND CONCLUSION 12](#summary-and-conclusion)

[3.0 REFERENCES 18](#references)

# 0.0 INTRODUCTION

The purpose of this chapter is to review the evidence of health effects
in humans resulting from exposure to formaldehyde.

Two approaches are used in this section:

1.  The potential health effects of formaldehyde in humans, reported as
    incident reports from different sources, are summarized.

2.  A literature search of health effects associated with formaldehyde
    exposure, including results of epidemiological studies, is
    summarized.

# 1.0 INCIDENT REPORT DATA ASSOCIATED WITH HEALTH EFFECTS 

The following databases have been consulted for incident data:

**[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.

**[Poison Control Centers]{.underline}** - as the result of a data
purchase by EPA, OPP received Poison Control Center data covering the
years 1993 through 2003 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.

**[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.

**[Incidents and Epidemiological Studies Published in Scientific
Literature]{.underline}** - Some incident reports and/or epidemiological
studies associated with formaldehyde related human health hazards are
published in the scientific literature.

##  [OPP's Incident Data System (IDS)]{.underline}

Seven incidents reported for human exposure to formaldehyde occurred in
hospital workers (sterilization of instruments and spill clean-up) and
in persons handling or being in close proximity to pesticide
formulations containing this active ingredient (in combination with
other chemicals). Five of the 7 incidents reported were solely due to
inhalation of these chemical vapors. In one incident, where deliberate
and intentional disposal of 9 gallons of formaldehyde (together with
other variable quantities of chemicals) into the school drains exposed
students to several mixtures of chemical vapors. One of the students
affected was hospitalized due to severe respiratory problems. In a
second incident, the person was exposed to a mixture of chemicals
(formaldehyde, glacial acetic acid and sodium meta-bisulfite) in a
holding tank, next to his work station; and suffered from insomnia,
disorientation, bronchitis, sore throat and severe pain in hands and
feet. Following a six month period, this person became totally
non-functional. In the third incident, respiratory and gastro-intestinal
tract problems were observed in 17 hospital workers who cleaned up
spills of chemicals containing 4% glutaraldehyde and 3% formaldehyde. In
the fourth incident, a technician working in proximity to glutaraldehyde
and formaldehyde experienced asthma, arrhythmia, rhinitis, and was
diagnosed as being sensitized to formaldehyde. Similar effects were
observed in the fifth incident of human exposures to formaldehyde in
combination with other chemicals.

The remaining 2 of 7 incidents occurred via combined routes (inhalation,
dermal and ocular). A hospital worker exposed to formaldehyde and
glutaraldehyde developed asthma, arrhythmia, airway disease, mucous in
the throat, shortness of breath, rhinitis, dermatitis, eye irritation,
focusing difficulties and symptoms of corneal burn. In another incident,
a female worker selling industrial/laundry chemicals and pesticides
(chlorinated organophosphorous pesticides, diazinon, malathion,
formaldehyde, methyl ethyl ketone, perchloroethylene, sodium cyanide,
benzene, toluene, vinyl chloride, DDT, chlordane, hepatochlor,
trichloroethene, sodium sulfate, sodium chloride, sodium hypochlorite,
chloroethene, herbicides, volatile organics, acid components, base
neutral compounds and dissolved metals) experienced headaches, mental
confusion, cutaneous T-cell lymphoma, syncopal spells, seizures,
dizziness, loss of equilibrium, nausea, dermatitis, skin irritation and
a rash, that continued for seven years.

The chemical formaldehyde is a known irritant when inhaled and can cause
severe dermal, ocular and gastro-intestinal illnesses. However, the
human incidents reported for formaldehyde do not reflect exposure to
this chemical alone, but in combination with other chemicals.

## 1.2 [Poison Control Center (1993 -- 2003)]{.underline}

There is no one incidence reported in the Poison Control Center Data.

[]{#__RefHeading___Toc189673199 .anchor}**1.3 [California Data - 1982
through 2004]{.underline}**

There are 116 incidences that have been reported in the California
Pesticide Surveillance Program Database (1982-2004) as definitely or
probably related to formaldehyde alone or in combination. As summarized
in Table 1, symptoms associated with eyes are the primary reported
illness in all the associated incidences. Nausea, dizziness, headache,
and sore throat are the primary systemic effects that have been
reported. The primary dermal effects that have been reported are rash,
burning sensation, itching, dry scaling irritation, cracking and
thickened skin, itching, and blisters and rash on hands.

As summarized in Table 2, although there are some people who were unable
to work after exposure for a certain period of time, no one was
hospitalized.

**Table 1. Cases Due to Formaldehyde Exposure in California Reported by
Type of Illness and Year, 1982-2004**

  -----------------------------------------------------------------------------------------
  **Year**    **Illness                                                         
              Type**                                                            
  ----------- ------------ --------- -------- ----------------- --------------- -----------
              **Systemic   **Eye**   **Skin   **Respiratory**   **Combination   **Total**
              ^a^**                  ^b^**                      ^c^**           

  **1982**    1            3         \-       \-                \-              4

  **1983**    1            \-        \-       \-                \-              1

  **1984**    \-           1         1        \-                \-              2

  **1985**    \-           \-        1        \-                \-              1

  **1986**    \-           1         \-       \-                \-              1

  **1987**    \-           2         \-       \-                \-              2

  **1988**    4            2         \-       \-                \-              6

  **1989**    8            7         1        10                9               17

  **1990**    \-           3         \-       2                 1               4

  **1991**    6            12        1        10                11              18

  **1992**    5            7         2        3                 4               13

  **1993**    1            3         \-       2                 1               5

  **1994**    1            2         \-       1                 1               3

  **1995**    4            5         1        2                 3               9

  **1996**    \-           3         2        1                 1               5

  **1997**    1            4         3        3                 3               8

  **1998**    1            5         2        3                 2               9

  **1999**    1            2         \-       1                 1               3

  **2001**    \-           3         \-       \-                \-              3

  **2002**    \-           1         \-       1                 \-              2

  **Total**   34           66        14       39                37              116
  -----------------------------------------------------------------------------------------

^a^ Category include cases where nausea, sore throat, dizziness,
headache and other systemic effects occurred.

