Environmental Health Perspectives • volume 118 | number 3 | March 2010 313

Review

Acute exposure to formaldehyde can cause 

eye, nose, throat, and skin irritation, whereas 

long-term exposure has been associated 

with certain cancers (e.g., sinonasal) as well 

as asthma (Daisey et al. 2003). Exposure to 

formaldehyde occurs in certain occupational 

settings (e.g., embalmers), but exposure via 

formaldehyde-emitting products such as particle board, urea formaldehyde insulation, 

carpeting, and furniture is more common 

(Garrett et al. 1999). In the United States, the 

legal occupational limit for short-term (i.e., 

< 15 min) formaldehyde exposure is 2 ppm, 

and the long-term limit (i.e., > 15 min) is 

0.75 ppm [Occupational Safety and Health 

Administration (OSHA) 2005]. In contrast, 

the National Institute for Occupational Safety 

and Health suggests that exposure be limited 

to much lower levels: 0.016 ppm (long term) 

and 0.1 ppm (short term). 

Much of the research regarding the 

health effects of formaldehyde has focused 

on cancer, whereas less attention has been 

paid to more common conditions such as 

asthma. In the United States, the prevalence 

of asthma is approximately 7% among adults 

and 9% among children (Akinbami et al. 

2009; Moorman et al. 2007). Among adults, 

some studies have reported a positive association between formaldehyde and asthma 

(Wieslander et al. 1997), while others have 

not (Krzyzanowski et al. 1990). It has been 

suggested that certain groups, specifically children, may be particularly sensitive to formaldehyde exposure; however, as with adults, 

the results have been inconsistent, with some 

studies reporting an association (Garrett 

et al. 1999) and others not (Symington et al. 

1991). All of these studies have specific limitations including small sample sizes (Delfino 

et al. 2003), the use of self-reported asthma 

(Smedje et al. 1997), and potential selection 

bias (Garrett et al. 1999). In addition, the 

extent of formaldehyde exposure varies widely 

across studies. For example, Mi et al. (2006)

reported a range of 3–20 μg/m3, whereas the 

range reported by Rumchev et al. (2002) was 

~ 0–224 μg/m3. However, the former study 

derived measurements from schools while 

the latter study obtained measurements from 

homes. Moreover, most studies are crosssectional and fail to provide information on 

exposure levels that reflect individual exposure (in magnitude and/or duration). 

Although there have been multiple 

reviews of the literature pertaining to formaldehyde and asthma in children, these have 

all been qualitative (Mendell 2007). The relationship between formaldehyde and respiratory symptoms has received attention recently 

because of concerns regarding air quality in 

mobile homes and travel trailers provided by 

the Federal Emergency Management Agency 

(FEMA) to displaced Gulf Coast residents 

in the aftermath of Hurricane Katrina. We 

conducted the current study, a systematic 

review of the literature regarding the potential 

association between formaldehyde exposure 

and asthma in children, to shed additional 

light on the issue.

Methods

This review was conducted using a modified 

version of the Meta-analysis of Observational 

Studies in Epidemiology (MOOSE) guidelines for the conduct of systematic reviews 

and meta-analysis of observational studies 

(Stroup et al. 2000). We identified studies 

through the PubMed/MEDLINE (National 

Library of Medicine 2009) and Google 

Scholar (2009) databases, employing a search 

strategy that combined text word (e.g., “formaldehyde and asthma and children”) and 

medical subject headings to identify reports 

regarding formaldehyde exposure and asthma. 

The reference lists of the identified studies 

were also reviewed to identify other relevant 

studies. Studies were initially selected if they 

appeared to contain qualitative or quantitative 

estimates for the association between formaldehyde exposure and asthma in children. 

We were specifically interested in studies that 

compared children with and without asthma 

with respect to formaldehyde exposure. All of 

the studies initially selected were in English.

