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Vaccinating welders against pneumonia
K. T. Palmer1 and M. P. Cosgrove2
1MRC Lifecourse Epidemiology Unit, University of Southampton, Southampton SO16 6YD, UK, 2TWI, Granta Park,
Great Abington, Cambridge CB21 6AL, UK.
Correspondence to: K. T. Palmer, MRC Lifecourse Epidemiology Unit, Southampton General Hospital, Tremona Road,
Southampton SO16 6YD, UK. Tel: +44 (0)2380 777624; fax: +44 (0)2380 704021; e-mail: email@example.com
Background In 2011, the Department of Health in England recommended that welders should each receive a
single dose of the 23-valent pneumococcal polysaccharide vaccine (PPV23).
To assess the evidence behind the advice and its practical implications.
Methods The review was informed by a systematic search in Medline, which related pneumonia to welding
and/or exposure to metal fume, and was supplemented using the personal libraries of the authors.
There is consistent evidence that welders die more often of pneumonia, especially lobar pneumonia,
are hospitalized more often for lobar and pneumococcal pneumonia, and more often develop invasive
pneumococcal disease (IPD). It is estimated that one case of IPD may be prevented over a 10-year
period by vaccinating 588 welders against pneumococcal infection.
Conclusions A good case exists that employers should offer PPV23 vaccination to welders and other employees
exposed to metal fume. Additionally, reasonable measures must be taken to minimize exposure to
welding fume, and welders should be encouraged not to smoke.
Infective risk; metal fume; occupation; pneumococcal.
The bacterium Streptococcus pneumoniae, otherwise
known as the pneumococcus, is commonly found in the
upper respiratory tract in healthy humans. Frequently,
the microorganism is carried as a commensal in the
nose or throat (by up to 70% of people), but among the
more than 90 different serotypes that exist, some may
give rise to serious infective illnesses, including pneu-
monia, septicaemia and meningitis. The term ‘invasive
pneumococcal disease’ (IPD) covers clinical conditions
where a pneumococcus is isolated from a normally ster-
ile body fluid such as blood or cerebrospinal fluid, and
this complication carries an appreciable case fatality
rate, estimated at perhaps 5–12% in adults of working
In November 2011, the Department of Health’s
‘Green Book’, ‘Immunisation against Infectious
Disease’, advised that welders should be added to the
list of patient groups for whom pneumococcal vac-
cination was recommended . In this review, we
summarize the evidential background to this recom-
mendation and discuss the implications of the advice
for occupational physicians who include welders among
the client populations they serve.
To inform the review, we conducted a search in Medline
covering the period 1950 to January 2012, in which we
combined terms for the exposure of interest, welding,
with the outcome of pneumonia. For the former, we used
a Medical Subject Heading (MESH) term for welding,
as well as text words for weld$, metal work$, metal fume
or welding fume; and for the latter, MESH terms for
pneumonia, bacterial pneumonia, pneumococcal pneu-
monia were used as well as pneumonia as a text word.
This search yielded 58 titles for screening, from which
we excluded irrelevant hits, reports on animal experi-
ments and studies focussed solely on metal fume fever
or metal pneumonitis. The bibliographies of retrieved
papers were checked for further information. Also, as a
significant proportion of the relevant research has been
undertaken by one of us (K.T.P.), and the other (M.P.C.)
has maintained an ongoing record of reports to advise
Occupational Medicine 2012;62:325–330
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TWI (formerly The Welding Institute), for completeness,
a check was made of the personal libraries available to us.
A report in 1980 by Beaumont and Weiss , on the
mortality experience of 8679 male members of a metal
trades union employed in shipyards, metal fabrica-
tion shops and small boat yards, recorded a significant
excess of deaths from pneumonia in welders relative
to that expected from rates in all US men. Five years
later, Newhouse et al.  also found a significant excess
death rate from pneumonia among welders employed at
a shipyard in north-east England compared with platers
and electricians from the same site.
Most information on the mortality of welders has
accrued, however, from the Decennial Supplements
on occupational mortality for England and Wales.
Successive analyses have demonstrated increased death
rates from pneumonia among welders in a pattern
that can be followed back for more than five decades.
