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com
Original article
1
Institute of Cancer
Epidemiology, Danish Cancer
Society, Copenhagen, Denmark
2
Department of Occupational
and Environmental Medicine,
Copenhagen University Hospital,
Bispebjerg, Denmark
Correspondence to
Else Ibfelt, Institute of Cancer
Epidemiology, Danish Cancer
Society, 49 Strandboulevarden,
Copenhagen DK-2100,
Denmark; else@cancer.dk
Accepted 11 February 2010
Published Online First
27 June 2010
772
Exposure to metal welding fume particles and risk for
cardiovascular disease in Denmark: a prospective
cohort study
Else Ibfelt,1 Jens Peter Bonde,2 Johnni Hansen1
ABSTRACT
Objectives To study welding fume particles in relation to
cardiovascular diseases.
Methods In 1986, 10 059 male metal workers in 75
welding companies were sent a questionnaire about
their welding experience and lifestyle (83.3% response
rate). Of these, 5866 were available for analysis and had
ever welded at baseline. Information on exposure to
welding fumes after 1986 was obtained by individual
linkage to the National Pension Fund. Lifelong exposure
to welding fume particles was estimated from
a jobeexposure matrix based on more than 1000
welding-specific measures of fume particles. Hospital
contacts for cardiovascular disease were obtained from
the Danish National Patient Registry by individual linkage.
The nine disease outcomes considered were acute
myocardial infarct (AMI), angina pectoris, other acute
ischaemic heart diseases, chronic ischaemic heart
disease (CHD), cardiac arrythmias, cardiac arrest, heart
failure, cerebral infarct, arterial embolism and
thrombosis. The cohort was followed up from baseline
until the end of 2006.
Results When the incidence of each of the nine
cardiovascular outcomes among welders was compared
with 5-year age- and calendar year-specific male national
rates, the number of observed cases significantly
exceeded that expected for AMI (standardised incidence
ratio, 95% CI) (1.12, 1.01 to 1.24), angina pectoris (1.11,
1.01 to 1.22), CHD (1.17, 1.05 to 1.31) and cerebral
infarct (1.24, 1.06 to 1.44). Internal comparisons of the
cohort with adjustment for tobacco smoking, alcohol and
hypertension medicines showed a significantly increasing
hazard rate ratio for CHD and non-significant increases
for AMI, angina pectoris and cerebral infarct with
increasing exposure to particles.
Conclusions This study supports the hypothesis that
exposure to welding processed particles increases the
risk for cardiovascular disease.
INTRODUCTION
Several studies conducted in Europe and the USA
during the past two decades have shown an asso-
ciation between the concentration of ultrafine
particles in ambient air and risk for cardiovascular
disease (CVD).1 Welders are exposed to much
higher concentrations of particles than the general
public2 3; investigation of CVD in this population,
therefore, contributes to elucidating associations
between ambient air pollution and cardiovascular
risk.
Metal welding consists of several processes that
may result in substantial exposure to particles,
fumes and gases. It is estimated that more than
Occup Environ Med 2010;67:772e777. doi:10.1136/oem.2009.051086
What this paper adds
< Few studies have investigated the relationship
between welding and the risk for cardiovascular
diseases; most found an increased risk,
although some did not find this association.
< Generally, previous studies lacked detailed
exposure measurements, combined many
cardiovascular diseases together, and rarely
adjusted for confounding.
< This study examines lifelong welding particulate
exposure in relation to risk for nine cardiovas-
cular outcomes adjusted for confounding by
smoking, alcohol and medicine use.
< Our study suggests that welders are at
increased risk for ischaemic and cerebrovas-
cular diseases.
1 million workers worldwide perform welding as
a part of their job.4 Particles in general are a source
of local irritation, as their physical, chemical or
biological properties can initiate an inflammatory
response. The inflammation may be acute and
easily healed, or it may become chronic.5 Studies of
exposure to welding fumes have shown that the
particles are in the ultrafine size range of
0.01e0.10 mm,6 and approximately 50%e75% are
of submicron size, with a diameter of 0.4e0.8 mm.7
As smaller particles penetrate further into the
airways, gases and other active species attached to
their surfaces are carried deeper into the lung.8 The
hypothesis has been proposed that inhaled particles
create pulmonary inflammation and a subsequent
systemic inflammatory response. This will increase
the probability of atherosclerosis, followed by other
cardiovascular events.9 The compounds of the
welding emission formed during the processes are
also suspected of increasing CVD, due to the
formation of, for example, ozone and carbon
monoxide.
Studies of ambient air pollution, in which the
level of exposure to ultrafine particles is usually
much lower than that experienced during welding
(at least 10e100-fold, depending on the welding
method and the place and time of air measure-
ments2 10 11), have shown acute effects on heart
rate, blood pressure and blood coagulation and
effects of more prolonged (chronic) exposure to air
pollution particles on the progression of athero-
sclerosis.1 12
Some of the few available studies on welding
have shown increased morbidity and mortality due
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to CVD,13e17 whereas others have shown no effect.18 19 Previous
studies of welders and CVD lacked detailed exposure measure-
ments (eg, duration, mass or number of particles inhaled),
combined all diagnoses of cardiovascular or ischaemic heart
disease, or recorded only mortality from CVD, and few studies
included adjustment for confounding by, for example, tobacco
smoking. In the study reported here, we estimated lifelong
exposure to welding fume particles, analysed doseeresponse
relationships for different diagnoses of cardiovascular diseases
and attempted to adjust for individual lifestyle risk factors.
METHODS
Study population
Potential study participants were selected from a cohort of 10
059 male production workers that was established in 1986 with
the aim of studying associations between metal welding and
lung cancer. The various steps of the construction of the cohort
have been described in detail elsewhere20 and are only
summarised here. In 1982, employees of 79 companies in
Denmark with metal welding activities were identified in
