The current investigation of employees in a car manufacturing plant in the UK detected 19 workers with EAA according to a strict case definition. During the investigation we also uncovered a large unknown outbreak of OA, with 74 workers diagnosed on the basis of serial peak flow records which are both reasonably sensitive and very specific for identifying patients with OA.21,22,25
A total of 87 workers met case definitions for OA and/or EAA and/or HF, an overall prevalence in the workforce of 10%. Half of the workers with OA had symptoms before 2003 (the date for new onset was defined as January 2003 or later based on the 12 index cases of EAA), suggesting that the outbreak of OA may have begun earlier than the outbreak of EAA.
We also identified workers with HF and work‐related chronic bronchitis, as well as single cases of histologically confirmed lipoid pneumonitis and Langerhans' cell histiocytosis and immunologically confirmed bronchopulmonary aspergillosis. The variety of different presentations of work‐related respiratory disease related to exposure to MWF in the current study is consistent with other outbreaks of EAA in the USA. Zacharisen et al
reported cases of EAA, asthma and bronchitis in a car engine manufacturing plant.26
Hodgson et al
found that many workers with EAA also had asthma, and there was at least one case of usual interstitial pneumonia and a case of sarcoidosis at the plant which produced titanium and steel parts for the aerospace industry.17
Similarly, in the present investigation 8 of the 19 workers who met the case definition for EAA also had peak flow variability consistent with the case definition for OA. EAA can produce findings of airways obstruction on spirometry, possibly due to associated bronchiolitis. It is conceivable that such airways obstruction would also show a work‐related pattern.
Before further interpreting the results, it is important that the methodological limitations are discussed. First, with 87 cases of work‐related respiratory disease observed at the factory, the size of the control group (n
50) may seem rather low. The number of controls had to be decided at the start of the investigation as the data collection had to happen for all at the same time, before the remedial action at the factory commenced. At that time the number of known (index) cases of EAA was only 12 and we were unaware of any cases of OA, so the sample size of 50 controls was thought to be reasonable. Second, a lower proportion of the control group worked in the manufacturing area compared with cases of OA and EAA and, as a consequence, they had less potential to be exposed to MWF. This was because the control population was selected from the asymptomatic workers identified from the screening questionnaire. The selection bias in the control group probably does not affect the results presented in this paper, as the focus of the paper is more about the epidemiology of those with respiratory illness. The results from this control group does reaffirm that working in the manufacturing area is associated with an increased risk of disease.
Another methodological issue is that the date of onset of symptoms was established retrospectively from the self‐completed questionnaire more than 15 months after the onset of the outbreak. Only 70 of the 146 workers with work‐related breathlessness were able to identify the month of onset. There were no contemporary surveillance data. With these caveats, there appears to be a peak incidence in March 2003, just before a new hydraulic oil for metal working machines was introduced in April 2003. The new hydraulic oil was more soluble in the MWF, increasing the concentration of tramp oil in the MWF. However, as the change in hydraulic oil occurred after the start of the outbreak, there is no clear evidence that this change is significant. The outbreak also coincided with reports of increased misting in the factory during the winter period when the roof louvers were closed.
Although factory records historically showed little bacterial growth, our own microbiological investigations in the factory found Acinetobacter
spp and Ochrabactrum anthropi
cultured from the washer fluid. DNA from these bacteria was also identified in the MWF from the largest sump, although there was no culture. No Mycobacterium
spp were identified either from culture or from DNA extraction. The Health and Safety Laboratory has carried out a parallel immunological investigation of the workers at the factory in the current investigation which is reported in detail elsewhere.20
MWF from the largest common sump at the time of the outbreak and extracts from cultures of Acinetobacter
spp, Ochrobactrum anthropi
spp were used to look for the presence of precipitating antibodies.20
In those with EAA, 59% had precipitating antibodies to at least one of the microbial species Acinetobacter
or to used sump oil, whereas precipitating antibodies were found in only 10% of those with OA and 5% of asymptomatic workers (controls).20
This is unlike other outbreaks of alveolitis where precipitating antibodies are commonly found in affected and asymptomatic subjects.27
No workers tested positive for precipitating antibodies to Mycobacteria
species. These results indicate that bacterial contamination of MWF—and in particular Acinetobacter
—had at least a contributory role in the cases of EAA.