During 1949–53, 70 deaths were observed compared
with 31 expected ; in 1959–63, 101 deaths with 54.9
expected ; and in 1970–72, 66 deaths versus 42.0
In 1994, an analysis covering the extended period
1979–80 and 1982–90 (disrupted by a year of industrial
action among the registrars of births and deaths) offered
greater statistical power to explore potential determi-
nants . This confirmed the association with welding
but went further in clarifying that the excess was attribut-
able largely to deaths from pneumonias other than bron-
chopneumonia (principally lobar pneumonia) and was,
moreover, limited to men below the normal retirement
age of 65 years (55 observed deaths from lobar pneu-
monia versus 21.6 expected). Thus, excess risk existed
for welders still in the occupation but not in men who
had retired from it, making confounding by smoking and
other non-occupational factors an unlikely explanation.
Finally, the heightened risk was found to apply to several
other occupations entailing exposure to metal fume, such
as moulders and coremakers and furnacemen in foun-
dries . When taken together, these findings suggested
that inhalation of metal fume increases susceptibility
to infectious pneumonia, and the effect was reversible
following cessation of exposure.
A subsequent mortality report extended observations
with the addition of data from the Registrar General’s
Supplements for 1910–12, 1930–32 and 1949–53 .
As in previous analyses, occupations with potential
exposure to metal fume, particularly welders, moulders,
coremakers and furnacemen, had significantly elevated
mortality from pneumonia. Excesses were also apparent
for metal grinders and polishers, although these were
less marked. Also, the excess mortality from pneumo-
nia in fume-exposed occupations was confined to men
of working age, while the at-risk occupations were found
not to have comparable excesses of lung cancer or of
mortality from non-respiratory infections, adding to the
evidence against confounding as an explanation.
In the years 1930–32 and 1949–53, unlike in later
reports, workers in ferrous foundries were distinguished
from foundrymen working other metals, and iron ore
miners from miners of tin, copper and other metal-
liferous ores. When disaggregated in this way, it was
found that the elevation of mortality from pneumonia
was generally more marked in those working with fer-
rous metal, with no consistent differences in mortality
from bronchitis. Similarly, during 1910–12, the risk of
death from pneumonia in iron founders was twice that
in brass founders, and that in iron miners and quarriers
was 50% greater than in lead miners, but there was no
corresponding excess mortality risk from bronchitis .
Generally, the pattern was considered compatible
with a specific hazard from iron, and multiple strands of
evidence indicate that free iron can promote infections in
biological systems, acting either as a growth nutrient for
microorganisms or as a cause of free radical injury (for a
full review see Palmer and Coggon ). Iron is seldom
‘free’ at body surfaces; instead, most of the body’s stores
are intracellular, in ferritin, haemosiderin and haem, and
the extracellular fraction is bound to high-affinity iron
binding proteins (transferrin in serum and lactoferrin in
external secretions) that keep the concentration of free
iron in equilibrium as low as 10–18 M (moles per litre).
However, a battle for free iron exists between host and
microorganisms, the normal flora of the respiratory tract
reflecting in part the nutrient-limited balance finally
achieved. In situations where the balance is disturbed,
for example when exogenous supplies of iron exceed the
capacity of the iron binding protein system, overgrowth
of organisms may be encouraged or free radical injury
of host defences against infection could ensue. Thus, an
‘iron hypothesis’ has been mooted to explain the consist-
ently higher risk of pneumonia in metal fume-exposed
Analysis of death certificates can only take matters so
far, being limited, for example, in its capacity to explore
the iron hypothesis, and whether risks are specific to
certain metal(s) or general to many metals, or to assess
whether the excess risk applies to all categories of pneu-
monia or only to those caused by certain microorgan-
isms. Another uncertainty is whether the effect of metal
fume is on the incidence of disease (the risk of acquiring
pneumonia) or on the case fatality rate (the risk of dying
once the disease has occurred).
To garner further information, a case–control study
was conducted during 1996–99 in Birmingham and
the West Midlands (chosen because of the relatively
high prevalence of occupational exposure to metal
fume in the local population) . In all, 525 working-
aged men of 20–64 years admitted to 11 hospitals with
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community-acquired pneumonia were interviewed about
their lifetime occupational history, including exposure to
metal fume, together with 1122 controls, admitted to
the same hospitals under the same medical teams with
Consistent with the mortality data, pneumonia overall
was found to be more common among welders and other
workers with exposure to metal fume than among work-
ers with non-exposed jobs; and risks were confined to
exposures in the previous 12 months (adjusted odds ratio
(OR) = 1.6, 95% confidence interval (CI) = 1.1–2.4)
and not apparent if the last exposure was more than a
year before (OR = 1.1). Also consistent with the mortal-
ity data, risks were higher where the X-rays (read blind to
occupational history) showed shadowing in a lobar or in
a segmental/subsegmental pattern than when the appear-
ance was one of bronchopneumonia (ORs for exposure
to any metal fume in the previous 12 months 1.8 and
1.8 respectively, versus 1.3 for bronchopneumonia).
