doi:10.1136/oem.2003.007476 

Occup. Environ. Med. 2004;61;193-200 

 

L E Pinkerton, M J Hein and L T Stayner 

 

exposed to formaldehyde: an update

Mortality among a cohort of garment workers

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Mortality among a cohort of garment workers exposed to

formaldehyde: an update

L E Pinkerton, M J Hein, L T Stayner

.............................................................................................................................. .

See end of article for

authors’ affiliations

.......................

Correspondence to:

Dr L E Pinkerton,

Epidemiology Section,

Industrywide Studies

Branch, Division of

Surveillance, Hazard

Evaluations and Field

Studies, The National

Institute for Occupational

Safety and Health, 4676

Columbia Parkway, R-15,

Cincinnati, OH 45226,

USA; LPinkerton@cdc.gov

Accepted 6 June 2003

.......................

Occup Environ Med 2004;61:193–200. doi: 10.1136/oem.2003.007476

Aims: To evaluate the mortality experience of 11 039 workers exposed to formaldehyde for three months

or more in three garment plants. The mean time weighted average formaldehyde exposure at the plants in

the early 1980s was 0.15 ppm but past exposures may have been substantially higher.

Methods: Vital status was updated through 1998, and life table analyses were conducted.

Results: Mortality from all causes (2206 deaths, standardised mortality ratio (SMR) 0.92, 95% CI 0.88 to

0.96) and all cancers (SMR 0.89, 95% CI 0.82 to 0.97) was less than expected based on US mortality

rates. A non-significant increase in mortality from myeloid leukaemia (15 deaths, SMR 1.44, 95% CI 0.80

to 2.37) was observed. Mortality from myeloid leukaemia was greatest among workers first exposed in the

earliest years when exposures were presumably higher, among workers with 10 or more years of

exposure, and among workers with 20 or more years since first exposure. No nasal or nasopharyngeal

cancers were observed. Mortality from trachea, bronchus, and lung cancer (147 deaths, SMR 0.98, 95%

CI 0.82 to 1.15) was not increased. Multiple cause mortality from leukaemia was increased almost twofold

among workers with both 10 or more years of exposure and 20 years or more since first exposure (15

deaths, SMR 1.92, 95% CI 1.08 to 3.17). Multiple cause mortality from myeloid leukaemia among this

group of workers was also significantly increased (8 deaths, SMR 2.55, 95% CI 1.10 to 5.03).

Conclusions: Results support a possible relation between formaldehyde exposure and myeloid leukaemia

mortality. Previous epidemiological studies supporting a relation between formaldehyde exposure and

leukaemia mortality have been primarily of formaldehyde exposed professional groups, not formaldehyde

exposed industrial workers. Limitations include limited power to detect an excess for rare cancers such as

nasal and nasopharyngeal cancers and lack of individual exposure estimates.

I

n 1988, Stayner and colleagues reported the mortality

experience of 11 030 employees with exposure to formaldehyde in three garment facilities in the USA.1 This

retrospective cohort mortality study was initiated after

Stayner et al observed significant excesses in mortality from

cancers of the buccal cavity, biliary passages and liver, and

other lymphatic and haematopoietic sites among garment

workers exposed to formaldehyde in a separate, but overlapping, proportionate mortality study.2 The main finding of

the cohort mortality study was an excess in mortality from

cancers of the buccal cavity (standardised mortality ratio

(SMR) 3.43) based on four observed deaths. Excesses in

mortality were also observed for cancers of the connective

tissue (SMR 3.64), trachea, bronchus, and lung (SMR 1.14),

pharynx (SMR 1.13), bladder (SMR 1.12), leukaemia (SMR

1.14), and other lymphopoietic neoplasms (SMR 1.70).1

Concern about the potential carcinogenicity of formaldehyde developed after formaldehyde was shown to cause

nasal squamous cell carcinomas in rats.3 4 In 1995, the

International Agency for Research on Cancer (IARC) classified formaldehyde as a probable human carcinogen with

sufficient evidence in experimental animals and limited

evidence in humans for the carcinogenicity of formaldehyde.5

The evidence for carcinogenicity in humans was considered

strongest for nasopharyngeal cancers. Three meta-analyses

have been conducted to evaluate the association between

formaldehyde exposure and cancers of the upper respiratory

tract and lung with somewhat discrepant results.6–8 One

meta-analysis also evaluated the association between formaldehyde exposure and other cancers.6 Excesses in leukaemia and brain cancer mortality were found among

formaldehyde exposed professional groups (for example,

pathologists, anatomists, and embalmers), but similar

excesses were not found among formaldehyde exposed

industrial workers.6 Because of continuing concern about

the possible human carcinogenicity of formaldehyde, we

extended the follow up of the cohort described by Stayner

and colleagues.1 The present report describes the mortality

experience of the cohort through 1998, an additional 16 years

of follow up.

METHODS

Cohort description

The cohort was assembled from the personnel records

obtained from three garment manufacturing facilities, which

will be referred to as plants 1, 2, and 3. Plants 1 and 3 were

located in Georgia; plant 2 was located in Pennsylvania.

These garment facilities produced shirts from fabrics which

were treated with formaldehyde resins to impart crease

resistance and other desirable properties. The fabrics emitted

formaldehyde gas resulting in potential occupational exposures. Employees who had worked at least three months after

formaldehyde was first introduced into the production

process were included in the cohort. Formaldehyde was first

introduced in 1959 at plants 1 and 2, and in 1955 at plant 3.

Clerical and administrative employees were not included. We

also reviewed documentation and data files from the original

study to identify employees who met the original cohort

criteria, but had been omitted. The final cohort included

............................................................... .