a survey. After exclusion of shipyards, because of possible
exposure to asbestos, 75 companies remained, employing about
60% of all Danish stainless-steel welders; five of the larger
companies had substantial numbers of mild-steel welders. All
men born before 1964 and employed by one of these companies
in the period April 1964eDecember 1984 for a minimum of
1 year were then identified from the computerised files of the
nationwide Danish Pension Fund.20 This pension scheme, with
compulsory membership for all wage earners aged 16e66 years,
contains the person’s name, the dates of the start and end of
each employment at company level (a unique company identi-
fication number is assigned for tax purposes) and the unique
personal identification number assigned by the Central Popula-
tion Registry to all residents of Denmark.21 These two registers
are regarded as both accurate and complete.21 In order to iden-
tify workers potentially exposed to welding, all the companies
were visited in 1986, and employees in departments with
welding activities were identified from independent information
in company records, foremen, long-term workers and other
sources. Information on emigration, disappearance and death for
each worker identified, was retrieved from the files of the
Central Population Registry, which was established in 1968. In
autumn 1986, all the workers (or spouses or long-term
colleagues of deceased or emigrated workers) were sent ques-
tionnaires eliciting information on lifetime exposure to welding
and other exposures such as tobacco smoking, use of medica-
tions and alcohol consumption. Non-respondents were
contacted up to three times. Responses were received from 8376
workers (83.3%). Of these, 6162 (74.6%) had ever welded at
baseline according to the questionnaire. We did not use men who
had never welded as an internal comparison group, as this group
was small and heterogeneous. We excluded three welders with
inconsistent personal identification numbers, eight welders who
immigrated to Greenland and 285 welders who had died before 1
January 1987, leaving 5866 men for the analyses.
Disease experience
Information on the occurrence of CVD in this population was
retrieved by linkage to the Danish National Patient Registry by
personal identification numbers. The welders were followed up
from the start of 1987 until the end of 2006. This computerised
register, with high validity,22 stores information on all persons
hospitalised in Denmark since 1 January 1977 and includes dates
of admission and discharge, codes for the primary diagnosis and up
Occup Environ Med 2010;67:772e777. doi:10.1136/oem.2009.051086
Original article
to 19 codes for additional diagnoses. Information on outpatients
was added on 1 January 1994. Until the end of 1993, diagnoses
were coded according to an extended Danish version of the
International Classification of Diseases, Revision 8 (ICD-8), and
after that date according to ICD-10. We defined the first occur-
rence of CVD as the date of first hospitalisation with CVD as
a main diagnosis after 1 January 1987; if a similar diagnosis had
been made earlier as a secondary diagnosis, however, we used this
to define the time of diagnosis. We excluded 236 welders’ hospi-
talisations with CVD diagnoses (main or secondary) that had
occurred between 1977 and the start of follow-up.
We considered nine main disease outcomes from ICD-8 and
ICD-10: acute myocardial infarct (AMI) (410, I21), angina
pectoris (413, I20), other acute ischaemic heart diseases (411,
I24), chronic ischaemic heart disease (CHD) (412, I25), cardiac
arrythmias (427, I48 and I49), cardiac arrest (none, I46), heart
failure (none, I50), cerebral infarct (433 and 434, I63) and arterial
embolism and thrombosis (444, I74).
Assessment of exposure to welding fumes
The questionnaire elicited information on the welding material
used (stainless or mild steel), welding process (manual metal arc,
tungsten inert gas, metal inert gas, metal active gas, spot or gas
welding), first year of welding, number of years welding in
various decades, use of exhaust ventilation and welding in
confined spaces. In an attempt to cover any exposure to welding
fumes after the baseline in 1986 and thereby obtain more
complete information about lifelong welding, we included data
from the National Pension Fund register on duration of
employment in welding companies after 1986.
To estimate total accumulated exposure to welding fume
particles before baseline, we used an exposure matrix based on
more than 1000 measurements of ambient air particles in the
workplace between 1971 and 1985 made by the Danish Welding
Institute and the National Institute of Occupational Health. Air
samples were collected on filters placed in the breathing zone
behind welding helmets. Filters used were pore size 0.8 mm, so
particles smaller than this did not contribute to the mass
measurements. Earlier exposures were estimated by extrapola-
tion, on the assumption of a declining trend in exposure in all
welding processes during 1971e1985. The database provided
geometric mean values (mg/m3) for exposure to particulates in
each welding process.23
By linking the exposure matrix to data from the question-
naires on decade, type of steel, welding process, frequency,
exhaust ventilation and welding in confined spaces, we were
able to compute the total of number of years that each man had
spent in welding and the particulate concentration in each
decade and for all decades. This gave a summary measure of
total exposure to welding fumes (mg/m33years) before baseline.
To obtain a measure of total lifelong exposure before and after
baseline, we calculated an average exposure for 1980e1986 (the
last interval of the questionnaire data) and multiplied it by
number of years in the welding industry after baseline. Total
exposure was calculated from data for 3499 welders for whom
consistent information on welding was available from the
questionnaire, and especially details on years, processes, etc, for
the period 1980e1986.
Statistical analysis
The risk for CVD was calculated from 1 January 1987, and
follow-up ended on the date of hospitalisation for CVD, death,
emigration from Denmark or 31 December 2006, whichever
came first.
773
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Original article
In the external analysis, we compared the incidence of CVD
among welders with 5-year age- and calendar year-specific
national rates among men, calculated from the CVD diagnosis in
the files of the Danish National Patient Registry. The expected