In total, we identified 18 articles that 

met the aforementioned criteria, and after 

a detailed review, determined that 10 articles contained information suitable for use 

in a systematic review. Three review articles 

were excluded (Burr 1999; Daisey et al. 

2003; Mendell 2007). Three additional 

articles were excluded because they were not 

asthma-­specific, but rather focused on respiratory symptoms (e.g., chest discomfort) or 

pulmonary function (Franklin et al. 2000; 

Symington et al. 1991; Wantke et al. 1996). 

Two studies were excluded because, although 

asthma-specific, they did not contain a reference or control group (Delfino et al. 2003; 

Erdei et al. 2003). For the 10 articles included, 

Address correspondence to G. McGwin, 1922 7th 

Ave. South, Suite 120, Birmingham, AL 35294 

USA. Telephone: (205) 975-3030. Fax: (205) 9753040. E-mail: mcgwin@uab.edu

G.M. has been paid as an expert witness regarding 

the health effects of formaldehyde exposure. The 

other authors declare they have no competing financial interests.

Received 29 June 2009; accepted 6 November 2009.

Formaldehyde Exposure and Asthma in Children: A Systematic Review

Gerald McGwin Jr.,1 Jeffrey Lienert,2 and John I. Kennedy Jr.3,4

1Department of Epidemiology, School of Public Health, University of Alabama at Birmingham, Birmingham, Alabama, USA; 2Franklin 

and Marshall College, Lancaster, Pennsylvania, USA; 3Department of Veterans Affairs Medical Center, Birmingham, Alabama, 

USA; 4Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, University of Alabama at Birmingham, 

Birmingham, Alabama, USA

Objective: Despite multiple published studies regarding the association between formaldehyde 

exposure and childhood asthma, a consistent association has not been identified. Here we report 

the results of a systematic review of published literature in order to provide a more comprehensive 

picture of this relationship.

Data sources: After a comprehensive literature search, we identified seven peer-reviewed studies 

providing quantitative results regarding the association between formaldehyde exposure and asthma 

in children. Studies were heterogeneous with respect to the definition of asthma (e.g., self-report, 

physician diagnosis). Most of the studies were cross-sectional. 

Data extraction: For each study, an odds ratio (OR) and 95% confidence interval (CI) for 

asthma were either abstracted from published results or calculated based on the data provided. 

Characteristics regarding the study design and population were also abstracted.

Data synthesis: We used fixed- and random-effects models to calculate pooled ORs and 95% CIs; 

measures of heterogeneity were also calculated. A fixed-effects model produced an OR of 1.03 (95% 

CI, 1.02–1.04), and random effects model produced an OR of 1.17 (95% CI, 1.01–1.36), both 

reflecting an increase of 10 μg/m3 of formaldehyde. Both the Q and I2 statistics indicated a moderate amount of heterogeneity.

Conclusions: Results indicate a significant positive association between formaldehyde exposure 

and childhood asthma. Given the largely cross-sectional nature of the studies underlying this metaanalysis, further well-designed prospective epidemiologic studies are needed.

Key words: asthma, children, epidemiology, formaldehyde, meta-analysis. Environ Health 

Perspect 118:313–317 (2010). doi:10.1289/ehp.0901143 available via http://dx.doi.org/ [Online 

6 November 2009]
McGwin et al.

314 volume 118 | number 3 | March 2010 • Environmental Health Perspectives

we abstracted information regarding study 

design and setting, subject response/participation rates, definition of asthma (e.g., physician 

diagnosis), sample size, average (minimum 

and maximum) formaldehyde levels, average 

age of study subjects, and quantitative estimates (or raw data) for the association between 

formaldehyde exposure and asthma as well as 

whether such estimates were adjusted and, if 

so, for what measures (Table 1). Three of 10 

studies did not contain actual formaldehyde 

measurements, and attempts to obtain this 

information from the study authors have been 

unsuccessful to date (Doi et al. 2003; Pati and 

Parida 2005; Tavernier et al. 2006).