Abbreviations: CI, confidence interval; LTAS, life table analysis system;

MCOD, multiple causes of death; NDI, National Death Index; PYAR,

person-years-at-risk; SMR, standardised mortality ratio; STEL, short term

exposure limit; TWA, time weighted average

www.occenvmed.com
11 098 workers, 11 029 of whom were in the original cohort

and 69 of whom were added. One individual in the original

cohort of 11 030 workers was deleted because he worked less

than three months after formaldehyde was introduced into

the production process. Finally, 59 (0.5%) of the 11 098

workers in the final cohort were excluded from the analysis

because their date of birth was unknown, resulting in 11 039

workers available for analysis.

Data on personal exposure levels of formaldehyde for 549

randomly selected employees in five different departments

(cutting, collar, parts, assembly, and packaging) are available

for 1981 (plant 1) and 1984 (plants 2 and 3).1 9 Briefly,

exposure to formaldehyde was similar across departments

and plants; the geometric mean eight hour time weighted

average (TWA) exposure to formaldehyde across all departments and plants ranged from 0.09 to 0.20 ppm. The overall

geometric mean concentration of formaldehyde was

0.15 ppm (geometric standard deviation 1.90). Area monitoring showed that the formaldehyde levels were essentially

constant without substantial peaks or intermittent exposures.

Additional information on the exposure levels found is

available elsewhere.1 9 Information on historical exposure

levels to formaldehyde was not available for these plants.

However, formaldehyde exposures were believed to have

been substantially higher in earlier years because the resin

systems used in treating permanent press fabrics had been

improved to reduce the amount of formaldehyde in the

fabrics. The current Occupational Safety and Health

Administration (OSHA) standard for formaldehyde exposure

is 2 ppm as a short term exposure limit (STEL) and 0.75 ppm

as an eight hour TWA.

Follow up

The vital status of all persons in the cohort was determined

through 31 December 1998. Follow up included inquiry

through the Social Security Administration, Internal Revenue

Service, US Postal Service, National Death Index (NDI), and

state bureaus of motor vehicles. Death certificates were

obtained from state vital records offices for some deceased

members of the cohort and coded by a trained nosologist

according to the revision of the International Classification of

Diseases in effect at the time of death. The causes of death for

other deceased members of the cohort were obtained from

the NDI.

Although vital status was updated for the workers in the

cohort, the work histories were not. We assumed that

exposure (employment) ceased in 1981 for plants 1 and 2

and in 1983 for plant 3 (that is, when the work histories were

ment was underestimated for 1230 (11.1%) of the 11 039

cohort members who were actively employed when the work

history records were obtained.

Analysis

The mortality experience of the cohort was analysed with the

use of the PC version of the National Institute for

Occupational Safety and Health (NIOSH) modified life table

analysis system (LTAS)10–12 (http://www.cdc.gov/niosh/

tindex.html). Each cohort member accumulated personyears-at-risk (PYAR) for each year of life after the three

month eligibility period until the date of death for deceased

cohort members, the date last observed for persons lost to

follow up, or the ending date of the study (31 December

1998) for cohort members known to be alive. In contrast,

PYAR were accrued until the ending date of the study for

persons lost to follow up in the original study. Cohort

members known to be alive after 1 January 1979 (the date

that the NDI began) and not identified as deceased were

assumed to be alive as of 31 December 1998. The PYAR were

stratified into five year intervals by age and calendar time and

were then multiplied by the appropriate US gender, race, and

cause specific mortality rates to calculate the expected

number of deaths for that stratum. At the time of the study,

the NIOSH LTAS only maintained US mortality rates through

1997. In order to calculate expected deaths through 1998, the

mortality rates for 1995–97 were used for 1998. The resulting

expected numbers were summed across strata to obtain cause

specific and total expected number of deaths. The ratio of

observed to expected number of deaths was expressed as the

standardised mortality ratio (SMR). Ninety five per cent

confidence intervals (CI) were computed for the SMRs

assuming a Poisson distribution for observed deaths. The

mortality analysis was repeated using Georgia or

Pennsylvania state mortality rates, as appropriate, to generate

expected numbers of death. In addition to analyses of

underlying cause of death, all causes listed on the death

certificate were analysed using multiple cause mortality

methods described by Steenland and colleagues.13 Multiple

cause analyses are particularly important for diseases that

may be prevalent at death but that are not the underlying

cause of death.13 In analyses using state or multiple cause

mortality rates, PYAR started to accumulate on 1 January

1960, when the rates were first available, or completion of the

three month eligibility period, whichever was later.

We stratified SMRs by duration of exposure (,3, 3–9, 10+

years), time since first exposure (,10, 10–19, 20+ years), and

year of first exposure (,1963, 1963–70, 1971+). The cut

points for time since first exposure and year of first exposure

were retained from the original study. For the analyses

stratified by duration of exposure (that is, duration of

employment after formaldehyde was introduced into the

process), the cohort was divided into three groups so that

each group had an approximately equal number of expected

deaths. Testing for heterogeneity and trend in the SMRs was

performed using the methods of Breslow and Day (1987).14

A sensitivity analysis was performed by replicating the life

table analyses under different assumptions in order to

evaluate the impact of underestimating duration of exposure

for cohort members who were actively employed when the

work history records were obtained. First, workers who were

still employed at the time the records were obtained were

assumed to have worked until age 65 years, the date last

observed, or the date the plant closed, whichever came first.

There were a small number of employees who were still

employed at the time the records were obtained who were

already beyond the age of 65 years. These workers were

assumed to have continued working for an additional 2 years

Main messages

N An excess in myeloid leukaemia mortality was

observed among a cohort of formaldehyde exposed

garment workers.

N Mortality from myeloid leukaemia was greatest among

workers first exposed in the earliest years when

exposures were presumably higher, among workers

with 10 or more years of exposure, and among

workers with 20 or more years since first exposure.

N The findings for leukaemia mortality are consistent with

the findings of several studies of formaldehyde

exposed professional groups.

