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Reference Dose for Chronic Oral Exposure (RfD)

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[UPDATE] The (inhaltion) portion of this assessment is currently under development and the latest draft can be 

found at, IRIS Toxicological Review of Formaldehyde (Inhalation) (External Review Draft)

0419

Formaldehyde; CASRN 50-00-0

Human health assessment information on a chemical substance is included in the IRIS database 

only after a comprehensive review of toxicity data, as outlined in the IRIS assessment development 

process. Sections I (Health Hazard Assessments for Noncarcinogenic Effects) and II (Carcinogenicity 

Assessment for Lifetime Exposure) present the conclusions that were reached during the 

assessment development process. Supporting information and explanations of the methods used to 

derive the values given in IRIS are provided in the guidance documents located on the IRIS 

website. 

STATUS OF DATA FOR Formaldehyde

File First On-Line 10/01/1989

Category (section) Status Last Revised
Oral RfD Assessment (I.A.) on-line 09/01/1990 

Inhalation RfC Assessment (I.B.) no data

Carcinogenicity Assessment (II.) on-line 05/01/1991 

_I. Chronic Health Hazard Assessments for Noncarcinogenic 

Effects

_I.A. Reference Dose for Chronic Oral Exposure (RfD)

Substance Name — Formaldehyde

CASRN — 50-00-0

Last Revised — 09/01/1990

The oral Reference Dose (RfD) is based on the assumption that thresholds exist for certain toxic 

effects such as cellular necrosis. It is expressed in units of mg/kg-day. In general, the RfD is an 

estimate (with uncertainty spanning perhaps an order of magnitude) of a daily exposure to the 

human population (including sensitive subgroups) that is likely to be without an appreciable risk of 

deleterious effects during a lifetime. Please refer to the Background Document for an elaboration of 

these concepts. RfDs can also be derived for the noncarcinogenic health effects of substances that 

are also carcinogens. Therefore, it is essential to refer to other sources of information concerning 

the carcinogenicity of this substance. If the U.S. EPA has evaluated this substance for potential 

human carcinogenicity, a summary of that evaluation will be contained in Section II of this file. 

__I.A.1. Oral RfD Summary

Critical Effect Experimental Doses* UF MF RfD

Reduced weight gain,

histopathology in rats

Rat 2-Year Bioassay

Til et al., 1989

NOAEL: 15 mg/kg/day

LOAEL: 82 mg/kg/day

100

 

1

 

2E-1

mg/kg/day

 

* Conversion Factors: none 

__I.A.2. Principal and Supporting Studies (Oral RfD)
Til, H.P., R.A. Woutersen, V.J. Feron, V.H.M. Hollanders, H.E. Falke and J.J. Clary. 1989. Two-year 

drinking water study of formaldehyde in rats. Food Chem. Toxicol. 27: 77-87. 

Formaldehyde was administered daily in drinking water to Wistar rats (70/sex/dose) for up to 24 

months at mean doses of 0, 1.2, 15, or 82 mg/kg/day for males and 0, 1.8, 21, or 109 mg/kg/day 

for females. Up to 10 rats/sex/dose were sacrificed and examined after 12 months and 18 months 

of treatment; the remainder was sacrificed and examined at 24 months. Mean body weights of the 

high-dose group were decreased in males from week 1 and in females from week 24 through 

termination. Food intake was significantly decreased in all high-dose males with females showing a 

similar but less consistent decrease in food intake. A 40% decrease in drinking water intake was 

reported in all high-dose animals while those rats receiving the middle dose showed a slight but 

generally insignificant decrease in liquid intake. Changes in urinalyses, and hematological and 

clinical chemistry parameters, were not dose-related, so were not considered to be related to 

formaldehyde intake. Among the high-dose males, significant decreases were seen in the absolute 

heart and liver weights at 18 months and at termination; in testes weights at 18 months; and in 

kidney weights at termination. High-dose females showed significant increases in the relative 

kidney weights at 12 and 24 months. Relative brain weights were significantly increased in highdose males at all three examination periods and in females at termination only. Relative testes 

weights were significantly increased in high-dose males at termination. These relative organ weight 

increases were generally ascribed to the decreased body weights observed. A significant increase in 

mortality among males receiving the 15 mg/kg/day dose was not considered toxicologically 

significant. 