number of CVD diagnoses was calculated by applying the
national gender-, age- and calendar time-specific rates to the
appropriate person-years under observation in each exposure
group. Standardised incidence ratios (SIRs) were calculated as
the observed incidence divided by that expected with a modified
version of the Person-Years (PYRS) software program.24 Signifi-
cance and 95% CIs were determined on the basis of the
assumption that the observed number of diagnoses of heart
disease in any category was Poisson distributed.
In the internal analyses, we compared the rates of CVD
among welders by number of years of welding with a lag time of
1 year and by estimated concentration of particles. We adjusted
for the effects of tobacco smoking (never, former or current
smoker), alcohol consumption (0e3.5, 4e20.5 or $21 drinks per
week), regular use of hypertension or ‘heart’ medicine within
1 year prior to baseline (yes or no) and calendar time. Tests for
interaction between covariates were performed for one pair at
a time using the Wald test statistics. No statistical significant
interactions were observed between exposure and covariates. We
performed sensitivity analyses after excluding welders who had
started welding before 1960 in order to minimise selection bias
due to the healthy worker effect. Cox regression analysis was
used to estimate hazard rate ratios (HRRs) for heart disease,
a measure of RR, with the Breslow method for ties. Age was
used as the underlying time scale to ensure that estimates were
based on comparisons of individuals of the same age. Estimated
lifelong exposure to welding particles (mg/m33years) was
included as a time-dependent variable, as duration of welding
included employment time both before and after the study
baseline. Two-sided 95% CIs were calculated for the HRRs with
the Wald test of the Cox regression parameter. The proportional
hazard assumption for the analysis was tested by KaplaneMeier
plots and the Schoenfeld test of proportional hazard assump-
tion. Cox regression analyses were performed with Stata
statistical software v 9.2.25
Table 1 Characteristics of 5866 welders at baseline, Denmark, 1987
Characteristic
Age (years), mean (SE)
Never smoked
Former smoker
Current smoker
Number of drinks (glass of beer, wine or spirits) per week
0e3.5
4e20.5
$21
Regular use of hypertension or ‘heart’
medicine within past year
Total number of years welding, mean (SE)
Before baseline (1924e1986)
After baseline (1987e2006)
Year started welding
<1960
1960e1969
1970e1986
Local exhaust used
Often or sometimes welded in confined
space
Cumulative estimated particulate exposure, mean mg/m33year (SE)
All years before baseline (1924e1986)
All years after baseline (1987e2006)
774
RESULTS
Of the 5866 welders, 1126 died before the end of follow-up, 51
emigrated from Denmark and 4689 were still alive at the end of
follow-up. Selected descriptive characteristics of the welders are
shown in table 1.
Table 2 gives the results of the external analysis. For four of
the nine CVD outcomes, the number of observed cases signifi-
cantly exceeded the number expected. We observed an increasing
risk with higher levels of particulate exposures for angina
pectoris, CHD and cerebral infarct, but the increase was signif-
icant only for cerebral infarct in the group exposed to >100 mg/
m33years. Increased risks for AMI and CHD were also seen for
a group of welders for whom inadequate data were available for
calculation of cumulative exposure.
In the internal analyses, we found no association between
total years of welding (duration) and risk for AMI, angina
pectoris, CHD or cerebral infarct, before or after adjustment for
calendar year, tobacco smoking, alcohol consumption and use of
hypertension or ‘heart’ medicine (data not shown).
Table 3 gives the estimates for cumulative exposure to
particulates after adjustment for potential confounders. A
significantly higher RR for CHD was found for welders exposed
to 10e50 mg/m33years (HRR 2.51, 95% CI 1.15 to 5.49) and
50e100 mg/m33years (2.79, 1.29 to 6.04) than those exposed to
0e10 mg/m33years (reference), while the risk for the group
with the highest exposure, >100 mg/m33years, was not
significantly increased (1.70, 0.78 to 3.72). Similar tendencies for
an exposureeresponse relationship were found for AMI, angina
pectoris and cerebral infarct, although these were not significant.
The unadjusted results (data not shown) were similar to those
found after adjustment.
When analysing exposure generated from data before baseline
only, the results were similar to those generated from lifelong
exposure shown in table 3, but with lower RR estimates. For the
three exposure categories 10e50, 50e100 and >100, the HRRs
for AMI were 1.04 (0.70 to 1.53), 1.31 (0.89 to 1.93) and 1.01
(0.68 to 1.52), for angina pectoris 1.04 (0.72 to 1.49), 1.27 (0.88
to 1.81) and 1.09 (0.75 to 1.58), for CHD 1.27 (0.82 to 1.96), 1.48
(0.96 to 2.28) and 0.95 (0.61 to 1.50) and for cerebral infarction
1.19 (0.65 to 2.17), 1.05 (0.57 to 1.95) and 1.39 (0.76 to 2.52).
After exclusion of welders who had started welding before
Welders
1960, the estimates for the group with the highest exposure
42.3 (0.16) (>100 mg/m33years) were increased, with HRRs of 1.24 (0.66
1077 (18.4%) to 2.36) for AMI, 1.28 (0.68 to 2.40) for angina pectoris, 1.87
1394 (23.8%) (0.72 to 4.85) for CHD and 2.14 (0.77 to 5.92) for cerebral
3376 (57.7%) infarct. The tests for trend, however, remained non-significant
(data not shown).
1.374 (23.5%)
3.895 (66.7%)
558 (9.7%)
DISCUSSION
381 (6.5%)
In our cohort of 5866 welders, we found significantly higher
risks for the four most frequent of nine cardiovascular outcomes
13.1 (0.13) (AMI, angina pectoris, CHD and cerebral infarct) than in the
5.6 (0.07) general population. The risks for AMI and CHD were increased
in a group of welders for whom data for calculation of cumu-
1572 (26.8%) lative particulate exposure were inadequate. It is possible that
2022 (34.5%) this is a group of vulnerable welders who were unable to fill in
2272 (38.7%) the questionnaire or did not work between 1980 and 1986 for
2435 (67.5%) various reasons.
2727 (48.1%) When comparing the welders internally, we also found an
approximate doseeresponse relationship between cumulated
exposure to particulates and each of the four diagnoses, although
53.1 (0.71)
the trend was not significant. The group with the highest
8.7 (0.18)
exposure had non-significantly lower risks for AMI, angina
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Original article