N There was no evidence of an association between

formaldehyde exposure and mortality from respiratory

cancers.

www.occenvmed.com
of employment beyond age 65 years in this cohort is 2.66

years. A second scenario assumed workers under age 65 who

were still employed at the time the records were obtained

continued to work until halfway between the date the records

were obtained and age 65, the date last observed, or the date

the plant closed, whichever came first. Under the two

scenarios described, the exposure duration category remained

unchanged for 10 735 (97.2%) of the 11 039 workers in the

analysis. Of the 1230 cohort members who were still

employed when the records were obtained, 915 (74.4%)

had already been employed 10 or more years.

We also calculated age adjusted rate ratios by exposure

duration, using the lowest exposure duration category as the

reference group, for mortality from selected cancers of a

priori interest using Poisson regression.

Based on previous studies, the primary a priori outcomes of

interest in this study were cancers of the upper respiratory

tract. Leukaemia and brain cancer were also a priori

outcomes of interest.

RESULTS

A total of 11 039 workers contributing 339 241 person-years

were included in the study. Table 1 shows the distribution of

the cohort by vital status, sex, race, plant, duration of

exposure, time since first exposure, and first year of exposure.

The cohort is primarily white (75.6%) and female (81.7%).

Roughly half (51.2%) of the workers are from plant 1. Causes

of death were obtained from death certificates or the NDI for

2195 (99.5%) of 2206 individuals known to be deceased.

Deaths with missing causes of death were included in the

other and unknown causes category. The duration of

exposure of the cohort is relatively short with a median of

3.3 years. Over 40% of the cohort was first exposed prior to

1963, with a median time since first exposure of 31.7 years.

causes of death by study period. Some findings for the 1955–

82 study period differ slightly from the results reported by

Stayner and colleagues in the original study, primarily

because of the differences described previously in the study

cohort and method for accruing PYAR for persons lost to

follow up. Overall, mortality from all causes (SMR 0.92, 95%

CI 0.88 to 0.96) was significantly less than expected.

Mortality from all malignant neoplasms was also significantly less than expected (SMR 0.89, 95% CI 0.82 to 0.97).

Mortality from pharyngeal cancer (three deaths, SMR 0.64,

95% CI 0.13 to 1.86), laryngeal cancer (three deaths, SMR

0.88, 95% CI 0.18 to 2.59), and trachea, bronchus, and lung

cancer (SMR 0.98, 95% CI 0.82 to 1.15) was not increased.

Two of the three cancers of the pharynx were cancers of the

hypopharynx; one was of an unspecified site within the

pharynx. No cancers of the nasopharynx (expected (exp)

0.96) or nose (exp 0.16) were observed. Mortality from

cancers of other parts of the respiratory system, a category

that includes nasal cancers, was increased (SMR 1.21, 95% CI

0.15 to 4.37), based on two cancers of the pleura. No

additional deaths from cancer of the buccal cavity were

observed in the analyses of underlying cause of death during

this update. Mortality from cancer of the buccal cavity (four

deaths, SMR 1.33, 95% CI 0.36 to 3.41) was increased, but the

observed excess was substantially less than the excess

observed in the previous study and not statistically significant. Mortality from brain cancer and leukaemia was

similar to that expected, with both SMRs equal to 1.09

(95% CI 0.66 to 1.71 and 0.70 to 1.62 for brain cancer and

leukaemia, respectively). Among outcomes other than those

of a priori interest, non-significant excesses were observed for

mortality from cancer of the connective and soft tissue (seven

deaths, SMR 1.57, 95% CI 0.63 to 3.24), prostate cancer (11

deaths, SMR 1.58, 95% CI 0.79 to 2.83), and, based on two

observed deaths each, other male genital cancer (SMR 3.89,

95% CI 0.47 to 14.04) and thyroid cancer (SMR 1.16, 95% CI

0.14 to 4.18). Among non-malignant causes of death,

mortality from cardiomyopathy, conductive disorders, and

other heart diseases (SMR 1.17, 95% CI 1.00 to 1.36) was

increased.

Table 3 shows the results of additional analyses to evaluate

mortality from heart disease and leukaemia in more detailed

subgroupings. Mortality was significantly increased for other

heart disease (SMR 1.43, 95% CI 1.10 to 1.83) and nonsignificantly increased for conductive disorders (SMR 1.32,

95% CI 0.97 to 1.74) and myeloid leukaemia (15 deaths, SMR

1.44, 95% CI 0.80 to 2.37). The underlying cause of death for

most of the deaths from other heart disease was heart failure.

The excess in myeloid leukaemia mortality was due to a nonsignificant increase in both acute myeloid leukaemia (nine

deaths, SMR 1.34, 95% CI 0.61 to 2.54) and chronic myeloid

leukaemia mortality (four deaths, SMR 1.39, 95% CI 0.38 to

3.56).

In order to evaluate whether regional variations in

mortality rates could explain the findings, analyses were

also conducted using state rates as the comparison population. Mortality from conductive disorders (SMR 0.72, 95% CI

0.53 to 0.95) and other heart disease (SMR 0.93, 95% CI 0.71

to 1.19) was not increased based on state rates. The results

using state rates and US rates were similar for the causes of

death of a priori interest (leukaemia, brain, and upper

respiratory cancers).

Table 4 shows the results from analysis stratified by

duration of exposure and time since first exposure for

selected causes of death with five or more observed deaths.