^b^ Category includes burning sensation, dry scaling irritation,
cracking and thickened skin, itching, and blisters and rash on hands.

^c^ Category includes combined effects to eye, skin, respiratory and/or
systemic effects.

**Table 2. Number of days lost from work or Hospitalized for Indicated
Number of Days after being Exposed to formaldehyde in California,
1982-2004.**

  ------------------------ ------------------------ ----------------------
                           **Number of Days lost    **Number of Persons
                           from work**              Hospitalized**

  **One day**              15                       \-

  **Two days**             6                        \-

  **3-5 days**             5                        \-

  **6-10 days**            \-                       \-

  **11-16 days**           1                        \-

  **Indefinite ^a^**       1                        \-

  **Unknown^b^**           11                       \-
  ------------------------ ------------------------ ----------------------

Note:

\(a\) An entry of indefinite indicates the event occurred, but the time
period is not known.

(b).An entry of unknown indicates no information was provided.

##  [Incidents and Epidemiological Studies Published in Scientific Literature]{.underline}

There are many reported incidents and epidemiological studies been
published in scientific literature.

[]{#__RefHeading___Toc189673201 .anchor}**[Non-Carcinogenic - Dermal
Exposure]{.underline}**

Formaldehyde is a dermal irritant and a dermal sensitization agent.
Engel and Calnan (1966) reviewed cases of dermatitis noted over three
years (1962-1965) in a car factory among 150 employees who handled
rubber weather strips coated with phenol-formaldehyde resins. A total of
50 cases of dermatitis were observed. The average duration of the
eruption was 12 weeks, however, in three cases it persisted up to 2.5
years. The eruption was generally an erythematous vesicular rash of the
fingers and hands. Exposure durations were for 1 day to two years before
the onset of the eruption, with an average period of contact of 17
weeks. 29 dermatitis patients were patch-tested. Among the patch-tested
patients, four (14%) gave a weak reaction to phenol alone, while 65% had
a positive reaction to the adhesive resins.

Japanese Contact Dermatitis Research Group (1982) summarized patch tests
with 2% formaldehyde (10 mg/cm^2^) performed at 17 Japanese hospitals on
more than 900 patients and healthy volunteer subjects. Irritation was
noticed in 2.78% and a delayed reaction in 2.62% of the patients.

One hundred-sixty-seven doctors, 92 dentists, and 333 nurses were
patch-tested with a standard panel of allergens plus allergens common to
their work environment (Rudzki et al.1989). Among nurses, formaldehyde
was the disinfectant that most frequently caused allergic reactions
(9.6%).

Sneddon (1968) monitored 13 staff members for 3 weeks in a haemodialysis
unit where formalin was used as a sterilant. Patch tests administered
with 3% formalin, 6/13 developed dermatitis, 4 of the 6 were positive in
patch test.

Dermal sensitization is induced only by direct skin contact with
formaldehyde solutions in concentrations higher than 2% (WHO 1989). In
sensitized patients, one of 5 volunteers reacted, under controlled
conditions, to a challenge concentration of 0.01% formaldehyde (Marzulli
and Maibach, 1973). Occluded patch test study of 20 sensitized subjects
and 20 healthy volunteers (Flyvholm et al. 1977). No skin irritation
occurred in the controls exposed to 1% formaldehyde. In sensitized
subjects, the frequency of response decreased with decreasing
formaldehyde concentrations as follows: 9/20 at 0.5%, 3/20 at 0.1%, 2/20
at 0.05%, and 1/20 at 0.025%. WHO (1989) concluded that the lowest patch
test challenge concentration in an aqueous solution reported to produce
a reaction in sensitized persons was 0.05%.

[]{#__RefHeading___Toc189673202 .anchor}**[Non-Carcinogenic - Inhalation
Exposure]{.underline}**

Formaldehyde has a pungent odor detectable at low concentrations, and
its vapor and solutions are known eye and upper respiratory irritants in
human beings. The common effects of formaldehyde exposure are various
symptoms caused by irritation of the mucosa in the eyes and upper
airways.

As summarized by NRC (2007), no reports of deaths in humans resulting
from inhaled formaldehyde were mentioned in the literature, and only a
few case reports of accidental inhalation exposures resulting in human
intoxication were found in the reviews consulted (IARC 1995; ATSDR 1999;
ACGIH 2001; Health Canada 2001; WHO 2002; Liteplo and Meek 2003; NAC
2003). Effects of formaldehyde at high but unreported concentrations
include tracheobronchitis and spasms and edema of the larynx (ACGIH
2001). Pulmonary edema, inflammation, and pneumonia occurred after
exposure to airborne formaldehyde at concentrations of 50 to 100 ppm
(ACGIH 2001).

Exposure to moderate levels of formaldehyde (1-3 ppm) can result in eye
and upper respiratory tract irritation (Weber-Tschoppe et al., 1977;
Kulle et al. 1987). Feinman (1988) states that most people cannot
tolerate exposures to more than 5 ppm formaldehyde in air; above 10-20
ppm symptoms become severe and shortness of breath occurs. High
concentrations of formaldehyde may result in nasal obstruction,
pulmonary edema, choking, dyspnea, and chest tightness (Porter, 1975;
Solomons and Cochrane 1984).

Health effects of low-level exposure to formaldehyde is also been
monitored Main and Hogan (1983). Among 21 subjects exposed to
formaldehyde (0.14 to 1.9 mg/m3) in a mobile home trailer were examined.
18 unexposed controls were included. No differences in lung function
were found between the two groups. However, there were significantly
more complaints of eye and throat irritation, headache, and fatigue
among the exposed.

Allergic reactions and asthma-like conditions also have been reported
following occupational exposures. A medical intern exposure to
formaldehyde over a period of 1 week developed dyspnea, chest tightness,
and edema, following a final 2 hour exposure to high concentrations of
formaldehyde (Porter 1975). Five workers exposed to high concentrations
of formaldehyde from urea-formaldehyde foam insulation experienced
intolerable eye and upper respiratory tract irritation, choking, marked
dyspnea, and nasal obstruction (Solomons and Cochrane, 1984). However,
the concentration of formaldehyde and the contribution of other airborne
chemicals were unknown in both of the reports (OEEHA 1999).