Table 2 Standardised incidence ratios (SIRs) and 95% CIs for selected cardiovascular diseases among
5866 male Danish welders followed up from 1986 to 2006 and compared with the general male
population
Cumulative particulate exposure
Cardiovascular disease (mg/m33years) Observed Expected SIR 95% CI
Acute myocardial infarct All 377 337.4 1.12 1.01 to 1.24
0e10 11 8.7 1.26 0.63 to 2.26
10e50 40 42.7 0.94 0.94 to 1.28
50e100 80 63.3 1.26 1.00 to 1.57
>100 76 77.3 0.98 0.77 to 1.23
Missing data* 170 145.4 1.17 1.00 to 1.36
Angina pectoris All 437 394.5 1.11 1.01 to 1.22
0e10 9 11.3 0.80 0.36 to 1.52
10e50 65 57.6 1.13 0.87 to 1.44
50e100 87 82.1 1.06 0.85 to 1.31
>100 101 90.4 1.12 0.91 to 1.36
Missing data* 175 153.1 1.14 0.98 to 1.33
Chronic ischaemic heart disease All 326 277.6 1.17 1.05 to 1.31
0e10 5 7.3 0.68 0.22 to 1.59
10e50 42 36.7 1.14 0.82 to 1.55
50e100 68 55.3 1.23 0.95 to 1.56
>100 65 65.3 1.00 0.77 to 1.27
Missing data* 146 15.2 1.29 1.09 to 1.52
Cerebral infarct All 169 136.5 1.24 1.06 to 1.44
0e10 2 3.4 0.58 0.07 to 2.10
10e50 21 16.7 1.26 0.78 to 1.92
50e100 30 25.6 1.17 0.79 to 1.67
>100 46 32.1 1.43 1.05 to 1.91
Missing data* 70 58.7 1.19 0.93 to 1.51
Other acute ischaemic heart disease All 14 13.02 1.08 0.59 to 1.80
Cardiac arrythmias All 237 233.5 1.01 0.89 to 1.15
Cardiac arrest All 32 33.7 0.95 0.65 to 1.34
Heart failure All 157 148.8 1.05 0.90 to 1.23
Arterial embolism and thrombosis All 11 15.3 0.72 0.36 to 1.29
*Welders for whom we had either incomplete information on duration of welding or no information on welding in the period 1980e86
for calculation of cumulative particulate exposure after baseline (from 1 January 1987).