Mortality from leukaemia, myeloid leukaemia, and acute

myeloid leukaemia was greatest among workers with 10 or

more years of exposure and among workers with 20 years or

Table 1 Characteristics of the study population

Excluded from analysis* 59

Number of workers 11039 (100%)

Race/sex

White male 1612 (14.6%)

Non-white male 403 (3.7%)

White female 6737 (61.0%)

Non-white female 2287 (20.7%)

Vital status (as of 31/12/1998)

Alive 8648 (78.3%)

Dead 2206 (20.0%)

Unknown 185 (1.7%)

Plant site

Plant 1 5647 (51.2%)

Plant 2 1851 (16.8%)

Plant 3 3541 (32.1%)

Year of birth

Median 1939

Range 1882–1960

Age at first exposure (years)

Median 26.2

Range 15.2–79.8

Year first exposed

Prior to 1963 4669 (42.3%)

1963–70 3813 (34.5%)

1971 or later 2557 (23.2%)

Duration of exposure

,3 years 5291 (47.9%)

3–9 years 3142 (28.5%)

10+ years 2606 (23.6%)

Time since first exposure

,10 years 330 (3.0%)

10–19 years 411 (3.7%)

20+ years 10298 (93.3%)

*Missing date of birth. No assumptions were made when date of birth

was missing. These workers were included in the original study by

Stayner and colleagues.1

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Table 2 Garment workers’ mortality results (US referent rates); update of cohort to 1998

Underlying cause of death

(ICD codes)`

Original study period (1955–82) Updated period (1983–98) Total study period (1955–98)

OBS SMR 95% CI OBS SMR 95% CI OBS SMR 95% CI

All deaths 635 0.80** 0.74 to 0.86 1571 0.98 0.93 to 1.03 2206 0.92** 0.88 to 0.96

All cancers (140–208) 193 0.86* 0.74 to 0.98 415 0.91 0.83 to 1.00 608 0.89** 0.82 to 0.97

Buccal and pharyngeal CA (140–149) 6 1.58 0.58 to 3.45 2 0.31 0.04 to 1.14 8 0.79 0.34 to 1.55

Buccal cavity (142–145) 4 3.53 0.96 to 9.02 0 0.00 0.00 to 1.98 4 1.33 0.36 to 3.41

Pharynx (146–149) 2 1.15 0.14 to 4.15 1 0.34 0.01 to 1.87 3 0.64 0.13 to 1.86

All digestive CA (150–159) 34 0.68* 0.47 to 0.95 82 0.81 0.65 to 1.01 116 0.77** 0.63 to 0.92

Oesophagus (150) 2 0.78 0.09 to 2.82 4 0.63 0.17 to 1.62 6 0.68 0.25 to 1.47

Stomach (151) 4 0.63 0.17 to 1.61 9 0.91 0.41 to 1.72 13 0.80 0.42 to 1.36

Colon (152–153) 18 0.85 0.50 to 1.34 31 0.74 0.50 to 1.05 49 0.77 0.57 to 1.02

Rectal (154) 1 0.21 0.01 to 1.19 6 0.89 0.32 to 1.93 7 0.61 0.25 to 1.26

Liver and biliary (155–156) 3 0.59 0.12 to 1.74 11 0.99 0.49 to 1.77 14 0.87 0.47 to 1.45

Pancreas (157) 6 0.64 0.23 to 1.39 20 0.87 0.53 to 1.35 26 0.81 0.53 to 1.18

All respiratory CA (160–165) 39 1.03 0.73 to 1.41 113 0.96 0.79 to 1.15 152 0.98 0.83 to 1.14

Larynx (161) 0 0.00 0.00 to 3.39 3 1.30 0.27 to 3.81 3 0.88 0.18 to 2.59

Trachea, bronchus, and lung (162) 39 1.08 0.77 to 1.48 108 0.94 0.77 to 1.14 147 0.98 0.82 to 1.15

Other respiratory (160, 163–165) 0 0.00 0.00 to 5.63 2 2.01 0.24 to 7.25 2 1.21 0.15 to 4.37

Breast CA (174–175) 33 0.70* 0.48 to 0.98 68 0.92 0.71 to 1.16 101 0.83 0.68 to 1.01

Female genital CA (179–184) 25 0.80 0.52 to 1.18 31 0.75 0.51 to 1.07 56 0.77 0.58 to 1.01

Male genital CA (185–187) 1 0.48 0.01 to 2.68 12 2.22* 1.15 to 3.89 13 1.74 0.93 to 2.98

Prostate CA (185) 0 0.00 0.00 to 2.15 11 2.10* 1.05 to 3.76 11 1.58 0.79 to 2.83

Other male genital CA (186–187) 1 2.79 0.07 to 15.51 1 6.41 0.16 to 35.59 2 3.89 0.47 to 14.04

All urinary CA (188–189) 5 0.83 0.27 to 1.94 7 0.49 0.20 to 1.01 12 0.59 0.30 to 1.03

Kidney (189.0–189.2) 2 0.57 0.07 to 2.04 3 0.36 0.07 to 1.06 5 0.42* 0.14 to 0.99

Bladder and other (188, 189.3–189.9) 3 1.20 0.25 to 3.51 4 0.66 0.18 to 1.69 7 0.82 0.33 to 1.69

All other and unspecified site CA

(170–173, 190–199) 30 1.10 0.74 to 1.57 61 1.13 0.87 to 1.46 91 1.12 0.90 to 1.38

Brain CA (191, 192) 5 0.72 0.23 to 1.69 14 1.34 0.73 to 2.24 19 1.09 0.66 to 1.71

Thyroid CA (193) 1 1.56 0.04 to 8.67 1 0.92 0.02 to 5.11 2 1.16 0.14 to 4.18

Connective and soft tissue (171) 4 3.14 0.86 to 8.03 3 0.94 0.19 to 2.76 7 1.57 0.63 to 3.24

Other/unspecified site CA (194–199) 18 1.32 0.78 to 2.09 36 1.13 0.79 to 1.57 54 1.19 0.89 to 1.55

All lymphatic and haematopoietic CA

(200–208) 20 1.01 0.62 to 1.56 39 0.96 0.68 to 1.31 59 0.97 0.74 to 1.26

Lymphosarcoma and reticulosarcoma

(200) 2 0.50 0.06 to 1.79 3 1.63 0.34 to 4.78 5 0.85 0.28 to 1.99

Hodgkin’s disease (201) 1 0.41 0.01 to 2.30 1 0.81 0.02 to 4.51 2 0.55 0.07 to 1.98