Consistent with the iron hypothesis, risks were high-
est of all when exposure in the past year was to ferrous
fumes but not to other metals or alloys (OR for lobar
pneumonia = 3.0, 95% CI = 1.4–6.7). Finally, in 43
cases where the pneumonia was confirmed as pneumo-
coccal, by recovery of S. pneumoniae from blood and/or
sputum, the OR for exposure to metal fume of any kind
was 1.8 and for exposure specifically to ferrous fume was
3.1 (95% CI = 1.0–9.5). The findings thus support the
hypothesis of a hazard that is reversible following cessa-
tion of exposure, which affects the incidence of disease
and not just its fatality, and which is linked in particu-
lar with recent exposure to ferrous metal fume and with
lobar and pneumococcal pneumonia.
Useful though this information is, the study could not
tie down precisely the time frame of risk as most workers
who were exposed in the previous 12 months had also
been exposed in the previous 7 days. Nor did it exclude
the possibility that other organisms could sometimes be
involved, as in men infected with Legionella, Mycoplasma
or Haemophilus influenzae the OR following exposure to
ferrous fume was 2.1. Finally, too few men were exposed
solely to nonferrous metal fumes to allow confident
exclusion of risks from these other sources of exposure.
Further corroboration of the findings came from
a study of mortality  in a large Swedish cohort of
construction workers, including 30 427 men with expos-
ure to metal fumes. Risks of death from pneumonia
were elevated 2.3-fold overall and 3.7- and 5.8-fold,
respectively, when lobar pneumonia and pneumococcal
pneumonia were analysed as subgroups of interest; while
the relative risk of infectious pneumonia was only 1.16 in
retired workers with former exposure.
Bringing the story up to date are one more analysis of
occupational mortality and a survey of patients hospital-
ized with IPD. In the first of these, Palmer et al.  pub-
lished risk estimates from the latest analysis of occupational
mortality for the Office for National Statistics (ONS) in
England and Wales during 1991–2000. Confirming earl-
ier observations, excesses of mortality were found from
pneumococcal and lobar pneumonia (54 deaths versus
27.3 expected) and from pneumonias other than bron-
chopneumonia (71 versus 52.4), but there were no
excesses of mortality from these causes at older ages or
from bronchopneumonia at any age. Despite potentially
better workplace controls on exposure, the hazard remains
manifest in the most recent national statistics. Elsewhere,
a study by Wong et al. , of cases of IPD confirmed at a
microbiological reference laboratory in Alberta, Canada,
implied a rate among welders of 22.7/100 000 popula-
tion/year, 2.7 times higher than in the general adult popu-
lation aged 18–65 years.
Deaths from pneumonia in young adults are rare,
as are deaths due to IPD [14,15], but the analysis by
Palmer et al.  found that the attributable mortality
from metal fume (45.3 excess deaths) in England and
Wales during 1991–2000 was not trivial compared with
an estimated 62.6 deaths from occupational asthma over
the same period. Using data from various sources, the
Health & Safety Executive has since made a similar esti-
mate of attributable mortality .
It may be said that, although efforts to control weld-
ing fume exposure at source are ongoing, this long-
standing hazard has been relatively underappreciated
in the UK, especially since the first report by Coggon
et al.  appeared in the Lancet in 1994 under the title
‘Lobar pneumonia: an occupational disease in welders’.
However, in 2001 the Norwegian Labour Inspection
Authority (NLIA) issued a warning to Norwegian phy-
sicians about the potentially lethal risk of fumes from
thermal metal work . The NLIA had received three
independent reports of deaths from pneumonia with
septicaemia among previously healthy men aged 50–55
years (all three exposed to welding fumes immediately
before they fell ill) and had also identified nine cases of
non-fatal pneumonia—three workers exposed to fumes
from cutting, grinding and welding were hospitalized
with lobar pneumonia, and six workers engaged on
reconstruction work inside a ship’s hull were managed as
outpatients . Case reports linking fatal pneumonia in
welders and metal fume-exposed occupations with atyp-
ical microorganisms also form a part of the record .