pectoris and CHD than the groups with intermediate exposure
when compared with the reference. It is possible that the group
with the highest exposure were selected ‘healthy workers’.
When we excluded welders who had started work before 1960 in
order to reduce this possible selection bias, the risk for the group
with the highest exposure increased but was still not signifi-
cantly higher than that of the group with the lowest exposure.
This may indicate that there is a threshold of exposure to
particles, a ‘healthy worker’ survivor effect or misclassification
of exposure.
One limitation is that particles less than 0.8 mm in size were
not included in the job-exposure matrix. Another is that the
effect of specific compounds involved in the welding processes is
not represented in the jobeexposure matrix algorithms used. In
particular, carbon monoxide and ozone generated from shielding
gases used in various welding processes are toxic to the respi-
ratory system, organs and blood. Carbon monoxide may have an
acute effect because of the formation of carboxyhaemoglobin
and have long-term effects via a possible atherogenic mecha-
nism.26 Ozone has been shown to affect levels of the cytokine
interleukin-6 in the bronchoalveolar lavage, which might
increase concentrations of plasma fibrinogen and thereby the
risk for ischaemic heart disease.16 Even though the questionnaire
provided information on specific welding processes and mate-
rials, it was not possible to construct ‘clean’ groups by type of
welding (eg, manual metal arc or metal active gas) or by expo-
sure to specific compounds, since the majority of the welders
worked with different methods over the years.
The major strengths of our study are the large cohort of
relatively young welders, detailed, prospectively obtained infor-
mation about welding processes and the long follow-up of
nearly 30 years. In Denmark, all residents have equal, free
admission to hospital, and, through the Danish National Patient
Registry, we were able to obtain information on all relevant
diseases that required hospitalisation. One limitation of the
study is that we did not have information on men with
cardiovascular disorders who were not admitted to hospital; for
instance, angina pectoris is sometimes treated by general prac-
titioners. As it is unlikely that welders are admitted more or less
often to hospital for a particular disease than the general
population, we consider that this limitation does not reduce the
validity of the study. Furthermore, we considered disease
outcomes that are usually treated in hospital.
Information on exposure to welding fumes before baseline
was obtained from self-reports by welders up to 40 years later.
Therefore, the details of welding processes, time spent welding
and working conditions might not be totally accurate for the
oldest group. Calculation of cumulative exposure to particulates
with the jobeexposure matrix and responses to a questionnaire
is not as precise as individual measurements of inhaled particles
for each welder. Therefore, some differential misclassification of
exposure might have occurred, resulting in underestimation of
the risk for CVD among the most heavily exposed men.27 28
The addition of information on estimated duration of welding
after baseline to the data from the questionnaire strengthens the
association of exposure during welding and CVD. The compulsory