Leukaemia (204–208) 9 1.14 0.52 to 2.17 15 1.05 0.59 to 1.74 24 1.09 0.70 to 1.62

Other lymphatic and haematopoietic

CA (202–203) 8 1.46 0.63 to 2.87 20 0.85 0.52 to 1.32 28 0.97 0.64 to 1.40

Benign and unspecified neoplasms

(210–239) 4 1.00 0.27 to 2.56 6 1.02 0.37 to 2.22 10 1.01 0.48 to 1.86

Tuberculosis (010–018) 1 0.45 0.01 to 2.49 2 1.60 0.19 to 5.77 3 0.86 0.18 to 2.52

Diabetes mellitus (250) 4 0.23** 0.06 to 0.60 29 0.65* 0.43 to 0.93 33 0.53** 0.37 to 0.75

Diseases of the blood (280–289) 1 0.30 0.01 to 1.69 9 1.29 0.59 to 2.45 10 0.98 0.47 to 1.79

Mental disorders (290–319) 1 0.17* 0.00 to 0.97 23 1.08 0.68 to 1.61 24 0.89 0.57 to 1.32

Non-malignant nervous system disease

(320–389) 3 0.27* 0.06 to 0.80 27 0.85 0.56 to 1.24 30 0.71 0.48 to 1.01

Heart disease (390–398, 402, 404,

410–414, 420–429) 179 0.81** 0.69 to 0.93 513 1.04 0.95 to 1.13 692 0.96 0.89 to 1.04

Ischaemic heart disease (410–414) 145 0.83* 0.70 to 0.98 333 1.01 0.90 to 1.12 478 0.95 0.86 to 1.03

Cardiomyopathy, conductive

disorders, and other heart diseases

(420–423, 425–428, 429.2–429.9) 25 1.03 0.67 to 1.53 150 1.19* 1.01 to 1.40 175 1.17* 1.00 to 1.36

Other circulatory disease (401, 403, 405,

415–417, 430–459) 61 0.79 0.60 to 1.01 167 1.02 0.87 to 1.19 228 0.95 0.83 to 1.08

Non-malignant respiratory disease

(460–519) 28 0.75 0.50 to 1.08 148 1.09 0.92 to 1.28 176 1.01 0.87 to 1.18

Chronic and unspecified bronchitis

(490–491) 4 2.51 0.68 to 6.43 2 0.76 0.09 to 2.76 6 1.42 0.52 to 3.10

Emphysema (492) 8 1.50 0.65 to 2.96 12 0.94 0.49 to 1.65 20 1.11 0.68 to 1.71

Asthma (493) 0 0.00 0.00 to 1.55 8 1.50 0.65 to 2.96 8 1.04 0.45 to 2.05

Pneumoconiosis and other respiratory

disease (470–478, 494–519) 5 0.42* 0.14 to 0.98 88 1.29* 1.03 to 1.58 93 1.16 0.93 to 1.42

Non-malignant digestive disease

(520–579) 32 0.71 0.49 to 1.00 51 0.79 0.59 to 1.04 83 0.76* 0.60 to 0.94

Cirrhosis of the liver (571) 18 0.73 0.44 to 1.16 13 0.53* 0.28 to 0.90 31 0.63** 0.43 to 0.89

Non-malignant genitourinary disease

(580–629) 12 1.02 0.53 to 1.78 33 1.17 0.80 to 1.64 45 1.12 0.82 to 1.50

Acute renal failure (580, 581, 584) 2 2.32 0.28 to 8.37 5 1.95 0.63 to 4.57 7 2.05 0.82 to 4.22

Chronic renal failure (582, 583,

585–587) 1 0.21 0.01 to 1.19 16 1.24 0.71 to 2.01 17 0.97 0.56 to 1.55

Non-malignant skin disease (680–709) 1 0.80 0.02 to 4.47 3 1.32 0.27 to 3.85 4 1.14 0.31 to 2.90

Non-malignant musculoskeletal disease

(710–739) 3 0.74 0.15 to 2.18 9 1.00 0.46 to 1.91 12 0.92 0.48 to 1.61

Ill defined conditions (780–796,

798–799) 5 0.45 0.15 to 1.05 8 0.56 0.24 to 1.10 13 0.51* 0.27 to 0.88

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more since first exposure. The SMR for myeloid leukaemia

among workers with both 10 or more years of exposure and

20 years or more since first exposure was 2.43 (seven deaths,

95% CI 0.98 to 5.01). Mortality from acute myeloid leukaemia

among this group of workers was similarly increased (five

deaths, SMR 2.51, 95% CI 0.81 to 5.85). Mortality from

cancer of the trachea, bronchus, and lung was inversely

related to duration of exposure and highest among workers

with less than 10 years since first exposure. There was no

clear pattern between mortality from prostatic cancer and

duration of exposure. Mortality from brain cancer, connective

tissue cancer, and cardiomyopathy, conductive disorders, and

other heart diseases was highest among workers with less

than three years of exposure.

The results stratified by duration of exposure were

essentially unchanged when the analyses were repeated

under different assumptions about the duration of

exposure for workers who were actively employed when

the work history records were obtained. The SMR for

myeloid leukaemia among workers exposed for 3–9 years

increased from 1.26 to 1.30 under the scenarios in which

individuals who were still employed when the work

history records were obtained were assumed to have

continued working; the SMR among workers exposed 10

or more years decreased from 2.19 to 2.13. Similar patterns

were observed across exposure duration categories in the

internal analysis for lung cancer, leukaemia, and brain

cancer. For example, the age adjusted rate ratio for leukaemia

among those exposed 3–9 years and 10 or more years was

0.67 (95% CI 0.21 to 2.17) and 1.25 (95% CI 0.46 to 3.43),

respectively, compared to workers exposed for less than three

years.