Gross examination at 12, 18, and 24 months revealed a raised, thickening of the limiting ridge of 

the forestomach in most high-dose rats and in some rats of both sexes from other groups. Irregular 

mucosal thickening of the forestomach and glandular stomach were seen in several rats of the highdose group and in occasional rats of other groups. The incidence of discoloration and irregularity of 

the kidney surface and atrophy of the testes was lower in the high-dose group as compared with 

controls. 

Significant histopathological changes of the gastrointestinal tract were found in high-dose males 

and females and included chronic atrophic gastritis of the glandular stomach from week 53 on, as 

well as focal ulceration and glandular hyperplasia at the terminal examination. The incidence of 

focal papillary epithelial hyperplasia and focal hyperkeratosis of the forestomach was significantly 

increased in both sexes at the terminal examination. These effects of formaldehyde on the gastric 

mucosa were considered cytotoxic in nature. A significant increase in the incidence of papillary 

necrosis of the kidneys was reported in both sexes of high-dose rats at the terminal examination. 

No treatment-related gastric tumors were observed in this study. The incidence and type of tumors 

observed in other organ systems were common to this strain and similar to those found in aging 

rats, 30 were not considered toxicologically significant. A NOAEL of 15 mg/kg/day in male rats was 

indicated in this study. 
Formaldehyde was administered daily in the drinking water of Sprague-Dawley rats (15/sex/dose) 

at doses equivalent to 0, 50, 100, or 150 mg/kg/day for 90 days (Johannsen et al., 1986). Male 

and female high-dose rats (150 mg/kg/day) and male rats receiving the 100 mg/kg/day dose 

showed a significant decrease in body weight gain. A dose-related decrease in the intake of drinking 

water was reported in both sexes of treated rats. Food intake and feed efficiency was comparable 

among all groups. No statistically significant differences were seen in urinalyses, or hematological 

and blood chemistry parameters. No treatment-related histopathological findings were observed. A 

NOAEL of 50 mg/kg/day was indicated for rats.

Similarly, formaldehyde was administered in the diet of pure-bred beagle dogs (4/sex/dose) at 

doses of 0, 50, 75, or 100 mg/kg/day for 90 days. A significant decrease in body weight gain was 

reported in the high-dose dogs of both sexes with no effect on weight gain at the two lower dose 

levels. A reduced food consumption and feed efficiency was observed in dogs at all treatment 

levels. No treatment-related effects were seen on hematological, blood chemistry, or urinalysis 

parameters, nor were any treatment-related lesions observed. The gastrointestinal mucosa was not 

affected by formaldehyde intake. A NOAEL of 75 mg/kg/day was indicated. 

Marks et al. (1980) administered formaldehyde as an aqueous solution to pregnant CD-1 mice at 

oral doses of 74, 148, and 185 mg/kg on days 6 to 15 of gestation. The high dose was lethal to

most of the treated mice by day 18. Mortality was 1/35 and 22/34 among dams treated at 148 and 

185 mg/kg/day, respectively. In the high-dose group, the number of resorption sites was increased 

and mean litter size was slightly decreased. No effects on fetus size, and no gross or microscopic 

skeletal or soft tissue abnormalities were observed. 

Hurni and Ohder (1973) exposed pregnant beagle dogs (9 to 11/group) to formaldehyde in the diet 

at levels of 125 or 375 ppm from 4 days after mating through day 56. Assuming that 1 ppm in the 

diet of a 10-kg dog consuming 250 g of dry chow/day equals 0.025 mg/kg/day (Lehman, 1959), 

this would correspond to doses of 3 or 9 mg/kg/day. The dogs were weighed weekly, and the pups 

were weighed at birth and twice weekly thereafter. Feeding of formaldehyde had no effect on 

pregnancy rate, maternal body weight, or duration of gestation. Mean litter sizes were within 

normal ranges. No effects were reported on growth or mortality. All pups were inspected for defects 

at birth and at 8 weeks postpartum. Stillborns, as well as pups dying before weaning, were 

autopsied and examined for internal and skeletal anomalies. Normal behavior, appearance, mobility 

and muscular coordination were reported for all dogs observed for up to 9 months. 