Once the relevant results from each study 

were extracted, we determined that homogenizing the individual study results using a 

single unit of formaldehyde measurement 

would be necessary. Because most studies 

reported their results as odds ratios (ORs) 

per 10-μg/m3 unit increase in formaldehyde, 

this was chosen as the common metric. Thus, 

results for those studies using different units 

were transformed. For example, if a study 

reported an OR reflecting a 1-μg/m3 increase 

in formaldehyde, the natural logarithm of 

the OR was calculated and multiplied by 10; 

this value was then exponentiated to obtain 

an OR for a 10-μg/m3 unit increase in formaldehyde. This process was repeated for the 

95% confidence interval (CI). Thus, for each 

study, an OR and 95% CI for the association 

between asthma and a 10-μg/m3 unit increase 

in formaldehyde exposure was obtained. One 

study (Zhao et al. 2008) provided two estimates: one for indoor and another for outdoor exposure, both of which were used. 

Pooled ORs and 95% CIs were obtained 

using inverse variance-weighted, fixed-effects, 

and random-effects models. We tested heterogeneity using the Q test and quantified with the 

I

2 statistic. Whereas the Q test only determines 

whether statistically significant heterogeneity 

exists, the I

2 statistic calculates the proportion 

of the variability that can be attributed to heterogeneity across the studies. I

2 values of 25%, 

50%, and 75% have been suggested as indicators of low, moderate, and high heterogeneity, 

respectively. Fixed-effects models are considered appropriate for values of < 50%, whereas 

for values of ≥ 50%, random-effects models are 

preferred. To evaluate whether the observed 

results were unduly influenced by any individual study and to determine if there was any 

publication bias, an influence plot and a funnel 

plot, respectively, were used. 

Results

Overall, 10 studies involving 6,387 participants including 635 with diagnosed or selfreported asthma were selected for systematic 

review, of which seven studies were able to be 

used in the meta-analysis involving a total of 

5,930 participants, 364 of whom had diagnosed asthma (Table 1). Most studies were 

cross-sectional; half relied on self-reported 

information on asthma diagnoses, whereas 

the remainder used actual physician diagnoses. Studies of the former type generally queried participants about whether they had ever 

been diagnosed with asthma, and thus those 

responding affirmatively are best characterized 

as prevalent cases. With respect to those studies using physician diagnosis, based on the 

study designs as they were described, it was 

frequently clear that those with asthma would 

also be best characterized as prevalent cases. 

In only one study was it entirely clear that 

the cases were truly incident (i.e., newly diagnosed). Participation rates ranged from 46% 

to 99%; however, this information was not 

available for half of the studies.

The results for each individual study as 

well as the fixed- and random-effects pooled 

ORs and 95% CIs are shown in Figure 1. The 

forest plots for both fixed- and random-effects 

models can be seen in Figures 1 and 2, respectively. The results of the fixed-effects model 

indicate a 3% increase (95% CI, 1.02–1.04, 

p < 0.0001) in asthma risk for each 10­μg/m3

unit increase in formaldehyde, whereas the 

random-effects model indicates a 17% increase 

(95% CI, 1.01–1.22, p = 0.0158). The Q and 

I

2 statistics were 14.28 (p < 0.0001) and 51%, 

respectively, indicating the presence of moderate between-study heterogeneity.

The influence plot indicated that one 

study (Rumchev et al. 2002) may have had 

Table 1. Summary of studies selected for inclusion in meta-analysis.

Source Setting Design

Asthma 

definition

Incident vs. 

prevalent 

cases

Participation 

rate Exposure

Formaldehyde 

levels (μg/m3)

No. 

(asthma)

OR (95% CI) per 

10-μg/m3 increase Adjusted

Mean 

age 

(years)

Krzyzanowski et al. 