Table 5 shows the results from analyses stratified by year of

first exposure. Mortality from brain cancer, leukaemia, and

myeloid leukaemia was highest among workers first exposed

prior to 1963, when exposures to formaldehyde were

presumably higher. Mortality from prostate cancer and

cancer of the trachea, bronchus, and lung was highest

among workers first exposed in 1971 or later.

Finally, one additional cancer of the buccal cavity was

detected in the multiple causes of death (MCOD) analysis

(five deaths, SMR 1.37, 95% CI 0.44 to 3.21). Seven

additional leukaemia deaths (SMR 1.19, 95% CI 0.81 to

1.68), including two additional myeloid leukaemia deaths

(SMR 1.38, 95% CI 0.80 to 2.20) and five additional

lymphocytic leukaemia deaths (SMR 1.11, 95% CI 0.48 to

2.19) were observed in the MCOD analysis. Among workers

with 10 or more years of exposure, multiple cause mortality

was significantly increased for leukaemia (17 deaths, SMR

1.78, 95% CI 1.04 to 2.86) and myeloid leukaemia (nine

deaths, SMR 2.24, 95% CI 1.02 to 4.25) and non-signficantly

increased for lymphocytic leukaemia (six deaths, SMR 2.12,

95% CI 0.78 to 4.62). The excess in leukaemia (26 deaths,

SMR 1.48, 95% CI 0.97 to 2.17) and myeloid leukaemia (15

deaths, SMR 2.02, 95% CI 1.13 to 3.34) mortality, based on

MCOD, was concentrated among workers with 20 or more

years since first exposure. All lymphocytic leukaemia deaths

occurred among workers with 10 or more years since first

exposure (10–19 years since first exposure: two deaths, SMR

1.75, 95% CI 0.21 to 6.31; 20 or more years since first

Underlying cause of death

(ICD codes)`

Original study period (1955–82) Updated period (1983–98) Total study period (1955–98)

OBS SMR 95% CI OBS SMR 95% CI OBS SMR 95% CI

Accidents (E800–E949) 52 0.89 0.67 to 1.17 48 1.02 0.75 to 1.36 100 0.95 0.77 to 1.16

Violence (E950–E978) 35 0.95 0.66 to 1.32 28 1.13 0.75 to 1.63 63 1.02 0.78 to 1.31

Other and unknown causes 1 20 1.05 0.64 to 1.63 52 0.94 0.70 to 1.23 72 0.97 0.76 to 1.22

OBS, observed number of deaths; SMR, standardised mortality ratio; CI, confidence interval; CA, cancer.

Results for all race/sex groups combined.

`International Classification of Diseases, 9th revision.

1Includes 11 observed deaths in total study period with missing death certificates.

*95% CI excludes the null value (1.0).

**99% CI excludes the null value (1.0).

Table 3 Garment workers’ mortality (since 1960) from leukaemia and heart disease

(US referent rates): update of cohort to 1998`

Cause of death (ICD codes)1 OBS SMR 95% CI

Leukaemia (204–208) 24 1.09 0.70 to 1.63

Lymphocytic leukaemia (204) 3 0.60 0.12 to 1.75

Myeloid leukaemia (205) 15 1.44 0.80 to 2.37

Acute myeloid leukaemia (205.0) 9 1.34 0.61 to 2.54

Chronic myeloid leukaemia (205.1) 4 1.39 0.38 to 3.56

Other and unspecified myeloid leukaemia (205.2–205.9) 1 2.15 0.05 to 11.94

Other and unspecified leukaemia (206–208) 6 0.92 0.34 to 2.00

Heart disease (390–398, 402–404, 410–414, 420–429) 691 0.97 0.90 to 1.04

Ischaemic heart disease (410–414, 429.2) 522 0.94 0.86 to 1.03

Cardiomyopathy (425) 19 0.99 0.59 to 1.54

Conductive disorders (426–427) 49 1.32 0.97 to 1.74

Other heart diseases (420–423, 428, 429.3–429.9) 62 1.43** 1.10 to 1.83

OBS, observed number of deaths; SMR, standardised mortality ratio; CI, confidence interval; CA = cancer.

Results for subtypes of myeloid leukaemia are for 1968, when US mortality rates for acute myeloid leukaemia and

chronic myeloid leukaemia were first available, through 1998. One chronic myeloid leukaemia death occurred

prior to 1968.

`Results for all race/sex groups combined.

1International Classification of Diseases, 9th revision.

*95% CI excludes the null value (1.0).

**99% CI excludes the null value (1.0).

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exposure: six deaths, SMR 1.14, 95% CI 0.42 to 2.48). Among

workers with both 10 or more years of exposure and 20 years

or more since first exposure, multiple cause mortality from

leukaemia was significantly increased almost twofold (15

deaths, SMR 1.92, 95% CI 1.08 to 3.17). Multiple cause

mortality from myeloid leukaemia was also significantly

increased among this group of workers (eight deaths, SMR

2.55, 95% CI 1.10 to 5.03). Multiple cause analyses were also

conducted for acute myeloid leukaemia beginning in 1968,

when US multiple cause mortality rates for acute myeloid

leukaemia were first available. The multiple cause SMR for

acute myeloid leukaemia was 1.25 (nine deaths, 95% CI 0.57

to 2.37) among the entire cohort, 1.91 (five deaths, 95% CI

0.62 to 4.45) among workers with 10 or more years of

exposure, and 1.84 (nine deaths, 95% CI 0.84 to 3.49) among

workers with 20 or more years since first exposure. No

cancers of the nasal cavities or nasopharynx were identified

in the MCOD analysis.

DISCUSSION

We observed a small increase in mortality from leukaemia

among a cohort of formaldehyde exposed garment workers.