Asthma has also been suggested in formaldehyde exposed occupational
workers (Burge 1985). Bronchial provocation tests with a mean
formaldehyde concentration of 4.8 mg/m3 (range not given) on 15
formaldehyde-exposed workers with symptoms suggesting occupation-related
asthma. 3 subjects with delayed bronchio-spasm and 6 with an immediate
reduction in forced expiratory volume in one second (FEV~1~).

One hundred nine workers and 254 control subjects were studied to
evaluate the effects of formaldehyde on the mucous membranes and lungs.
A modified, respiratory symptom questionnaire and spirometry were admin
to all study participants before and after their work shift, and
formaldehyde levels were determined for each test subject. Over the
course of the monitored work shift, test subjects demonstrated a
dose-dependent excess of irritant symptoms and a statistically
significant decline in certain lung function parameters. Baseline
spirometry values were not significantly different between test and
control groups, and formaldehyde-exposed workers did not report an
excess of respiratory symptoms. Formaldehyde is a dose-dependent
irritant of the eyes & mucous membranes at low-level exposures. It can
exert a small, across-shift effect on airways but after a mean exposure
of 10 yr does not appear to cause permanent respiratory impairment.
(Horvath et. al. 1988)

The effect of formaldehyde exposure on medical students conducting
dissections in the gross anatomy laboratory course was evaluated
(Fleischer 1987). By using self-administered questionnaires designed to
assess the frequency of occurrence of various symptoms associated with
the acute effects of formaldehyde exposure. The questionnaires were
given to a cohort of 1st-yr medical students on completion of the gross
anatomy lab course. Air sampling of formaldehyde levels in the anatomy
labs was carried out on one day during the time in which these students
were conducting dissections. Although the results of the air sampling
showed formaldehyde levels to be well below current occupational
standards, significant numbers of students reported experiencing
symptoms associated with formaldehyde exposure. In addition, it was
found that female students were 3 times more likely to report
formaldehyde-related symptoms than male students.

In a similar study, a group of 24 physical therapy students dissected
cadavers for 3-hour periods per week over 10 weeks. Estimates of
breathing zone formaldehyde concentrations ranged from 0.49 to 0.93 ppm
(geometric mean 0.73±1.22 ppm). The peak expiratory flow rate (PEFR),
the only pulmonary function variable measured in this study, was
measured before and after each exposure period. Mean baseline PEFR
declined by about 2%. Postexposure PEFR means were 1--3% lower than
preexposure PEFR means during the first 4 weeks, but this difference was
not apparent during the last 6 weeks. Fourteen weeks after the end of
the 10-week period, the mean PEFR for the group returned to the
preexposure baseline value (Kriebel et al. 1993).

A prospective evaluation of pulmonary function and respiratory symptoms
among 103 medical students exposed at a TWA concentration that was
generally less than 1 ppm with peak exposures less than 5 ppm was
conducted over a 7-month period. Acute symptoms of eye and respiratory
irritation were significantly associated with such exposure (Uba et al.
1989). Formaldehyde exposed workers (\<1 mg/m3 with some higher peak
values not stated) in a formaldehyde manufacturing factory . Nasal
symptoms in 30 workers, about 40% of the workers had rhinitis with nasal
obstruction and discharge (Wilhelmsson and Holmstrom, 1987).

38 employees exposed to formaldehyde when working with acid-hardening
lacquers and 18 nonexposed control persons employed at the same company
were examined to determine lung function (spirometry and nitrogen
washout), total immunoglobulin blood concentration, and work-related
symptoms. The mean exposure to formaldehyde during an 8-hr workday was
0.40 mg/m3 air, and the mean exposure to peak values was 0.70 mg/m3.
Mean exposure to solvents was low, i.e., approximately 1/10 of the
hygienic effect. The workers were employed for an average of 7.8 years;
estimates of formaldehyde concentrations in workplace air ranged from
0.2 to 2.1 ppm with a TWA mean of 0.3 ppm. Eye, nose, and throat
irritation was more common in exposed persons than in controls. Monday
morning, after two exposure-free days, forced vital capacity (FVC)
values were found to have declined by 0.24 L and forced expiratory
volume in 1 sec (FEV ~1~) by 0.21 L, compared with normal values
(Alexandersson. and Hedenstierna 1988).

Since January 1978 , the Wisconsin Division of Health has collected air
samples and environmental data on mobile homes, conventional homes, and
offices that have particleboard in their construction and foam
insulation. The median formaldehyde concentration was 0.47 ppm (range \<
0. 1-3.68 ppm) and a positive (inverse) association was present between
age of the structure and formaldehyde concentration. The greatest
prevalence of symptoms was for irritation of mucous membranes, but of
the 256 subjects, 53% reported headaches and 38% reported difficulty in
sleeping. Among infants and young children, vomiting, diarrhea, and
respiratory problems were identified as particularly important
conditions. The relationship between smoking and formaldehyde
concentration in the dwelling was examined; smoking did not
significantly increase formaldehyde concentration in the home at the
time of concentration measurement (Dailly et al., 1981a and 1981b;
Hanrahan et al. 1981 and 1984).

On December 1, 1978, a meeting was held in Washington, D.C. to exchange
information dealing with the assessment of potential health problems
associated with formaldehyde emissions following the installation of
urea-formaldehyde foam insulation. Representatives of eleven states
reported on complaints from residents of a total of 39 homes and
apartments. At least two atmospheric samples were collected during each
investigation. Shortly after the meeting, the State of Colorado,
Department of Law, Office of the Attorney General issued a warning. It
stated that, \" ... urea-formaldehyde foam has characteristics which may
adversely affect health...persons exposed to the substance may
experience any one or all of the following symptoms: Difficulty in
breathing, watery eyes, nasal congestion, ear, nose and throat
irritation, upper respiratory stress, nausea, headache, difficulty in
sleeping, disorientation, skin rashes, dizziness, vomiting, diarrhea,
and asthmatic attacks.\" It was noted that 80 percent of the atmospheric
sample results were less than 0.5 ppm formaldehyde (Wilson, 1987)