1990

United 

States

Cross-sectional Self-report Prevalent Unknown Home ≤ 50 to > 87.5 298 (47) 1.07 (0.81–1.43) No 9.3

Smedje et al. 1997 Sweden Cross-sectional Self-report Prevalent 82% School < 5 to 10 627 (40) 2.59 (1.10–6.19) Yes 13–14

Garrett et al. 1999 Australia Cross-sectional Diagnosis Prevalent Unknown Home < 20 to > 50 148 (53) 1.27 (1.04–1.55) No 10.2

Smedje and Norbäck 

2001

Sweden Cohort Self-report Incident 66% School < 5 to 72 1,258 (56) 1.20 (0.80–1.70) Yes 10.3

14.3

Rumchev et al. 2002 Australia Case–control Diagnosis Unclear Unknown Home < 10 to > 60 192 (88) 1.03 (1.02–1.04) Yes 1.9

Doi et al. 2003 Japan Case–control Diagnosis Prevalent Unknown NA NA 155 (122) NA NA 9.4

Mi et al. 2006 China Cross-sectional Self-report Prevalent 99% School 3 to 20 1,414 (44) 1.30 (0.72–2.32) Yes 13.0

Tavernier et al. 2006 United 

Kingdom

Case–control Diagnosis Prevalent 46% Home NA 130 (65) a Yes 8.1

Pati et al. 2005 India Case–control Diagnosis Unclear Unknown Home NA 172 (84) b NA NA

Zhao et al. 2008 China Cross-sectional Self-report Prevalent 90% School 1 to 5 1,993 (36) 0.12 (0.0008–17.32) Yes 12.8

Zhao et al. 2008 China Cross-sectional Self-report Prevalent 90% Outdoor 5 to 7 1,993 (36) 581.59 (0.06–2263796.94) Yes 12.8

NA, not applicable. 

aElevated (nonsignificant) ORs for living room and bedroom formaldehyde levels. bIndoor exposure to formaldehyde significantly increased the risk of asthma.

Figure 1. Forest plot of the relative risk estimates and their 95% CIs from the studies included in the metaanalysis of the association between formaldehyde exposure and asthma in children based upon a fixedeffects model.

0.1 1 10

Decreased risk Increased risk

Study OR (95% CI) OR (95% CI) Weight %

Krzyzanowski et al. 1990

Smedje et al. 1997

Garrett et al. 1999

Smedje and Norbäck 2001

Rumchev et al. 2002

Mi et al. 2006

Zhao et al. 2008 (school)

Zhao et al. 2008 (outdoor)

Overall (fixed)

1.070 (0.810–1.420)

2.590 (1.090–6.140)

1.270 (1.040–1.550)

1.200 (0.820–1.750)

1.030 (1.020–1.040)

1.300 (0.960–1.750)

0.120 (0.010–17.66)

581.6 (0.090–357E4)

1.030 (1.020–1.040)

0.0

0.0

0.0

0.0

99.0

0.0

0.0

0.0
Formaldehyde exposure and asthma in children

Environmental Health Perspectives • volume 118 | number 3 | March 2010 315

an undue influence on the study results (data 

not shown). When this study was excluded,

the resulting ORs from fixed- and random-effects models were 1.24 (95% CI, 1.09–1.42) 

and 1.24 (95% CI, 1.07–1.44), respectively 

(Table 2). The Q and I2 statistics were 6.76 

and 11.2%, respectively.

Table 2 presents the pooled results stratified according to specific study characteristics. Based on the fixed-effects model, the 

OR for self-reported asthma was 1.22 (95% 

CI, 1.02–1.46), whereas the OR for diagnosed asthma was 1.03 (95% CI, 1.02–1.04). 