The NLIA urged physicians to inquire about occu-
pational exposures in working-aged patients with pneu-
monia, but the more direct and pressing need, to ensure
effective controls, has been problematic for several rea-
sons. Although some data suggest that chronic exposure
to metal fume blunts responsiveness to inhaled particu-
late matter (favouring the free radical injury hypothesis)
, the exact underlying mechanisms remain elusive,
and mechanistic chamber experiments are currently in
progress (K. T. Palmer, personal communication). In the
absence of suitable biomarkers of risk, the dose–response
K. T. PALMER AND M. P. COSGROVE: VACCINATING WELDERS AGAINST PNEUMONIA 327
by guest on July 4, 2015
relationship and the level below which exposures should
be controlled have not yet been defined.
However, the writers of the Green Book, the Joint
Committee on Vaccination and Immunisation (JCVI),
have now acted on available evidence to advise personal
protection for workers . Specifically, they advise that
‘There is a strong association between welding and the
development of pneumococcal disease, particularly lobar
pneumonia . . . . Therefore, welders who have not received
the pneumococcal polysaccharide vaccine (PPV23)
previously, should be offered a single dose of 0.5 ml of
PPV23 vaccine . . . Employers should ensure that provi-
sion is in place for workers to receive PPV23.’
Much is known about the properties and efficacy
of this vaccination and about alternative choices .
Several vaccines for pneumococcal pneumonia are avail-
able worldwide. The vaccine commonly given in child-
hood in the UK, the pneumococcal conjugate vaccine,
prevents infection with seven different serotypes, while
the vaccine given in adulthood, PPV23, contains purified
capsular polysaccharide from each of 23 capsular types
The vaccine is safe, and most healthy adults develop
a good antibody response to a single dose of PPV by
the third week following immunization. PPV23 will not
prevent pneumococcal pneumonia arising from a sero-
type absent in the vaccine, pneumonias caused by other
microorganisms, or pneumonitis secondary to inhalation
of metal fume. However, the 23 types included in the
vaccine account for 96% of the pneumococcal isolates
that cause serious infection in the UK, and PPV has
been estimated by a Cochrane review to be 74% effect-
ive (95% CI = 56–85%) in preventing IPD, with similar
estimates in relation to the prevention of pneumococcal
Following a single injection, post-immunization
antibody levels usually begin to wane after about
5 years, although the length of protection is not known.
Assuming that it lasts at least 10 years and that its effi-
cacy in welders matches that estimated in the Cochrane
meta- analysis, the incidence of IPD in welders should
fall from the 22.7/100 000/year estimated by Wong et al.
 to <6/100 000/year, and about 588 welders (95%
CI = 363–1551) would need to be vaccinated to prevent
one case of this disease in 10 years. If the case fatality rate
were 12% , 4900 welders would need vaccination to
avoid one death over the 10-year period. The first ratio
looks reasonable compared with the 500 healthy US
physicians who would need to take aspirin every year
to prevent myocardial infarction (MI) or death over the
period, and the 700 patients who would need to take sim-
ple anti-hypertensives each year to prevent one stroke,
MI or death ; while the second can be compared
with the roughly 2400 deaths/year  prevented by
fitting front and rear seat belts to 31 million cars on UK
roads (assuming that 31 million × 4 seat belts will pre-
vent 24 000 deaths if cars have a useful life of 10 years,
this equates to 5166 seat belt fittings per life saved per
Whom to vaccinate and when?
The Green Book guidance does not specify the types of
welding or welder that should be covered, the evidence
being of a nature that does not allow clear distinctions to
be drawn. Certainly, employees who regard themselves
as welders should be offered vaccination with PPV23,
but there are many workers who undertake some welding
as part of their job, and it would seem prudent to extend
the offer of vaccination to this group as well if welding is
undertaken on a regular basis.