Respiratory health of plywood workers occupationally exposed to
formaldehyde is been studied in several epidemiological studies. 93
plywood workers were compared with a group of 93 nonexposed subjects.
The plywood workers were employed for a mean of 6.2±2.4 years in
workplaces with estimated formaldehyde air concentrations ranging from
0.22 to 3.48 ppm. The mean product of employment duration times
workplace air formaldehyde concentration was 6.2 ppm/year (sd 2.72
ppm/year) for the exposed group of workers; division of this value by
the average duration of employment (6.2 years) arrives at an estimated
average exposure concentration of 1 ppm formaldehyde. Reported average
respirable and total wood-dust concentrations in workplace air were 0.60
and 1.35 mg/m3, respectively. The percentages of subjects with abnormal
values for a number of pulmonary function variables (e.g., FEV~1~ and
FEF25--75) were significantly higher in the group of plywood workers
compared with a group of nonexposed subjects. Mean values of baseline
FEV1 and FEFR25--75, after adjustment for dust exposure, were reportedly
statistically significantly lower in the exposed group of workers
compared with the nonexposed group (FEV~1~ 2.78 L \[sd 0.41\] versus
2.82 L \[sd 0.3\]; and FEF25--75 3.14 L/second \[sd 0.76\] versus 3.44
L/second \[sd 0.78\]). Malaka and Kodama (1990) noted that although the
small differences were statistically significant, their clinical
significance was unclear.

Biopsy evaluation of the interior turbinate nasal mucosa of 20 men
(average age, 36 years) who had been exposed at 0.1 to 1.1 ppm
formaldehyde during particle board processing for an average of 7 years
(Edling et al. 1985) The histopathological findings were compared to
those from a reference group of 25 men, but who were without
occupational exposure to "irritating agents." Five of the
formaldehyde-exposed men had swollen or dry changes, or both, of the
nasal mucosa; microscopic evaluation revealed a loss of cilia and goblet
cells, squamous metaplasia, and, in some individuals, mild dysplasia.

In a perspective study, Alexandersson, et al (1989) studied the
pulmonary function in wood workers exposed to formaldehyde. Employees
exposed to formaldehyde in the woodworking industry (N = 47) and
nonexposed control subjects (N = 20) were examined in 1980 by spirometry
and the nitrogen washout technique. A transient impairment of lung
function was noted over a work shift. Five years later, 21 subjects were
still experiencing exposure to formaldehyde. A transient decrease in
lung function was again found over a work shift, as evidenced by a
reduction in forced mid-expiratory (FEF25-75) of 0, 15 l/s and an
increase in closing volume (CV%) of 3.0% in nonsmokers. Significant
decreases in forced expired volume in 1 s as a percent of forced vital
capacity (FEV 1.0/FVC) and FEF25-75 were also noted over the 5 y in
nonsmokers (0.4% and 0, 2 l s/y, respectively, after correction for
normal aging). After 4 wk of no exposure (holidays), FEF25-75 and forced
expired vital capacity (FVC, FEV1.0) returned to normal in the smoking
group. Lung function in workers improved less during the holiday. A
dose-response relationship was found between exposure to formaldehyde
and decrease in lung function. Thus, industrial exposure to formaldehyde
causes transient lung function impairment over a work shift, with a
cumulative effect over the years. The impairment, however, can be
reversed with 4 wk of no exposure.

Histological changes in nasal tissue specimens were examined from a
group of 70 workers in a chemical plant that produced formaldehyde and
formaldehyde resins for impregnation of paper, a group of 100 furniture
factory workers working with particle board and glue components, and a
nonexposed, control group of 36 office workers in the same village as
the furniture factories (Holmstrom et al. 1989) . Mean durations of
employment were 10.4 years for the chemical workers and 9.0 years for
the furniture workers. Estimates of personal breathing zone air
concentrations ranged from 0.04 to 0.4 ppm for the chemical workers,
from 0.16 to 0.4 ppm for the furniture workers, and from 0.07 to 0.13
ppm in the late summer for the office workers with a year-round office
worker median reported as 0.07 ppm with no standard deviation. The mean
wood dust concentration in the furniture factory was reported to have
been between 1 and 2 mg/m3. Nasal histology scores ranged from 0 to 4
for the chemical workers, from 0 to 6 for the furniture workers, and
from 0 to 4 for the office workers. The mean histological score for the
chemical workers, but not the furniture workers, was significantly
different from the control score, thus supporting the hypothesis that
the development of nasal lesions is formaldehyde-related and not
obligatorily related to a possible interaction between formaldehyde and
wood dust. The most severe epithelial change (light or moderate
dysplasia) was found in two furniture workers. Among the control workers
(not exposed to wood dust), loss of cilia, goblet cell hyperplasia, and
cuboidal and squamous cell metaplasia replacing the columnar epithelium
occurred more frequently than in the control group of office workers.
Within both groups of formaldehyde-exposed workers, no evidence was
found for associations between histological score and duration of
exposure, index of accumulated dose, or smoking habit.

Horvath et al. (1988) studied the effects of formaldehyde on the mucous
membranes and lungs in an industrial population. 109 workers and 254
control subjects were studied to evaluate the effects of formaldehyde on
the mucous membranes and lungs. A modified, respiratory system
questionnaire and spirometry were administered to all study participants
before and after their work shift, and formaldehyde levels were
determined for each test subject. Estimated TWA formaldehyde
concentrations ranged from 0.17 to 2.93 ppm (mean 0.69 ppm). Median
concentrations of airborne nuisance particulates (i.e., wood dust) in
the particle board plant were 0.38 and 0.11 mg/m3 for total and
respirable particulates, respectively. Over the course of the monitored
work shift, test subjects demonstrated a dose-dependent excess of
irritant symptoms and a statistically significant decline in certain
lung function parameters. Formaldehyde is a dose-depended irritant of
the eyes and mucous membranes at low-level exposures. It can exert a
small, across-shift effect on airways but after a mean exposure of ten
years does not appear to cause permanent respiratory impairment.