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Original article

Table 3 Adjusted HRRs and 95% CIs for cardiovascular disease among 3499 welders according to
accumulated exposure to particles
Cumulative particulate
Cardiovascular disease exposure (mg/m33years) N* No. of cases HRRy 95% CI
Acute myocardial infarct 0e10 (reference) 37991 17 1 e
10e50 163075 67 1.11 0.65 to 1.89
50e100 184292 96 1.43 0.85 to 2.41
>100 150199 80 1.03 0.61 to 1.74
Log-rank test, c2¼5.95, p¼0.114
Test for trend, c2¼0.00, p¼0.969

Angina pectoris 0e10 (reference) 44954 17 1 e

10e50 194825 80 1.23 0.73 to 2.08
50e100 226162 107 1.41 0.84 to 2.36
>100 181557 95 1.21 0.72 to 2.03

Log-rank test, c2¼2.26, p¼0.521

Test for trend, c2¼0.22, p¼0.637

Chronic ischaemic heart disease 0e10 (reference) 31613 7 1 e

10e50 131588 61 2.51 1.15 to 5.49
50e100 162675 83 2.79 1.29 to 6.04
>100 143045 60 1.70 0.78 to 3.72

Logerank test, c2¼13.56, p¼0.004

Test for trend, c2¼0.27, p¼0.606

Cerebral infarct 0e10 (reference) 15477 7 1 e

10e50 63815 32 1.32 0.58 to 3.01
50e100 76279 32 1.17 0.52 to 2.67
>100 66747 52 1.54 0.70 to 3.39

Log-rank test, c2¼2.44, p¼0.486

Test for trend, c2¼1.12, p¼0.290
Results for welders who answered all the questions necessary for calculation of their cumulative exposure across all years and who
answered questions about smoking, alcohol consumption and use of medicines.
*Numbers correspond to data split on every incidence of each disease for all welders, in order to include the time-dependent variable,
duration of welding after baseline. As each man contributed a different number of years for each incidence, each was included more
than once in the analysis.
yAdjusted for calendar year, tobacco smoking, alcohol consumption and use of hypertension or ‘heart’ medicine.