Seidenberg et al. (1987) evaluated formaldehyde in the Chernoff/Kavlock developmental toxicity 

screen. Formaldehyde was administered by gavage at 540 mg/kg/day to pregnant ICR/SIM mice on 

gestation days 8 through 12. The mice were allowed to deliver, then several neonatal growth and 

viability parameters were measured in the offspring. Comparative statistical analysis of these 

parameters between treated animals and concurrent (vehicle-treated) controls revealed no 

significant effect on any perinatal parameter examined. 
__I.A.3. Uncertainty and Modifying Factors (Oral RfD)

UF — An uncertainty factor of 100 was used to account for the inter- and intraspecies differences. 

MF — None 

__I.A.4. Additional Studies/Comments (Oral RfD)

Based on this 2-year study in rats in which a NOAEL is identified, the uncertainty factor of 100 is 

considered appropriate for extrapolating results to humans. This study consisted of adequate 

numbers of animals of both sexes as well as a thorough examination of toxicological and 

histological parameters. 

Takahashi et al. (1986) conducted a two-stage carcinogenesis bioassay in male Wistar rats. The 

animals were administered N-methyl-N'-nitro-N- nitrosoguanidine (MNNG) at 100 mg/L in the 

drinking water for the first 8 weeks of the study, followed by administration of 0.5% formalin (dose 

not specified) in the drinking water during weeks 8 through 40. Other groups of animals received 

just MNNG or formalin (dose not specified). The animals were sacrificed at the termination of dosing 

and the stomachs were examined grossly and microscopically. The actual doses of formaldehyde 

received by the test animals is not known, because dose concentrations were not reported, and 

drinking water consumption was not measured. Formalin did not produce malignant tumors when 

given alone. In animals receiving just formalin, forestomach papillomas occurred in 8/10 animals. 

In rats given MNNG alone, adenocarcinoma of the pylorus occurred in 1/30 rats, preneoplastic 

hyperplasia of the pylorus occurred in 7/30 rats, and adenocarcinoma of the duodenum occurred in 

3/30 rats. In the group administered both MNG and formalin, forestomach papillomas occurred in 

15/17 animals, adenocarcinoma of the pylorus in 4/17, preneoplastic hyperplasia of the pylorus in 

7/17, and adenocarcinoma of the duodenum in 1/17. 

__I.A.5. Confidence in the Oral RfD

Study — High

Database — Medium

RfD — Medium

Confidence in the critical study is high since it consisted of adequate numbers of animals of both 

sexes, as well as a thorough examination of toxicological and histological parameters. Confidence in 

the database is medium as several additional chronic bioassays and reproductive and 

developmental stuides support the critical effect and study. Medium confidence in the RfD follows. 

__I.A.6. EPA Documentation and Review of the Oral RfD
Source Document — U.S. EPA, 1989

Other EPA Documentation — None

Agency Work Group Review — 11/17/1989, 05/17/1990, 06/20/1990 

Verification Date — 06/20/1990 

__I.A.7. EPA Contacts (Oral RfD)

Please contact the IRIS Hotline for all questions concerning this assessment or IRIS, in general, at 

(202)566-1676 (phone), (202)566-1749 (FAX) or hotline.iris@epa.gov (internet address). 

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_I.B. Reference Concentration for Chronic Inhalation Exposure (RfC)

Substance Name — Formaldehyde

CASRN — 50-00-0

Not available at this time.

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_II. Carcinogenicity Assessment for Lifetime Exposure

Substance Name — Formaldehyde

CASRN — 50-00-0

Last Revised — 05/01/1991

Section II provides information on three aspects of the carcinogenic assessment for the substance 

in question; the weight-of-evidence judgment of the likelihood that the substance is a human 

carcinogen, and quantitative estimates of risk from oral exposure and from inhalation exposure. 