[]{#__RefHeading___Toc189673203 .anchor}**[Non-Carcinogenic - Oral
Exposure]{.underline}**

Only limited acute cases with oral exposure to formaldehyde have been
published in scientific literature. Burkhart et al (1990) reported a
case of a 58-year-old man swallowed 4 ounces of formalin (517 mg
formaldehyde/kg) in a suicide attempt. The man was found unconscious by
a co-worker about 1 hour after his shift began. In the emergency room,
the subject regained consciousness but was lethargic. Laboratory results
indicated significant acidosis. Approximately 3 hours after ingesting
the formalin, the patient complained of abdominal pain and began
retching without emesis; he was admitted for observation and treated
with ethanol. The patient\'s abdominal pains became more severe and he
had difficulty breathing. At 5.5 hours after ingestion, the patient
became obtund, and both his respiratory rate and blood pressure fell
significantly; he was intubated and placed on 100% oxygen. Shortly
thereafter, the patient began to experience seizures; treatment with
diazepam and phenytoin was unproductive, but pancuronium was effective
in treating the seizures. Intravenous bicarbonate and ethanol therapies
were begun after the seizures started. The patient was transported for
dialysis, but on arrival, had clinical signs of intravascular
coagulopathy. He subsequently sustained a cardiac arrest from which he
could not be revived. At autopsy, the patient's stomach was hard, white,
and leathery; the esophagus and intestines appeared to be normal.

A 41-year-old woman swallowed 120 mL formalin (37% formaldehyde
solution; 624 mg formaldehyde/kg). The woman was brought to the
emergency room within 30 minutes. The patient complained of abdominal
pain and subsequently lost consciousness. Upon admission, the patient
was cyanotic, apneic, and hypotensive. Laboratory results indicated
significant acidosis. The patient was intubated, ventilation was
initiated, and gastric lavage was performed. Intravenous fluid therapy
consisting of Ringers solution followed by 5% dextrose, epinephrine, and
sodium bicarbonate was initiated and the patient was transferred to
intensive care. The patient was maintained via endotracheal respiration
and dopamine therapy. The patient became anuric approximately 7.5 hours
after admission, and her health continued to deteriorate over the next
day; she died 28 hours after admission (Eells et al. 1981)

Kochhar et al (1986) reported a case of a 26-year-old woman ingested 234
mg/kg formaldehyde. Extensive gastrointestinal damage was exhibited.
Immediately after ingesting formaldehyde, the patient experienced
repeated vomiting with occasional streaks of blood. Anti-emetics and
antacids were prescribed but did not relieve symptoms. Examination of
the oropharynx revealed ulceration and sloughing of the soft palate and
posterior pharyngeal wall. Indirect laryngoscopy revealed ulceration of
the epiglottis, pyriform fossae, and arytenoids. At 96 hours, an upper
gastrointestinal endoscopy revealed that the esophageal mucosa was
edematous and ulcerated with patches of black slough along the entire
length. Areas of the stomach were hyperemic, and there was superficial
ulceration in the distal body and antrum; the duodenal mucosa appeared
normal. The patient underwent a feeding jejunostomy and made an
uneventful recovery. At 4 weeks, a repeat endoscopy revealed a normal
esophagus. The stomach appeared normal with the exception of slight
hyperemia and limited distensibility of the antrum. Barium examination
revealed scarring of the antrum and distal portion of the gastric body.
At 6 weeks, the patient was asymptomatic.

[]{#__RefHeading___Toc189673204 .anchor}**[Mutagenic and Carcinogenic
Effects]{.underline}**

Formaldehyde has been demonstrated to be genotoxic in a wide variety of
experimental systems both in vitro in animal and human cells and in vivo
in animals (IARC 1995). As summarized in Table 3, there are some
epidemiological studies associated with potential formaldehyde exposure
with the mutagenic concern of formaldehyde.

More than forty epidemiological studies have examined the carcinogenic
potential of formaldehyde in animals and humans. The findings from those
studies have been evaluated by a number of agencies and committees
engaged in setting regulatory standards and guidelines (IARC 1995,
2004,, 2006 ; Paustenbach et al. 1997; ATSDR 1999; ACGIH 2001; WHO 2002;
EPA 2003; NAC 2003).

Some epidemiologic studies (ATSDR 1999) have found an excess number of
nasopharyngeal cancers. There are two meta-analyses (Blair et al. 1990;
Partanen 1993) reported a relationship between exposure to formaldehyde
and the occurrence of nasopharyngeal cancer was observed, However, those
associations were relatively weak (relative risks \[RR\] = 2.1 \[95%
confidence interval (CI) = 1.1-3.5\] and 2.7 \[95% CI = 1.4-5.6\] in
Blair et al. \[1990\] and Partanen \[1993\], respectively).

In a more recently published meta-analysis (Collins et al. 1997), this
correction for the underreporting was made. In addition, the exposure
potential for the jobs included in the analysis was evaluated. The
authors concluded that the epidemiological studies do not support a
causal relationship between formaldehyde exposure and nasopharyngeal
cancer.

The follow-up study by Hauptmann et al. (2003, 2004) of the National
Cancer Institute (NCI) retrospective cohort mortality study of U.S.
workers involved in the production or use of formaldehyde represents the
best available data set for quantitative cancer risk assessments of
lymphohematopoietic cancers and nasopharyngeal tumors based on human
data. The NCI study is a large epidemiology study, and it provides
individual quantitative exposure estimates for the workers.

The analyses conducted by the Agency are based on the
lymphohematopoietic (Hauptmann et al., 2003) and nasopharyngeal
(Hauptmann et al., 2004) cancer results from the NCI follow-up study.
This is the largest study of the three independent studies, and it is
the only one of the three with sufficient individual exposure data for
exposure-response modeling. The NCI cohort consisted of 25,619 workers
(88% male) employed in any of the 10 plants prior to 1966; the current
follow-up analyzes 8,486 deaths (178 attributed to lymphohematopoietic
malignancy and 9 to nasopharyngeal cancer). A detailed exposure
assessment was conducted for each worker based on exposure estimates for
different jobs held and tasks performed (Stewart et al., 1986). Exposure
estimates were made using several different metrics - peak exposures,
average intensity, cumulative exposure, and duration of exposure.
Respirator use and exposures to formaldehyde particles and other
chemicals were also considered. Significant increases in relative risk
for lymphohematopoietic cancer were observed primarily for myeloid
leukemia and Hodgkin's disease and for the peak exposure and average
intensity exposure metrics. For the nasopharyngeal cancers, significant
trends were observed for the cumulative and peak exposure metrics.