For the random-effects model, the ORs for 

self-reported and diagnosed asthma were 

1.26 (95% CI, 0.97–1.64) and 1.12 (95% 

CI, 0.88–1.44), respectively. When stratified according to study design, the ORs for 

cross-sectional studies were 1.25 (95% CI, 

1.08–1.44) for fixed effects and 1.26 (95% 

CI, 1.03–1.55) for random effects. There was 

only one cohort study and one case–control 

study; the results of these individual studies appear in Table 1. With respect to the 

exposure setting (home vs. school), assuming fixed effects, the OR was 1.03 (95% CI, 

1.02–1.04) for home exposure, whereas for 

school exposure the OR was 1.32 (95% CI, 

1.05–1.66). For the random-effects model, 

the OR for home exposure was 1.10 (95% 

CI, 0.95–1.27), and the OR for school exposure was 1.33 (95% CI, 1.02–1.74). Only one 

study (Zhao et al. 2008) evaluated outdoor 

exposure, and its results appear in Table 1. 

Finally, the fixed- and random-effects results 

for the four studies (Mi et al. 2006; Smedje 

and Norbäck 2001; Smedje et al. 1997; Zhao 

et al. 2008) that provided participation rates 

(66%, 82%, 90%, and 99%) were stronger 

than the results for those for which participation rates were unknown.

The funnel plot did not show evidence 

of publication bias either with or without 

Rumchev et al. 2002 (data not shown). 

Discussion

Asthma is a disorder characterized by episodic symptoms and a physiology associated 

with airway hyperresponsiveness, bronchoconstriction, and excessive mucus production. Fundamentally, asthma is a disorder 

with inflammation of airways that creates 

a microenvironment capable of reacting to 

specific and/or nonspecific stimuli with a 

stereotypic pathogenic response. Although 

debate on the topic continues, multiple studies have suggested a link between inhalation 

exposure to formaldehyde and the development of airway hyperresponsiveness and 

asthma (Thompson et al. 2008). Several 

mechanisms have been identified that provide 

plausible connections between formaldehyde 

exposure and airways disease. Formaldehyde 

is a well-recognized irritant affecting multiple tissues; it has been demonstrated to 

provoke transient decline in pulmonary function (Paustenbach et al. 1997). As a small 

molecule, formaldehyde may associate with 

larger protein molecules (e.g., albumin) to 

create newly antigenic moieties. Such exposure presumably would provoke formation 

of specific IgE antibodies that could bind to 

mast cells and, upon subsequent exposure, 

lead to mast cell degranulation and the elaboration of mediators traditionally associated 

with the asthmatic (early- and late-phase) 

response. Alternatively, formaldehyde inhalation, through its nonspecific irritant effect, 

could provoke mucosal inflammation in airways. If the resultant inflammatory response 

is T helper-2 dominant, cytokine mediators 

typically associated with asthma [interleukin 

(IL)-4, IL-5, IL-9, IL-13] would subsequently 

be produced (Elias et al. 2003). Recently, 

formaldehyde has also been demonstrated to 

alter thiol biology, leading to the accelerated 

reduction of the endogenous bronchodilator 

S-nitrosoglutathione, thus providing another 

putative mechanistic link between formaldehyde exposure and airways disease (Thompson 

et al. 2008).

The results of this study, which pooled the 

results of seven published studies, suggest a 

positive relationship between formaldehyde 

exposure and childhood asthma. To place the 

observed results (OR of 1.17 per 10-μg/m3

increase) in context, when compared with individuals with no formaldehyde exposure, those 

with the highest levels of exposure reported in 

Figure 2. Forest plot of the relative risk estimates and their 95% CIs from the studies included in the metaanalysis of the association between formaldehyde exposure and asthma in children based on a randomeffects model.

0.1 1 10

Decreased risk Increased risk

Study OR (95% CI) OR (95% CI) Weight %

Krzyzanowski et al. 1990

Smedje et al. 1997

Garrett et al. 1999

Smedje and Norbäck 2001

Rumchev et al. 2002

Mi et al. 2006

Zhao et al. 2008 (school)

Zhao et al. 2008 (outdoor)

Overall (random)

1.070 (0.810–1.420)

2.590 (1.090–6.140)

1.270 (1.040–1.550)

1.200 (0.820–1.750)

1.030 (1.020–1.040)

1.300 (0.960–1.750)

0.120 (0.010–17.66)

581.6 (0.090–357E4)

1.170 (1.010–1.360)

15.0

3.0

22.0

11.0

35.0

14.0

0.0

0.0

Table 2. Pooled ORs and 95% CIs for fixed- and random-effects models.