The quantitative risk estimates are presented in three ways. The slope factor is the result of 

application of a low-dose extrapolation procedure and is presented as the risk per (mg/kg)/day. The 

unit risk is the quantitative estimate in terms of either risk per ug/L drinking water or risk per 

ug/cu.m air breathed. The third form in which risk is presented is a drinking water or air 

concentration providing cancer risks of 1 in 10,000, 1 in 100,000 or 1 in 1,000,000. The rationale 
and methods used to develop the carcinogenicity information in IRIS are described in The Risk 

Assessment Guidelines of 1986 (EPA/600/8-87/045) and in the IRIS Background Document. IRIS 

summaries developed since the publication of EPA's more recent Proposed Guidelines for 

Carcinogen Risk Assessment also utilize those Guidelines where indicated (Federal Register 

61(79):17960-18011, April 23, 1996). Users are referred to Section I of this IRIS file for 

information on long-term toxic effects other than carcinogenicity. 

_II.A. Evidence for Human Carcinogenicity

__II.A.1. Weight-of-Evidence Characterization

Classification — 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. 

__II.A.2. Human Carcinogenicity Data

Limited. At least 28 relevant epidemiologic studies have been conducted. Among these, two cohort 

studies (Blair et al., 1986, 1987; Stayner et al., 1988) and one case-control study (Vaughan et al., 

1986a,b) were well-conducted and specifically designed to detect small to moderate increases in 

formaldehyde-associated human risks. Blair et al. studied workers at 10 plants who were in some 

way exposed to formaldehyde (largely through resin formation) and observed significant excesses 

in lung and nasopharyngeal cancer deaths. Despite a lack of significant trends with increasing 

concentration or cumulative formaldehyde exposure, lung cancer mortality was significantly 

elevated in analyses with or without a 20-year latency allowance. No explicit control was made for 

smoking status. Stayner et al. reported statistically significant excesses in mortality from buccal 

cavity tumors among formaldehyde-exposed garment workers. The highest SMR was for workers 

with long employment duration (exposure) and follow-up period (latency). The Vaughan et al. nasal 

and pharyngeal cancer case-control study examined occupational and residential exposures, 

controlling for smoking and alcohol consumption. It showed a significant association between 

nasopharyngeal cancer and having lived 10 or more years in a mobile home, especially for mobile 

homes built in the 1950s to 1970s, a period of increasing formaldehyde- resin usage. No exposure 

measurements were available. 

The 25 other reviewed studies had limited ability to detect small to moderate increases in 

formaldehyde risks owing to small sample sizes, small numbers of observed site-specific deaths, 

and insufficient follow-up. Even with these potential limitations, 6 of the 25 studies (Acheson et al., 
1984; Hardell et al., 1982; Hayes et al., 1986; Liebling et al., 1984; Olsen et al., 1984; Stayner et 

al., 1985) reported significant associations between excess site-specific respiratory (lung, buccal 

cavity, and pharyngeal) cancers and exposure to formaldehyde. Some of these studies looked at 

potential confounders (such as wood-dust exposure) in greater detail; they did not discern 

sinonasal cancer incidence excesses of the size predicted. Others (Liebling et al., 1984; Stayner et 

al., 1985) overlapped the Acheson et al. (1984), Hardell et al. (1982) and Hayes et al. (1986) 

studies; the improved design and nonoverlapping portions of the later studies (Blair et al., 1986; 

Stayner et al., 1988) reinforce the conclusions of the earlier studies. Analysis of the remaining 19 

studies indicate that leukemia and neoplasms of the brain and colon may be associated with 

formaldehyde exposure. The biological support for such postulates, however, has not yet been 

demonstrated. Although the common exposure in all of these studies was formaldehyde, the 

epidemiologic evidence is categorized as "limited" primarily because of the possible exposures to 

other agents. Such exposures could have contributed to the findings of excess cancers. 

__II.A.3. Animal Carcinogenicity Data

Sufficient. Consequences of inhalation exposure to formaldehyde have been studied in rats, mice, 

hamsters and monkeys. The principal evidence comes from positive studies in both sexes of two 

strains of rats (Kerns et al., 1983; Albert et al., 1982; Tobe et al., 1985) and males of one strain of 

mice (Kerns et al., 1983), all showing squamous cell carcinomas.