With respect to the subtypes of lymphohematopoietic malignancy, the
strongest exposure-response relationships were observed for Hodgkin's
disease and myeloid leukemia for both the peak exposure and average
intensity exposure metrics. The (all) lymphohematopoietic malignancies
category also showed a highly significant trend for the peak exposure
metric and a significant trend with the average intensity metric, and
this was the category selected for the cancer risk analyses presented
here. While other lymphohematopoietic cancer subtypes did not exhibit
statistically significant increases, many did suggest increases in
relative risk with formaldehyde exposure, and the subtype analyses were
generally based on small numbers of cases (i.e., lower statistical
power). Furthermore, as noted by the NCI investigators, "although the
accuracy of death certificates for lymphohematopoietic malignancies is
generally high, classification of subtypes of leukemia and lymphoma from
death certificates is less accurate than from hospital records."
Finally, the all lymphohematopoietic cancer category contains the most
data, and the results are more stable.

Formaldehyde has been also been demonstrated to be associated with
leukemia in workers. However, the evidence of causing leukemia or other
nonrespiratory cancers in humans has been considered weaker than that
for high-dose formaldehyde exposures to cause nasopharyngeal cancers on
the basis of pharmacokinetic and toxicologic evidence (BEST, 2007)

The Agency's IRIS program grouped formaldehyde as a B1 (probable human
carcinogen) based on limited evidence in humans, and sufficient evidence
in animals. Human data include nine studies that show statistically
significant associations between site-specific respiratory neoplasms and
exposure to formaldehyde or formaldehyde-containing products. An
increased incidence of nasal squamous cell carcinomas was observed in
long-term inhalation studies in rats and in mice. The classification is
supported by in vitro genotoxicity data and formaldehyde\'s structural
relationships to other carcinogenic aldehydes such as acetaldehyde.

# SUMMARY AND CONCLUSION 

Although there are many reported incidences been reported associated
with formaldehyde exposure, only limited incidences are associated with
when formaldehyde is used as for antimicrobial agent (biocide).
Formaldehyde is a dermal irritant and a dermal sensitizer. The primary
dermal effects that have been reported are rash, burning sensation,
itching, dry scaling irritation, cracking and thickened skin, itching,
and blisters and rash on hands. Acute exposure, symptoms associated with
eyes are the primary reported illness in all the associated incidences.
Nausea, dizziness, headache, and sore throat are the primary systemic
effects that have been reported. Allergic reactions and asthma-like
conditions also have been reported following occupational exposures.
Only limited acute cases with oral exposure to formaldehyde have been
published in scientific literature. Formaldehyde has been demonstrated
to be genotoxic in many reported epidemiological studies. Formaldehyde
exposure has been associated respiratory cancer (especially
nasopharyngeal cancer), leukemia, and other nonrespiratory cancers in
humans. The Agency's IRIS program grouped formaldehyde as a B1
carcinogen.