Fixed effects Random effects

No. of 

studies

OR (95% CI) per 

10-μg/m3 increase p-Value Q I 2

OR (95% CI) per 

10-μg/m3 increase p-Value

All studies 7 1.03 (1.02–1.04) < 0.0001 14.28 51.0 1.17 (1.01–1.36) 0.0202

Excluding Rumchev et al. 6 1.24 (1.09–1.42) 0.0013 6.76 11.3 1.24 (1.07–1.45) 0.0026

Diagnosis method

Self-reported 6 1.21 (1.02–1.46) 0.0158 6.66 24.9 1.26 (0.97–1.64) 0.0446

Diagnosed 2 1.03 (1.02–1.04) < 0.0001 4.22 76.3 1.12 (0.88–1.44) 0.1711

Study design

Cohort 1 1.20 (0.80–1.70) 0.1711

Case–control 1 1.03 (1.02–1.04) < 0.0001

Cross-sectional 6 1.25 (1.08–1.44) 0.0013 6.72 25.6 1.26 (1.03–1.55) 0.0122

Exposure setting

Home 3 1.03 (1.02–1.04) < 0.0001 4.29 53.4 1.10 (0.95–1.27) 0.1056

School 4 1.32 (1.05–1.66) 0.0082 3.48 13.8 1.33 (1.02–1.74) 0.0179

Participation rate

 > 60% 4 1.34 (1.00–1.81) 0.0519 5.66 29.3 1.43 (0.92–2.23) 0.1139

Unknown 3 1.03 (1.02–1.04) < 0.0001 4.29 30.1 1.09 (0.96–1.25) 0.1924
McGwin et al.

316 volume 118 | number 3 | March 2010 • Environmental Health Perspectives

the seven studies (i.e., 80 μg/m3) would have

3.5-times higher odds of asthma. The results 

reported herein are consistent with much of 

the previously published literature regarding 

the association between formaldehyde exposure and childhood asthma. This should not be 

surprising in that many of these studies serve as 

the foundation of our meta-analysis. However, 

in addition to the seven studies included in 

the meta-analysis, two additional studies, each 

reporting a positive association, could not be 

included, yet they provide further support 

for the observed quantitative results (Pati and 

Parida 2005; Tavernier et al. 2006). Tavernier 

et al. (2006) reported elevated but not statistically significant ORs for specific levels of 

formaldehyde exposure; unfortunately, the 

authors did not provide the actual, quantitative 

values associated with those levels. Similarly, 

Pati and Parida (2005) simply reported that, 

“indoor exposure to formaldehyde . . . significantly increased the risk of having asthma.” 

Additionally, Symington et al. (1991) compared the prevalence of respiratory symptoms 

exhibited by children living within 1 mile of 

a formaldehyde-emitting foundry with that of 

children living in other areas and reported no 

differences (Symington et al. 1991). Franklin 

et al. (2000) determined that individuals with 

a home formaldehyde concentration of at least 

50 ppb had a significantly increased volume of 

exhaled nitric oxide, which serves as a marker 

of airway inflammation (Franklin et al. 2000). 

Venn et al. (2003) did not observe an association between persistent wheezing and formaldehyde exposure; however, among children with 

persistent wheezing, those reporting frequent 

nighttime symptoms had higher formaldehyde 

levels compared with those not experiencing 

nocturnal symptoms (Venn et al. 2003). Erdei 

et al. (2003) reported a significant increase in 

immune biomarkers in children exposed to 

high amounts of formaldehyde (Erdei et al. 