For the CIIT, Kerns et al. (1983) exposed about 120 animals/sex/species (Fischer 344 rats and 

B6C3F1 mice) to 0, 2, 5.6 or 14.3 ppm, 6 hours/day, 5 days/week for 24 months. Five animals per 

group were sacrificed at 6 and 12 months and 20 per group were killed at 18 months. At 24 and 27 

months the number sacrificed is unclear. The studies were terminated at 30 months. From the 12th 

month on, male and female rats in the highest dose group (14.3 ppm) showed significantly 

increased mortality compared with controls. In the 5.6- ppm group, male rats showed a significant 

increase in mortality from 17 months on. Female mice showed generally comparable survival across 

dose groups, as did male mice, but the male mice as a whole showed increased mortality because 

of housing problems. Squamous cell carcinomas were seen in the nasal cavities of 51/117 male rats 

and 52/115 female rats at 14.3 ppm (HDT) by experiment's end (as many as 35 carcinomas had 

been identified in males by month 18 based on EPA analysis notes and Kerns (Chart 8). At 5.6 ppm, 

1/119 male rats and 1/116 female rats showed squamous cell carcinomas of the nasal cavity. No 

such tumors were seen at 0 or 2 ppm. Polypoid adenomas of the nasal mucosa were seen in rats at 

all doses (0 ppm: 1/118 M, 0/114 F; 2 ppm: 4/118 M, 4/118 F; 5.6 ppm: 6/119 M, 0/116 F; 14.3 

ppm: 4/117 M, 1/115 F) in a significant dose-related trend, albeit one that falls off after a peak. 

Among the mice, squamous cell carcinomas were seen in two males at 14.3 ppm. No other lesions 

were noteworthy. 

Sellakumar et al. (1985) exposed male Sprague-Dawley rats, 100/group, 6 hours/day, 5 days/week 

for lifetime to 10 ppm HCl and to 14 ppm formaldehyde. This was a combined exposure HCl and 
formaldehyde were administered simultaneously, and each was administered separately. An equal 

number of rats received an air control. HCl was administered to determine if tumor response was 

enhanced by an additional irritant effect or by the combining of formaldehyde and HCl to form bis-

(chloromethyl)ether (BCME). Groups receiving formaldehyde alone or with HCl showed an increase 

in nasal squamous cell carcinomas; those without formaldehyde were free of carcinomas and other 

tumors (0/99 in each group), although rhinitis and hyperplasia were of comparable incidence.

Tobe et al. (1985) conducted a 28-month study of male Fischer 344 rats (about 2 weeks younger 

than those in Kerns et al., 1983). Groups of 32 rats were exposed 6 hours/day, 5 days/week to 0, 

0.3, 2.0, 3,3, or 15 ppm formaldehyde in aqueous solution methanol; another group of 32 was 

exposed to methanol only (vehicle control). Animals were sacrificed at 12, 18, and 24 months. 

Exposure to 15 ppm ended at 24 months; at that point, mortality was 88%. At 28 months mortality 

was 60% in the control group and 32% in the 0.3 dose group. Squamous cell carcinomas were seen 

at 15 ppm in 14/27 rats surviving past 12 months, compared with 0/27 in the controls. No polypoid 

adenomas were observed; the increased incidences of rhinitis and hyperplasia were dose-related. 

While these three rodent studies are principal in the weight-of-evidence, inhalation studies have 

been carried out in other strains and species. Dalbey (1982), as part of a promotion experiment, 

exposed male Syrian golden hamsters to 10 ppm formaldehyde 5 times/week, 5 hours/day 

throughout their lifetimes, 132 animals were untreated controls. Although survival time was 

significantly reduced in the treated group, no tumors were observed in either treated or control 

groups. Rusch et al. (1983) carried out a 6-month toxicity study in 6 male cynomolgus monkeys, 

40 F344 rats (20M, 20F), and 20 Syrian golden hamsters (10M, 10F) with 22 hours/day, 7 

days/week exposure to three levels of formaldehyde with corresponding controls. The highest dose 

tested was 2.95 ppm. The short duration of the assay, the small sample sizes, and, possibly, the 

low concentrations tested, limited the sensitivity of the assay to detect tumors. In the highest dose 

group in both rats and monkeys, incidences of squamous metaplasia/hyperplasia of the nasal 

turbinates were significantly elevated. 