The overall levels of mist from both MWF and mineral oil sources were unremarkable, with most levels below the then MWF guidance value of 1 mg/m3
and the mineral oil in air guidance value of 3 mg/m3
The Health and Safety Executive (the UK regulatory body for health and safety) has since withdrawn these guidance values.28
The highest number of cases was in one of the assembly areas which was about 30 metres from the common sump, suggesting that the causative aerosol was relatively widespread. Two washers vented inside the factory and were also in the northern end of the factory. Given the wide distribution of disease in the factory, the most likely cause was an aerosol from either the metalworking and/or washing operations, although no material within this mist has been confirmed as a specific causal agent.
The potential of other exposure factors as a cause of this outbreak was considered. Metal particles can produce an intrapulmonary inflammatory response29
and some specific metals are well recognised causes of OA. These are mainly platinum salts, chrome, cobalt and, to a lesser extent, zinc and nickel. At the factory the engines were made of aluminium alloy. There was no platinum, chrome or nickel. There was one machine where hard metal valve rings were machined. Cobalt levels in the MWF were insignificant and levels were checked in the urine of workers and were normal. There is some doubt as to whether aluminium alone can cause OA. The main work on aluminium and asthma comes from smelters where aluminium sodium fluoride is a possible cause. It has never been described in those working with cold aluminium. There were no sources of nitrogen oxides (no heating of the metal). However, the potential for other chemical constituents to be either causal or to have had a co‐effect cannot be discounted. The Health and Safety Executive has compiled a list of the constituents and contaminants of the MWF and wash fluids at the factory which were considered in the original investigation as possible causes of either EAA or OA (see online supplement available at http://thorax.bmj.com/supplemental
During bronchial challenge tests two workers (one with OA and one with EAA) confirmed reactions to the used MWF taken from the common sump but not the clean MWF. The used MWF will contain material from the aluminium alloy castings, microbial contamination and added biocides, pH adjusters, etc. The lack of reaction to the unused MWF indicates that the chemical constituents alone were unlikely to have caused the disease.
As a consequence of this outbreak UK policy has changed, firstly for the users of MWF and secondly for those affected by EAA. First, the “lessons learned” from this outbreak have been published by the Health and Safety Executive on their website (this is available in the online Appendix at http://thorax.bmj.com/supplemental
), detailing the practical implications for other users of MWF.28
This outbreak showed that adhering to the guidance standards of oil mist did not prevent respiratory disease23,24
and has led to their withdrawal by the Health and Safety Executive. Furthermore, the Health and Safety Executive has since issued new guidance on safe working practices that includes a requirement for respiratory surveillance. They have subsequently carried out a national survey of large users of MWF in 2005/6 to identify the extent to which guidance was being followed, with many deficiencies noted.30
Second, there is an anomaly in that OA due to oil mists is compensatable in the UK through a no‐fault compensation system from the UK Government's Department for Work and Pensions, but EAA due to anything other than fungal or avian antigens is not.31
OA is known to adversely affect income and clinical outcome,32,33
whereas the impact of EAA is likely to be at least as important. In July 2006 the Industrial Injuries Advisory Council (who advise the Department of Work and Pensions of the list of prescribed diseases for compensation) recommended that the occupational coverage for EAA should include exposure to mists from MWF.34
This has now had ministerial approval and “work involving exposure to MWF” as a cause of EAA was added to the list of prescribed diseases on 6 April 2007.31
Finally, it is of interest to note what happened after the outbreak at the factory. After the assessment at the factory in June 2004 a series of control measures was introduced including:28
- replacing MWF in the large common sumps;
- cleaning machines with individual sumps (both metalworking and washing) which were heavily contaminated with bacteria and then refilling them with fresh fluid;
- treating other less contaminated sumps with biocide;
- supplying employees with respiratory protection with powered respirators for those with known disease; and
- instituting respiratory surveillance for all employees.
Continued surveillance using occupational PEF records was carried out for those with OA, and a few had persistent OA despite the extensive control measures. The factory went into administration in April 2005. The machinery was subsequently bought by Nanjing Automobile (Group) Corporation and removed to China. Nanjing has been warned about the risks.