+----------+---------------------+-------------------------------------+
| **Table  |                     |                                     |
| 3. Human |                     |                                     |
| Epidemi  |                     |                                     |
| ological |                     |                                     |
| Studies  |                     |                                     |
| as       |                     |                                     |
| sociated |                     |                                     |
| P        |                     |                                     |
| otential |                     |                                     |
| M        |                     |                                     |
| utagenic |                     |                                     |
| Activity |                     |                                     |
| of       |                     |                                     |
| Form     |                     |                                     |
| aldehyde |                     |                                     |
| Ex       |                     |                                     |
| posure** |                     |                                     |
+==========+=====================+=====================================+
| **R      | **Study Design**    | **Results**                         |
| eference |                     |                                     |
| Infor    |                     |                                     |
| mation** |                     |                                     |
+----------+---------------------+-------------------------------------+
| Ballarin | 15 nonsmoking       | Nasal mucosal cells from exposed    |
| C, Sarto | workers (8 males, 7 | workers exhibited significantly     |
| F,       | females) who worked | increased incidence of micronuclei  |
| Gi       | in a plywood        | (0.9 versus 0.25 for controls),     |
| acomelli | factory for         | chronic inflammation, and a         |
| L, et    | cytopathologic      | significantly higher frequency of   |
| al.      | changes in nasal    | squamous metaplasia cells           |
| 1992.    | mucosal cells, were | (histological score: 2.3 versus     |
| Micron   | evaluated and the   | 1.6) than cells from control        |
| ucleated | results were        | workers. Micronuclei were found     |
| cells in | compared to matched | mainly in the ciliated cells.       |
| nasal    | controls. Mean      |                                     |
| mucosa   | levels of exposure  |                                     |
| of       | to formaldehyde     |                                     |
| form     | ranged from 0.07 to |                                     |
| aldehyde | 0.08 ppm in the     |                                     |
| -exposed | sawmill and         |                                     |
|          | shearing press      |                                     |
| workers. | departments to 0.32 |                                     |
| Mutat    | ppm in the          |                                     |
| Res      | warehouse. The      |                                     |
| 280:1-7. | total range of      |                                     |
|          | exposure in all     |                                     |
|          | areas containing    |                                     |
|          | formaldehyde vapors |                                     |
|          | was 0.06--0.49 ppm. |                                     |
|          | Workers were also   |                                     |
|          | exposed to wood     |                                     |
|          | dust.               |                                     |
+----------+---------------------+-------------------------------------+
| Berke,   | Cytologic study of  | Among formaldehyde-exposed workers  |
| J.H.     | the nasal mucosa of | with personal monitoring data,      |
| (1987):  | four groups of      | exposures ranged from 0.02 to 2.0   |
| C        | employees either    | ppm. A statistically significant    |
| ytologic | engaged in          | (p=0.04) overall prevalence of      |
| Exa      | phenol-formaldehyde | nasal erythema, edema, and fissures |
| mination | impregnation or who | among the nonsmokers was found      |
| of the   | were not known to   | which Berke concluded was           |
| Nasal    | have experienced    | consistent with localized tissue    |
| Mucosa   | regular             | irritation as a consequence of      |
| in       | occupational        | formaldehyde exposure. Two people   |
| Form     | formaldehyde        | with nasal polyps were confirmed    |
| aldehyde | exposure. Berke     | among the 42 formaldehyde workers,  |
| -Exposed | used historical,    | and none were found among the 38    |
| Workers. | environmental       | controls. Berke concluded that      |
| J.       | occupational        | there was, however, no significant  |
| Occup.   | hygiene data where  | association between formaldehyde    |
| Med.     | formaldehyde        | exposure and "abnormal" nasal       |
| 29:      | excursions to 9 ppm | mucosal cytology after              |
| 681-684. | were documented     | simultaneously controlling for age  |
|          | (with alleged       | and smoking habits.                 |
|          | excursions to 15    |                                     |
|          | ppm). Smoking       |                                     |
|          | habits, measured as |                                     |
|          | pack-years, were    |                                     |
|          | very similar for    |                                     |
|          | the exposed and     |                                     |
|          | control groups.     |                                     |
+----------+---------------------+-------------------------------------+
| Ch       | The lymphocytes     | The level of chromosomal            |
| ebotarev | sister chromatic    | aberrations in formaldehyde-exposed |
| AN,      | exchanges (SCEs) of | workers was 2.76%, which was        |
| Titenko  | 40 wood-working     | significantly elevated compared to  |
| NV,      | employees and 22    | spontaneous chromosomal aberrations |
| S        | control workers     | in controls (1.64%, p\<0.05). The   |
| elezneva | were examined for   | incidence of chromosomal breakage   |
| TG, et   | chromosomal         | in exposed workers (2.95%) was      |
| al.      | aberrations, SCEs,  | significantly greater than the      |
| 1986.    | and unscheduled DNA | frequency of spontaneous breakage   |
| Co       | repair or           | (1.64%, p\<0.05). No differences    |
| mparison | synthesis.          | between exposed and control         |
| of the   |                     | subjects were seen for SCEs either  |
| ch       |                     | at baseline (8.01 versus 8.24       |
| romosome |                     | exchanges per cell) or after        |
| aber     |                     | induction with the genotoxin        |
| rations, |                     | thiotepa (23.32 versus 25.78        |
|          |                     | exchanges per cell). There were no  |
| sister   |                     | differences between                 |
| c        |                     | formaldehyde-exposed and control    |
| hromatid |                     | samples in unscheduled DNA repair   |
| ex       |                     | rates at baseline (335.2 versus     |
| changes, |                     | 341.9) or after treatment with      |
| and      |                     | hydroxyurea (179.8 versus 194.2).   |
| uns      |                     | However, when treated with          |
| cheduled |                     | thiotepa, unscheduled DNA repair    |
| DNA      |                     | rates in lymphocytes from           |
| s        |                     | formaldehyde-exposed workers were   |
| ynthesis |                     | lower than those from control       |
| when     |                     | workers (217.2 versus 270.4,        |
| ev       |                     | p\<0.05).                           |
| aluating |                     |                                     |
| the      |                     |                                     |
| muta     |                     |                                     |
| genicity |                     |                                     |
| of       |                     |                                     |
| envir    |                     |                                     |
| onmental |                     |                                     |
| factors. |                     |                                     |
| Cytol    |                     |                                     |
| Genet    |                     |                                     |
| 2        |                     |                                     |
| 0:21-26. |                     |                                     |
+----------+---------------------+-------------------------------------+
| Fleig I, | Chromosome analyses | There were no differences between   |
| Petri N, | were performed on   | exposed and control groups in the   |
| Stocker  | 15 exposed and 15   | incidence of chromosomal            |
| WG, et   | non-exposed         | aberrations. The mean frequency of  |
| al.      | employees from      | aberrant metaphases among           |
| 1982.    | formaldehyde        |                                     |
| Cyt      | manufacturing       | formaldehyde-exposed persons was    |
| ogenetic | facilities. Exposed | 3.07 versus 3.33% in controls. No   |
| analyses | workers had an      | correlation was found between       |
| of blood | average duration of | formaldehyde exposure levels and    |
| lym      | exposure of 28      | the number of aberrant metaphases.  |
| phocytes | years (range 23--35 |                                     |
| of       | years). Average     |                                     |
| workers  | exposure            |                                     |
| exposed  | concentrations did  |                                     |
| to       | not exceed 5 ppm    |                                     |
| form     | prior to 1971 and 1 |                                     |
| aldehyde | ppm after 1971. The |                                     |
| in       | formaldehyde        |                                     |
| form     | exposures of        |                                     |
| aldehyde | individual workers  |                                     |
| manuf    | were classified     |                                     |
| acturing | into one of the     |                                     |
| and      | three following     |                                     |
| pro      | categories:         |                                     |