This excess was primarily driven by a moderate increase in

myeloid leukaemia mortality. There was also a non-significant increase in lymphocytic leukaemia mortality, based on

MCOD, especially among workers with 10 or more years of

exposure. Lymphocytic leukaemia mortality was not

increased in the underlying cause of death analysis, but in

the USA, the five year survival rate for chronic lymphocytic

leukaemia, which is more common than acute lymphocytic

y y p

exposure (US referent rates); update of cohort to 1998`

Cause of death (ICD codes)1

Duration of exposure Time since first exposure

,3 years

SMR (OBS)

3–9 years

SMR (OBS)

10+ years

SMR (OBS)

,10 years

SMR (OBS)

10–19 years

SMR (OBS)

20+ years

SMR (OBS)

All deaths 1.03 (754) 0.89 (689)** 0.85 (763)** 0.79 (216)** 0.78 (379)** 0.98 (1611)

All cancers (140-208) 1.04 (221) 0.85 (180)* 0.81 (207)** 0.84 (56) 0.80 (115)* 0.93 (437)

Trachea, bronchus, and lung CA (162) 1.26 (61) 1.07 (47) 0.67 (39)** 1.77 (14) 0.97 (25) 0.92 (108)

Prostate CA (185) 1.83 (4) 0.43 (1) 2.46 (6) – (0) 0.70 (1) 1.99 (10)

Brain CA (191, 192) 1.45 (9) 0.94 (5) 0.86 (5) 0.82 (2) 0.97 (4) 1.20 (13)

Connective and soft tissue CA (171) 2.42 (4) 2.26 (3) – (0) 2.30 (1) 2.15 (2) 1.30 (4)

Leukaemia (204–208) 0.96 (7) 0.72 (5) 1.53 (12) 0.68 (2) 0.65 (3) 1.31 (19)

Myeloid leukaemia (205) 0.83 (3) 1.26 (4) 2.19 (8) 0.90 (1) 0.40 (1) 1.91 (13)*

Acute myeloid leukaemia (205.0) 0.44 (1) 1.53 (3) 2.02 (5) – (0) – (0) 1.93 (9)

Heart disease (390–398, 402, 404,

410–414, 420–429)

1.15 (210) 0.93 (225) 0.88 (257)* 0.80 (48) 0.88 (117) 1.00 (527)

Ischaemic heart disease (410–414) 1.11 (139) 0.93 (161) 0.86 (178)* 0.92 (40) 0.92 (94) 0.96 (344)

Cardiomyopathy, conductive

disorders, and other heart diseases

(420–423, 425–428, 429.2–429.9)

1.45 (58)** 1.01 (48) 1.10 (69) 0.90 (5) 0.94 (17) 1.21 (153)*

OBS, observed number of deaths; SMR, standardised mortality ratio; CA, cancer.

Results for myeloid leukaemia and acute myeloid leukaemia are for 1960 and 1968, respectively, when US population rates for myeloid leukaemia and acute

myeloid leukaemia were first available, through 1998.

`Results for all race/sex groups combined.

1International Classification of Diseases, 9th revision.

*95% CI excludes the null value (1.0).

**99% CI excludes the null value (1.0).

Test for trend, p,0.05.

Table 5 Garment workers’ mortality (since 1955) from selected causes by year of first exposure (US referent rates); update of

cohort to 1998`

Year of first exposure

Cause of death (ICD codes)1

Prior to 1963

SMR (OBS)

1963–70

SMR (OBS)

1971 or later

SMR (OBS)

All deaths 0.91 (1543)** 0.97 (494) 0.88 (169)

All cancers (140–208) 0.86 (412)** 0.94 (142) 1.11 (54)

Trachea, bronchus, and lung CA (162) 0.86 (89) 1.06 (39) 1.83 (19) *

Prostate CA (185) 1.32 (5) 1.64 (4) 2.80 (2)

Brain CA (191,192) 1.17 (14) 0.97 (4) 0.76 (1)

Connective and soft tissue CA (171) 1.10 (3) 2.47 (3) 1.95 (1)

Leukaemia (204–208) 1.23 (19) 0.81 (4) 0.56 (1)

Myeloid leukaemia (205) 1.61 (11) 1.15 (3) 1.02 (1)

Acute myeloid leukaemia (205.0) 1.81 (8) — (0) 1.60 (1)

Heart disease (390–398, 402, 404, 410–414, 420–429) 0.93 (516) 1.04 (131) 1.14 (45)

Ischaemic heart disease (410–414) 0.90 (357)* 1.05 (88) 1.40 (33)

Cardiomyopathy, conductive disorders, and other heart

diseases (420–423, 425–428, 429.2, 429.9)

1.18 (128) 1.24 (37) 0.88 (10)

OBS, observed number of deaths, SMR, standardised mortality ratio, CA, cancer.

Results for myeloid leukaemia and acute myeloid leukaemia are for 1960 and 1968, respectively, when US population rates for myeloid leukaemia and acute

myeloid leukaemia were first available, through 1998.

`Results for all race/sex groups combined.

1International Classification of Diseases, 9th revision.

*95% CI excludes the null value (1.0).

**99% CI excludes the null value (1.0).

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mortality, especially underlying cause mortality, may not be

a sensitive outcome measure for lymphocytic leukaemia.

Myeloid leukaemia mortality was highest among workers

with 10 or more years of exposure, among workers with 20 or

more years since first exposure, and among workers who

were first exposed prior to 1963 when exposures were

presumably higher, which is consistent with the hypothesis

that the observed excess in myeloid leukaemia mortality is

related to formaldehyde exposure. Because formaldehyde is

water soluble, highly reactive, and rapidly metabolised,

carcinogenic effects at sites distant from the portal of entry

are considered less likely than carcinogenic effects at the sites

of direct contact.16 17 However, transport of formaldehyde to

distant sites and subsequent carcinogenic effects cannot be

excluded. Our finding of an excess in leukaemia mortality is

consistent with several studies of formaldehyde exposed

professional groups.6 In contrast, mortality from leukaemia

was not increased among 26 561 workers employed at 10 US

formaldehyde producing or using plants,18 or among 14 037

men employed at six British formaldehyde producing or

using plants.19 Both of these studies included workers who

were exposed to much higher levels of formaldehyde

(.2 ppm) than those measured at the plants in this study

in the 1980s. Workers in our study were probably exposed to

higher concentrations of formaldehyde in earlier years than

in the 1980s, but the level of exposure is unknown.