__II.A.4. Supporting Data for Carcinogenicity 

Mutagenic activity of formaldehyde has been demonstrated in viruses, Escherichia coli, 

Pseudomonas fluorescens, Salmonella typhimurium and certain strains of yeast, fungi, Drosophila, 

grasshopper and mammalian cells (Ulsamer et al., 1984). Formaldehyde has been shown to cause 

gene mutations, single strand breaks in DNA, DNA-protein crosslinks, sister chromatid exchanges 

and chromosomal aberrations. Formaldehyde produces in vitro transformation in BALB/c 3T3 mouse 

cells, BHK21 hamster cells and C3H-10Tl/2 mouse cells, enhances the transformation of Syrian 

hamster embryo cells by SA7 adenovirus, and inhibits DNA repair (Consensus Workshop on 

Formaldehyde, 1984). 
When inhaled, acetaldehyde, the closest aldehyde to formaldehyde in structure, causes cancers in 

the nose and trachea of hamsters, and nasal cancers in rats. 

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_II.B. Quantitative Estimate of Carcinogenic Risk from Oral Exposure

None.

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_II.C. Quantitative Estimate of Carcinogenic Risk from Inhalation 

Exposure

Inhalation Unit Risk — 1.3E-5 per (ug/cu.m) 

Extrapolation Method — Linearized multistage procedure, additional risk 

Air Concentrations at Specified Risk Levels: 

Risk Level Concentration

E-4 (1 in 10,000) 8E+0 ug/cu.m

E-5 (1 in 100,000) 8E-1 ug/cu.m

E-6 (1 in 1,000,000) 8E-2 ug/cu.m

__II.C.2. Dose-Response Data for Carcinogenicity, Inhalation Exposure

Tumor Type — squamous cell carcinoma

Test Animals — Rat/F344, males

Route — inhalation

Reference — Kerns et al., 1983 

----------- Dose -----------

Administered

(ppm)

Human Equivalent

(mg/kg)/day

Tumor

Incidence
0 0 0/156

2 2 0/159

5.6 5.6 2/153

14.3 14.3 94/140

__II.C.3. Additional Comments (Carcinogenicity, Inhalation Exposure)

In the Kerns et al. (1983) study, rats that died at 11 months (prior to appearance of the first 

squamous cell carcinoma) were not considered at risk. Those sacrificed at 12 and 18 months were 

treated as though they would have responded in the same proportion as rats remaining alive at the 

respective sacrifice times and those living beyond 24 months were included with animals sacrificed 

at 24 months. From the estimates of the probability of death with tumor within 24 months and its 

variance, the number of animals at risk and the number with tumors were derived for a 24-month 

study with no 12- or 18-month kills. These rounded numbers are shown above and were used for 

significance tests and modeling. 

The unit risk should not be used if the air concentration exceeds 8E+2 ug/cu.m, since above this 

concentration the unit risk may not be appropriate. 

__II.C.4. Discussion of Confidence (Carcinogenicity, Inhalation 

Exposure)

The experimental range is close to expected human exposures. Estimated lifetime excess risks from 

six epidemiologic studies are close to upper bound risks based on animal data (usually within 1 

order of magnitude for four types of estimated occupational and residential exposure). Animalbased estimates derived using time in the model were similar but would have required the use of 

more assumptions in the calculations. Three non-zero doses were used in addition to controls in the 

study on which calculations are based, with a large number of animals per group. Male and female 

incidences were close throughout the exposure groups. 

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_II.D. EPA Documentation, Review, and Contacts (Carcinogenicity 

Assessment)

__II.D.1. EPA Documentation

Source Document — U.S. EPA, 1987
The OTS Assessment of Health Risk has received wide internal and external review. 

__II.D.2. EPA Review (Carcinogenicity Assessment)

Agency Work Group Review — 02/03/1988

Verification Date — 02/03/1988 

__II.D.3. EPA Contacts (Carcinogenicity Assessment)

Please contact the IRIS Hotline for all questions concerning this assessment or IRIS, in general, at 

(202)566-1676 (phone), (202)566-1749 (FAX) or hotline.iris@epa.gov (internet address). 

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_III. [reserved]

_IV. [reserved] 

_V. [reserved]

_VI. Bibliography 

Substance Name — Formaldehyde

CASRN — 50-00-0

Last Revised — 08/01/1991

_VI.A. Oral RfD References

Hurni, H. and H. Ohder. 1973. Reproduction study with formaldehyde and hexamethylenetetramine 

in beagle dogs. Food Cosmet. Toxicol. 11: 459-462. 