| cessing. | Category 1:         |                                     |
| J Occup  | exposure 25% of    |                                     |
| Med      | the maximum         |                                     |
| 24:10    | workplace           |                                     |
| 09-1012. | concentration       |                                     |
|          | (MAK); Category 2:  |                                     |
|          | exposure up to a    |                                     |
|          | maximum of 60% MAK; |                                     |
|          | and Category 3:     |                                     |
|          | exposure up to 100% |                                     |
|          | of the MAK.         |                                     |
|          | Peripheral blood    |                                     |
|          | samples were        |                                     |
|          | collected from each |                                     |
|          | worker and          |                                     |
|          | lymphocytes were    |                                     |
|          | separated and       |                                     |
|          | cultured for 70--72 |                                     |
|          | hours at 37 C.    |                                     |
|          | Cells were          |                                     |
|          | subsequently fixed  |                                     |
|          | and examined for    |                                     |
|          | chromatid- and      |                                     |
|          | chromosome-type     |                                     |
|          | aberrations.        |                                     |
+----------+---------------------+-------------------------------------+
| Goh &    | The chromosomal     | Aneuploidies, chromosomal structure |
| Cestero  | patterns of direct  | abnormalities, and chromosomal      |
| (1979)   | bone                | breaks were seen in the metaphase.  |
| Chr      |                     |                                     |
| omosomal | marrow preparations |                                     |
| abnor    | from 40 patients    |                                     |
| malities | undergoing          |                                     |
| in       | maintenance         |                                     |
|          | haemo-dialysis were |                                     |
| mai      | studied. During the |                                     |
| ntenance | period of this      |                                     |
| hemo     | study, each patient |                                     |
| dialysis | could have received |                                     |
| p        | up to 126 ± 50 mg   |                                     |
| atients. | of formaldehyde     |                                     |
| J. Med., | during each         |                                     |
| 10:      | dialysis.           |                                     |
| 167-174. |                     |                                     |
+----------+---------------------+-------------------------------------+
| Shaham   | The formation of    | Exposure to formaldehyde resulted   |
| J,       | DNA-protein cross   | in a significant increase in the    |
| Bomstein | links in peripheral | incidence of DNA-protein cross      |
| Y,       | white blood cells   | links. Mean (±sd) incidences in     |
| Meltzer  | of occupationally   | exposed and nonexposed workers were |
| A, et    | exposed workers     | 28±6 and 22±6%, respectively.       |
| al.      | (n=12) and          | Within the exposed workers group,   |
| 1996a.   | unexposed controls  | technicians had significantly       |
| DNA      | (n=8) was measured. | greater levels of DNA-protein cross |
| -protein | The average length  | links than physicians (32.3±4.3 and |
| cro      | of occupational     | 26.3±4.4%, respectively). A linear  |
| sslinks, | exposure was 13     | relationship between years of       |
| a        | years. All subjects | exposure and DNA-protein cross      |
| b        | completed a         | links formation was also detected.  |
| iomarker | questionnaire       | When the data were analyzed         |
| of       | regarding           | considering worker smoking habits,  |
| exposure | demographics,       | DNA-protein cross links were        |
| to       | occupational and    | consistently elevated among         |
| formal   | medical background, | formaldehyde-exposed versus         |
| dehyde - | and smoking and     | corresponding controls (p=0.03).    |
| *in      | hygiene habits.     | The authors concluded that          |
| vitro*   | Venous blood        | DNA-protein cross links can be used |
| and *in  | samples were        | as a biomarker of exposure;         |
| vivo*    | collected from each | however, the assay measures         |
| studies. | worker and were     | DNA-protein cross links in general, |
| Carcin   | processed to        | not those specific to formaldehyde  |
| ogenesis | isolate DNA-protein | cross link formation.               |
| 17:      | cross links.        |                                     |
| 121-125. | Personal and room   |                                     |
|          | concentrations of   |                                     |
|          | formaldehyde were   |                                     |
|          | collected at        |                                     |
|          | various periods     |                                     |
|          | during the working  |                                     |
|          | day among the       |                                     |
|          | exposed subjects,   |                                     |
|          | with formaldehyde   |                                     |
|          | room concentrations |                                     |
|          | ranging from 1.38   |                                     |
|          | to 1.6 ppm.         |                                     |
|          | Personal monitoring |                                     |
|          | devices indicated   |                                     |
|          | formaldehyde        |                                     |
|          | concentrations of   |                                     |
|          | 2.8--3.1 ppm during |                                     |
|          | peak work and an    |                                     |
|          | average             |                                     |
|          | concentration of    |                                     |
|          | 1.46 ppm at times   |                                     |
|          | when work was       |                                     |
|          | usually completed.  |                                     |
+----------+---------------------+-------------------------------------+
| Vasudeva | The effects of      | There was no difference in the      |
| N, Anand | formaldehyde        | incidences of chromosomal           |
| C. 1996. | exposure on the     | aberrations among the exposed and   |
| Cyt      | incidence of        | control groups. The mean            |
| ogenetic | chromosomal         | frequencies of aberrant metaphases  |
| ev       | aberrations in      | in the exposed and control groups   |
| aluation | peripheral blood    | were 1.2 and 0.9%, respectively.    |
| of       | lymphocytes of 30   | There was no correlation between    |
| medical  | medical students    | reported irritant effects of        |
| students | exposed to          | formaldehyde and the number of      |
| exposed  | formaldehyde vapors | aberrant metaphases, and the        |
| to       | at concentrations   | authors concluded that exposure to  |
| form     | of \<1 ppm for 15   | formaldehyde at concentrations seen |
| aldehyde | months were         | in this study does not lead to      |
| vapor in | examined.           | chromosomal aberrations.            |
| the      | Questionnaires      |                                     |
| gross    | established that    |                                     |
| anatomy  | the participants    |                                     |
| di       | were healthy and    |                                     |
| ssection | had insignificant   |                                     |
| level. J | medical histories.  |                                     |
| Am Coll  |                     |                                     |
| Health   |                     |                                     |
| 44:      |                     |                                     |
| 177-179. |                     |                                     |
+----------+---------------------+-------------------------------------+
| Yager    | Peripheral          | Breathing-zone monitoring revealed  |
| JW, Cohn | lymphocytes from    | mean exposure of 1.2 ppm (range     |
| KL,      | eight anatomy       | 0.73--1.95 ppm). A small average    |
| Spear    | students exposed to | increase in the incidence of SCE    |
| RC, et   | for                 | was observed in the lymphocytes of  |
| al.      | maldehyde-embalming | the students after exposure         |
| 1986.    | solution over a     | (7.2/cell) when compared to values  |
| Sister-c | 10-week course were | obtained before exposure            |
| hromatid | examined for sister | (6.39/cell)                         |
| e        | chromatid exchange  |                                     |
| xchanges | (SCE). Results were |                                     |
| in       | compared with       |                                     |
| lym      | preexposure values  |                                     |
| phocytes | for each student.   |                                     |
| of       |                     |                                     |
| anatomy  |                     |                                     |
| students |                     |                                     |
| exposed  |                     |                                     |
| to       |                     |                                     |
| formal   |                     |                                     |
| dehyde-e |                     |                                     |
| mbalming |                     |                                     |
| s        |                     |                                     |
| olution. |                     |                                     |
| Mutat    |                     |                                     |
| Res      |                     |                                     |
| 174:     |                     |                                     |
| 135-139. |                     |                                     |
+----------+---------------------+-------------------------------------+

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