2003). Doi et al. (2003) found only 2 of 122 

asthmatic children have formaldehyde-specific 

IgE and concluded that formaldehyde is not 

a risk factor for childhood asthma (Doi et al. 

2003). 

By its nature, a systematic review incorporates many individual studies, each of 

which has its own limitations, and not surprisingly, our analysis revealed low to moderate between-study heterogeneity. Ultimately 

much of the heterogeneity appears to be 

attributed to a single study (Rumchev et al. 

2002). The reason this study stands out can 

be partly ascribed to the precision of the OR 

for the association between formaldehyde 

and asthma; additionally, this study is unique 

in that the mean age of the participants was 

< 2 years. Infants and younger children may 

be even more vulnerable than older children 

to the effects of formaldehyde because of

the small caliber of their airways. When the 

analysis was conducted without this study, 

the results of the fixed- and random-effects 

models were highly consistent, and there was 

a decrease in the measures of heterogeneity. 

Beyond the influence of the Rumchev et al. 

(2002) study, a number of study-specific limitations must also be mentioned. First, several studies used self-reported information 

on ever having been diagnosed with asthma 

(e.g., Krzyzanowski et al. 1990; Smedje and 

Norbäck 2001). However, research indicates 

that there is a high level of agreement between 

self-reported and physician-diagnosed asthma 

such that this issue is likely of minimal concern (Rönmark et al. 1999). Moreover, when 

stratified by asthma definition, the results were 

largely consistent. Another limitation faced 

by several studies is selection bias (Garrett 

et al. 1999; Rumchev et al. 2002; Tavernier 

et al. 2006). For example, Rumchev et al. 

(2002) hypothesized that because their study 

focused on indoor environmental risk factors 

for asthma, it was likely that the people who 

were most interested in this topic were more 

likely to participate in the study. The authors 

also suggested that selection bias may have 

arisen from low and potentially differential 

participation rates; however, they describe a 

number of strategies that were employed to 

minimize this problem. Although some studies provided adjusted estimates, others did 

not. Thus, our pooled results may be subject 

to residual confounding. The extent of this 

problem is a function of the individual study 

weights; the two studies that did not provide adjusted estimates generally had higher 

weights than those that did. Finally, the 

temporal relationship between etiologically 

relevant formaldehyde exposure and asthma 

cannot be established in most of the studies included in our analysis because of their 

cross-sectional designs. As a result, our pooled 

results are largely cross-sectional in nature,

and the measured formaldehyde levels do not 

reflect personal exposures. This problem is 

compounded by the inclusion of those studies 

wherein “ever asthma” was used as an indication of a positive outcome, because such a 

definition will capture transient outcomes 

whose etiology may lie in acute exposures that 

occurred in the distant past and may not be 

captured by current exposure levels. The study 

by Smedje and Norbäck (2001) does not suffer from this potential limitation given its 

use of a cohort study design. The inability 

to quantify etiologically relevant formaldehyde levels is attributable to several factors. 

Formaldehyde levels were not measured at the 

same time of the year from one study to the 

next. This is important, because formaldehyde 

levels can vary with temperature and humidity. Whereas formaldehyde levels were measured at the subjects’ home in some studies, 

others focused on the school setting. Taken 

together, the implication is that the observed 

formaldehyde levels and their association with 

asthma may not reflect the true the magnitude of formaldehyde exposure, specifically 

that preceding asthma onset.

Conclusions

Subject to the limitations discussed above, the 

results of this systematic review suggest that 

there is a positive association between formaldehyde levels and childhood asthma. Taken 

in conjunction with a plausible biological 

mechanism, the results of this study provide 

important evidence regarding the potential 

causal link between formaldehyde and asthma 

in children. This is not to suggest that closure 

can be brought to this issue. Well-designed 

prospective epidemiologic studies are needed 

to shed additional light on this issue. 

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