Johannsen, F.R., G.J. Levinskas and A.S. Tegeris. 1986. Effects of formaldehyde in the rat and dog 

following oral exposure. Toxicol. Lett. 30: 1-6. 

Marks, T.A., W.C. Worthy and R.E. Staples. 1980. Influence of formaldehyde and sonacide 

(potentiated acid glutaraldehyde) on embryo and fetal development in mice. Teratology. 22: 51-58. 

Seidenberg, J.M., D.G. Anderson and R.A. Becker. 1986. Validation of an in vivo developmental 

toxicity screen in the mouse. Teratol. Carcinogen. Mutagen. 6: 361-374. 
Takahashi, M., R. Hasegawa, F. Furukawa, K. Toyoda, H. Sato and Y. Hayashi. 1986. Effects of 

ethanol, potassium metabisulfite, formaldehyde and hydrogen peroxide on gastric carcinogenesis in 

rats after initiation with N-methyl- N'nitro-N'nitrosoguanidine. Jap. J. Cancer Res. 77: 118-124. 

Til, H.P., R.A. Woutersen, V.J. Feron, V.H.M. Hollanders, H.E. Falke and J.J. Clary. 1989. Two-year 

drinking water study of formaldehyde in rats. Food Chem. Toxicol. 27(2): 77-87. 

U.S. EPA. 1989. Draft Drinking Water Health Advisory for Formaldehyde. Office of Drinking Water, 

Washington, DC. 

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_VI.B. Inhalation RfC References

None

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_VI.C. Carcinogenicity Assessment References

Acheson, E.D., M.J. Gardner, B. Pannett, H.R. Barnes, C. Osmond and C.P. Taylor. 1984. 

Formaldehyde in the British Chemical Industry. The Lancet. p. 611-615.

Albert, R.E., A.R. Sellakumar, S. Laskin, M. Kuschner, N. Nelson and C.A. Snyder. Gaseous 

formaldehyde and hydrogen chloride induction of nasal cancer in the rat. J. Natl. Cancer Inst. 

68(4): 597-603.

Blair, A., P.A. Stewart, R.N. Hoover, et al. 1986. Mortality among industrial workers exposed to 

formaldehyde. J. Natl. Cancer Inst. 76(6): 1071-1084. 

Blair, A., P. Stewart, P.A. Hoover, et al. 1987. Cancers of the nasopharynx and oropharynx and 

formaldehyde exposure. J. Natl. Cancer Inst. 78(1): 191-193. 

Consensus Workshop on Formaldehyde. 1984. Deliberations of the Consensus Workshop on 

Formaldehyde, October 3-6, 1983. Little Rock, AK. (Final report)

Dalbey, W.E. 1982. Formaldehyde and tumors in hamster respiratory tract. Toxicology. 24: 9-14.
Hardell, L., B. Johansson and O. Axelson. 1982. Epidemiological study of nasal and nasopharyngeal 

cancer and their relation to phenoxy acid or chlorophenol exposure. Am. J. Ind. Med. 3: 247-257. 

Hayes, R.B., J.W. Raatgever, A. de Bruyn and M. Gerin. 1986. Cancer of the nasal cavity and 

paranasal sinuses, and formaldehyde exposure. Int. J. Cancer. 37: 487-492.

Kerns, W.D., K.L. Pavkov, D.J. Donofrio, E.J. Gralla and J.A. Swenberg. 1983. Carcinogenicity of 

formaldehyde in rats and mice after long-term inhalation exposure. Cancer Res. 43: 4382-4392.

Liebling, T., K.D. Rosenman, H. Pastides, R.G. Griffith and S. Lemeshow. 1984. Cancer mortality 

among workers exposed to formaldehyde. Am. J. Ind. Med. 5: 423-428. 

Olsen, J.H., S.P. Jensen, M. Hink, K. Faurbo, N.O. Breum and O.M. Jensen. 1984. Occupational 

formaldehyde exposure and increased nasal cancer risk in man. Int. J. Cancer. 34: 639-644.

Rusch, G.M., J.J. Clary, W.E. Rinehart and H.F. Bolte. 1983. A 26-week inhalation toxicity study 

with formaldehyde in the monkey, rat and hamster. Toxicol. Appl. Pharmacol. 68: 329-343.