routine registration of employment in the Danish Pension Fund
register ensures that there is no selection of individuals or missing
or incorrect reporting of employment. One limitation in the
calculation of cumulative exposure after baseline was the lack of
information on whether the work specifically included welding
and whether the welders continued to have the same hours and
processes reported in 1986. Also, we assumed that there was no
change in exposure after 1980e1986. The semi-quantitative esti-
mate of exposure to particulates is therefore an approximate
measure of the true lifelong exposure. We consider, however, that it
is a more informative, complete measure than measures based on
total number of years welding (used in other studies) or cumula-
tive exposure calculated only from data before baseline.
True risk can be underestimated when the morbidity rates of
welders are compared with those of the total population (given
no confounding from other exposures), because the general
population includes sick and disabled people who are unable to
work.16 In our internal analysis, we were able to lessen this
possible bias and potential confounding by including tobacco
smoking, alcohol consumption and use of hypertension or
‘heart’ medicines. These exposures had, however, only
a marginal influence on the results. Data on these lifestyle
factors were only collected at one time point and we had no
information about changes over time. Smoking exposure is likely
to have decreased since 1986, and if so our results of welding
effect may be underestimated. Alcohol consumption is likely to
have stayed the same over the years for this group of people. The
number of welders using hypertension or ‘heart’ medicine is
likely to increase as the cohort grows older, but is only relevant
for a smaller group and can be an intermediate step before
experiencing a CVD diagnosis. We had no information on other
risk factors for CVD, such as obesity, high intake of fatty foods,
low vegetable intake and low physical activity.29 As we found an
approximate doseeresponse relationship between exposure to
welding particles and CVD, the increased risk is unlikely to be
due only to other, unknown confounders.
Few other studies have investigated the risk for CVD in
welders, and half of them addressed only mortality from such
causes. One Danish cross-sectional study of AMI and three
cohort studies of mortality due to ischaemic heart disease found
positive associations with welding, the results being: OR 2.1
(95% CI 1.05 to 4.30) only for welders with blood type O,
unadjusted17; standardised mortality ratio (SMR) 1.06 (1.02 to
1.11) in the 1970 census and SMR 1.35 (1.10 to 1.64) in the 1990
census, unadjusted16; SMR 1.51 (1.00 to 2.18) and SMR 1.79
(p<0.05) for welders who had worked $20 years, adjusted for
smoking14; and SMR 1.30 (1.04 to 1.56), unadjusted.15 A cohort
study of 236 workers showed increased risks adjusted for
smoking for angina pectoris and chest pain, with prevalence
ratios of 2.61 (1.2 to 5.7) and 2.27 (1.5 to 4.9), respectively, and
a non-significant effect for AMI (prevalence ratio 1.37, 0.7 to
2.8).13 The risk estimate for AMI observed in our study is within

776 Occup Environ Med 2010;67:772e777. doi:10.1136/oem.2009.051086

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the range of the prevalence ratio from this study. In a cohort
study of ischaemic heart disease in construction workers, no
effect was found (RR 1.01, 0.95 to 1.08) in 831 workers exposed
to metal fumes.19 In a study of pooled data for 11 092 welders in
135 companies in nine countries, no significant effect was found
(SMR 94, 86 to 103), but the inclusion criteria for different
countries differed, and all diseases of the circulatory system
combined (ICD-8: 390e458) were considered.18
Our finding of an increased risk for ischaemic heart disease in
welders is supported by most of these studies, and the elevated
risks are close to our estimates. The two studies that did not find
increased risks were unable to analyse doseeresponse relation-
ships, addressed all ischaemic heart disease or circulatory diag-
noses or did not include adjustment for smoking. In addition,
other studies found acute effects on intermediate cardiovascular
outcomes after exposure to welding fumes: cardiac autonomic
control,30 aortic augmentation31 and acute systematic inflam-
mation,32 which further support our results. Studies on ambient
air pollution have also shown associations with cardiac
arrhythmias mostly in patients with underlying cardiac
disease,33 however, we did not find such association in this
study.
In conclusion, this study supports the hypothesis that expo-
sure during welding increases the risk for cardiovascular and
cerebrovascular disease. As the particles in welding fumes are
likely to be of ultrafine or nano sizes, like particles from traffic
and combustion pollution, we consider that our results are
relevant in the discussion of the health hazards of environ-
mental pollution from particulates in general. However, very
small particles are usually measured in numbers, a quantitative
measurement we did not have for our cohort of welders. Further
studies on numbers of ultrafine and nano sized welding particles
and diseases of the lungs and cardiovascular system will be
needed to answer questions about the health hazards of these
particles in general. Also questions about specific welding
compounds and CVD risk could be addressed in future studies
analysing air samples or questionnaires aimed at welders
working with specific welding processes only.
Acknowledgements We are indebted to Klaus S Hansen for providing access to
the data on the cohort of welders, to Andrea Meersohn for help with data
processing and to Kirsten Frederiksen for statistical assistance.
Funding This study was supported by a grant from the Danish Working Environment
Research Fund. The funding source had no role in the design or analysis of the study or
in the decision to submit the manuscript for publication.
Competing interests None.
Contributors JH and JPB designed and planned the study and developed the
protocol. EI and AM carried out the statistical analyses. EI, JH and JBP interpreted the
final data analyses and wrote the manuscript.
Provenance and peer review Not commissioned; externally peer reviewed.
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Exposure to metal welding fume particles and

risk for cardiovascular disease in Denmark: a
prospective cohort study
Else Ibfelt, Jens Peter Bonde and Johnni Hansen

Occup Environ Med 2010 67: 772-777 originally published online June
27, 2010
doi: 10.1136/oem.2009.051086

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