For other groups, risk assessment will determine
whether exposure is improbable, possible or likely. For
example, most employees are not exposed to metal fume
from well-enclosed automated laser welding and cutting,
unless they need to enter the laser welding room shortly
after the cessation of laser or hybrid welding; the metal
fume produced from high-velocity oxyfuel coating should
be removed by the extraction system before an operator
re-enters the room; and there should be no concern in
relation to plastic, electron beam and friction stir weld-
ing, or work on laser metal or powder bed deposition
or cold spray technologies. Ultimately, however, as the
risk-conferring exposures are not closely defined, there
is a case for making offer of a one-off vaccination liberal
No Department of Health funding is available for
PPV23 to be given in welders, so employers will need to
fund the vaccination programme, which is estimated to
cost around £30 per vaccination. The obligation to vac-
cinate may be seen in the same light as that on hospital
managers under the Health and Safety at Work etc. Act
to ensure that certain categories of health care worker
at higher risk of hepatitis B infection receive the offer of
appropriate immunization—it is a necessary cost to the
There is current uncertainty regarding the optimum
timing of vaccination. An argument can be advanced for
offering vaccination to welders only at older ages (e.g.
over 50 years). Immunity may last only a few years ,
no booster is presently recommended (because of an
increased risk of side-effects) and the incidence of IPD
climbs at older ages, being low in young adults .
Thus, as absolute risk is higher at older ages, a bigger
absolute risk reduction may be anticipated among older
welders than among younger ones. Set against this, the
act of withholding vaccination would require a judgement
about the likelihood a welder would remain exposed at
the qualifying older age, and would deny protection in
328 OCCUPATIONAL MEDICINE
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the interim to those destined to discontinue exposure
before then. In view of the uncertainties, the JCVI did
not recommend an age restriction. Hopes exist that a
polyvalent pneumococcal conjugate vaccine, currently
under testing in adults, will provide a more lasting
immune memory (A. Hall, personal communication)
and could potentially be used for re-vaccination, in which
case timing of vaccination will become less important.
In the meantime, the uncertain duration of afforded
protection serves to remind that prevention at source is
paramount. Vaccination should not be seen by employ-
ers as an alternative to adequate fume control or by
welders as a reason to neglect the controls that employ-
ers have provided. Always using appropriate and effect-
ive local exhaust ventilation (LEV), keeping the LEV
hood near the work-piece, not placing the welder’s face
in the plume, wearing appropriate personal protective
equipment (using an ‘improved’ rather than a ‘standard’
helmet), always cleaning the work-piece prior to welding
to remove contaminants, undertaking other tasks (e.g.
grinding) away from the area in which welding is taking
place if possible or at least using an appropriate mask
will all help to minimize exposure to welding fume and
metal particulates in welders. A recent recommendation
by the Dutch welding community (www.5xbeter.nl) to
‘count to five’ after completing welding before lifting
the helmet is also worth following, as this will allow
time for agglomeration and aggregation of fume par-
ticles, rendering them non-respirable. Ensuring good
general ventilation and extraction in laser and electron
beam welding and high-velocity oxyfuel coating, and
allowing time to pass for fumes to cool before entering
the room are all sensible preventive actions.
Finally, as tobacco smoking increases the risk of IPD
, it is good practice to discourage welders from
smoking or exposing their non-smoking co-workers to
environmental tobacco smoke.
On the strength of this review we venture to make five
(i) Occupational health providers and employers should
offer welders and other employees who are exposed
to metal fume a single dose of PPV23.
(ii) Welders and other employees exposed to metal
fume should continue to control the amount of
fume that they are exposed to by all reasonably pos-
(iii) Ongoing efforts should be made to encourage weld-
ers to discontinue or avoid taking up smoking, not
only to reduce their risk of infectious pneumonia
but also that of more major and more likely threats
to their health from cardiovascular and chronic
obstructive pulmonary disease.
(iv) Research should be undertaken into the long-term
effectiveness of pneumococcal vaccine (and its opti-
mum timing) in preventing pneumococcal pneumo-
nia and IPD in welders, controlling as appropriate
for tobacco smoke exposure, co-morbidity and his-
tory of metal fume exposure.
(v) Physicians should monitor periodic updates to the
Green Book in case a more effective and long-lived
vaccine or suitable booster vaccine comes to the fore.
K.T.P. is in receipt of core funding from the Medical Research
Council. Certain of the work reviewed on pneumonia and met-
al fume was funded also by the Health and Safety Executive,
the Office for National Statistics, the Worshipful Company of
Blacksmiths and the Colt Foundation.
Conflicts of interest
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The athletic shadow of Millennium Man with his
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city, its five white Olympic rings and the iconic Opera
House—a motif echoed in the smoke plume of his torch
and repeated on his legs. The blue background mimick-
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Captain Robert Dover opened the first Olimpicks
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