Sellakumar, A.R., C.A. Snyder, J.J. Solomon and R.E. Albert. Carcinogenicity of formaldehyde and 

hydrogen chloride in rats. Toxicol. Appl. Pharmacol. 81: 401-406.

Stayner, L.S., A.B. Smith, G. Reeve, et al. 1985. Proportionate mortality study of workers in the 

garment industry exposed to formaldehyde. Am. J. Ind. Med. 7: 229-240.

Stayner, L.T., L. Elliott, L. Blade, R. Keenlyside and W. Halperin. 1988. A retrospective cohort 

mortality study of workers exposed to formaldehyde in the garment industry. Am. J. Ind. Med. 

13(6): 667-682.

Tobe, M., T. Kaneko, Y. Uchida, et al. 1985. Studies of the inhalation toxicity of formaldehyde. 

National Sanitary and Medical Laboratory Service (Japan). p. 1-94.

Ulsamer, A.G., K.C. Gupta, M.S. Cohn and P.W. Preuss. 1982. Formaldehyde in indoor air: Toxicity 

and risk. In: Proceed. 75th Ann. Meet. Air Pollut. Control Assoc. 16 p.

U.S. EPA. 1987. Assessment of Health Risk to Garment Workers and Certain Home Residents from 

Exposure to Formaldehyde. Office of Toxic Substances, Washington, DC. 

Vaughn, T.L., C. Strader, S. Davis and J.R. Daling. 1986a. Formaldehyde and cancers of the 

pharynx, sinus and nasal cavity: I. Occupational exposures. Int. J. Cancer. 38: 677-683.
Vaughn, T.L., C. Strader, S. Davis and J.R. Daling. 1986b. Formaldehyde and cancers of the 

pharynx, sinus and nasal cavity: II. Residential exposures. Int. J. Cancer. 38: 685-688. 

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_VII. Revision History

Substance Name — Formaldehyde

CASRN — 50-00-0 

Date Section Description

10/01/1989 II. Carcinogen summary on-line

10/01/1989 VI. Bibliography on-line

12/01/1989 I.A. Oral RfD now under review

02/01/1990 VI. Supplementary data on-line

09/01/1990 I.A. Oral RfD summary on-line

09/01/1990 II. Text edited

09/01/1990 VI.A. Oral RfD references added

01/01/1991 II. Text edited

01/01/1991 II.C.1. Inhalation slope factor removed (global change)

05/01/1991 II.C.1. Corrected units in risk level concentrations

08/01/1991 VI.A.&C. Citations clarified

01/01/1992 IV. Regulatory Action section on-line

04/01/1997 III., IV., 

V.

Drinking Water Health Advisories, EPA Regulatory Actions, and Supplementary 

Data were removed from IRIS on or before April 1997. IRIS users were directed 

to the appropriate EPA Program Offices for this information.

01/02/1998 I., II. This chemical is being reassessed under the IRIS Program.

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_VIII. Synonyms

Substance Name — Formaldehyde

CASRN — 50-00-0

Last Revised — 10/01/1989

 50-00-0 

 ALDEHYDE FORMIQUE (FRENCH) 

 ALDEHYD MRAVENCI (CZECH) 

 ALDEIDE FORMICA (ITALIAN) 

 BFV 

 FA 

 FORMALDEHYD (CZECH, POLISH) 

 FORMALDEHYDE 

 FORMALDEHYDE SOLUTION (DOT) 

 FORMALIN 

 FORMALITH 

 FORMIC ALDEHYDE 

 FORMOL 

 FYDE 

 HOCH 

 IVALON 

 KARSAN 

 LYSOFORM 

 METHANAL 

 METHYL ALDEHYDE 

 METHYLENE GLYCOL 

 METHYLENE OXIDE 

 MORBICID 

 NCI-C02799 

 OPLOSSINGEN (DUTCH) 

 OXOMETHANE 

 OXYMETHYLENE 

 PARAFORM 

 POLYOXYMETHYLENE GLYCOLS 

 RCRA WASTE NUMBER U122 

 SUPERLYSOFORM 

 UN 1198 (DOT) 

 UN 2209 (DOT)