Investigators also found no evidence for an increased risk

of leukaemia among US automotive iron foundry workers

exposed to formaldehyde20 or among men in the Danish

Cancer Registry who had their longest work experience at a

formaldehyde using or producing company.21 Wong reported

an excess in leukaemia among a small cohort,22 but the

observed excess was based on only two observed deaths and

the study plant was included in the large US study18 of

formaldehyde using or producing facilities in which no excess

in leukaemia mortality was found.6 Most previous studies of

formaldehyde exposed workers have not evaluated cell type

specific leukaemia mortality. However, the observed excess in

myeloid leukaemia mortality is consistent with studies of

formaldehyde exposed professional groups in which the risk

of cell type specific leukaemia mortality was evaluated.23–26

Several reasons have been postulated for the observed risk

of leukaemia among formaldehyde exposed professional

groups versus industrial cohorts, including the possibility

that the increased risk of leukaemia mortality observed in

professional groups is due to occupational exposures other

than formaldehyde.6 Diagnostic bias has also been suggested

as a possible explanation since professional groups may

receive better medical care than the general population.6

Neither of these possibilities are likely explanations for the

findings in this study. Industrial hygiene surveys conducted

at the time of the original study did not identify any chemical

exposures at the study plants other than formaldehyde which

were likely to influence the study findings.1 Diagnostic bias is

also less likely in this study of garment workers than in

studies of medical professionals such as pathologists. Internal

analyses were conducted for mortality from leukaemia to

address the potential problems associated with using the US

general population as the reference population and comparing SMRs across subgroups of the cohort. Similar patterns of

risk were observed across exposure duration categories in the

internal analyses. However, we could only crudely adjust for

age in the internal analysis, because of the limited number of

observed deaths.

There is little evidence for an increased risk of mortality

from respiratory cancers in this update. Although the original

study reported an excess in mortality for both lung and

pharyngeal cancer, we did not observe an excess in mortality

cancer mortality was increased among workers first exposed

during the most recent years when exposures to formaldehyde were the lowest. Lung cancer mortality was also

increased among workers with the shortest duration of

exposure and time since first exposure. These findings

suggest that the excess in lung cancer mortality observed

among some groups of workers in this cohort is due to factors

other than formaldehyde exposure. Some investigators have

concluded that formaldehyde exposure is most likely to cause

nasopharyngeal and nasal cancers.5–7 No nasal or nasopharyngeal cancers were observed in this study.

Cancers of the buccal cavity are also biologically plausible

since direct contact with formaldehyde may occur in the

buccal cavity. There were no additional deaths from buccal

cancer, based on underlying cause of death, observed in this

update. The excess risk of mortality from buccal cancer that

was noted in the original study decreased considerably from

an SMR of 3.43 to an SMR of 1.33. Buccal cancer mortality

was not increased in previous meta-analyses of the carcinogenic effects of formaldehyde.6 7

Mortality from cardiomyopathy, conductive disorders, and

other heart disease was increased based on US population

mortality rates. There is no known association between

inhalational exposure to formaldehyde and heart disease.16

The results from the analysis using state rates suggest that

the finding may be related to regional differences. Mortality

from cardiomyopathy, conductive disorders, and other heart

diseases was also highest among workers with less than three

years of exposure, suggesting that this finding is not related

to formaldehyde exposure.

This study had limited power, despite the large cohort size,

to detect an excess in mortality from some of the cancers of a

priori interest. The power of this study to detect a twofold or

greater increase in mortality from nasopharyngeal cancer and

from nasal cancer was only 13% and 16%, respectively. In

addition, exposure-response relations could only be evaluated

using duration of exposure. This may have introduced some

misclassification and biased the exposure-response relation

towards the null since exposures probably decreased substantially over time as improvements were made in the resin

systems used to treat fabrics. Other limitations include the

relatively low levels of formaldehyde since at least 1981 to

which workers in this study were exposed, the lack of data on

formaldehyde levels prior to 1981, the lack of data on other

risk factors for cancers of interest, and the reliance on

mortality data only. Although the work history records for

this study were obtained in the early 1980s and were not

updated, the sensitivity analysis suggests that the impact of

not updating the work histories is minimal. Strengths of the

current study include the large cohort size, the inclusion of

many women, the lack of other occupational exposures at the

study plants that are likely to have influenced the study

findings, the long period of follow up, and the evaluation of

multiple cause mortality in addition to underlying cause

mortality.

In summary, the results, although not conclusive, support

a possible relation between formaldehyde exposure and

myeloid leukaemia mortality. The findings for leukaemia

mortality are consistent with the findings of several studies of

professional groups exposed to formaldehyde, but are in

contrast to other large studies of formaldehyde exposed

industrial workers. We found no evidence of an association

between formaldehyde exposure and mortality from respiratory cancers. An increased risk of mortality from buccal

cancer, based on four observed cancers, was observed, but the

results from this update are far weaker than those from the

previous study and not supported by other epidemiologic

studies. Non-significant excesses in mortality were observed

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between the observed excesses and duration of exposure.

Limitations of the study include limited power to detect an

excess in mortality from rare cancers and lack of individual

exposure estimates.

Authors’ affiliations

.....................

L E Pinkerton, M J Hein, Industrywide Studies Branch, Division of

Surveillance, Hazard Evaluations and Field Studies, The National

Institute for Occupational Safety and Health, Cincinnati, Ohio, USA

L T Stayner, Risk Evaluation Branch, Education and Information Division,

The National Institute for Occupational Safety and Health, Cincinnati,

Ohio, USA

The manuscript was written by employees of the US government as part

of their official duties; the work is therefore not subject to copyright.

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