Abstract

A 52-year-old man was referred with chronic cough of increasing severity over the last 4 years. The cough was productive of green sputum and he experienced coughing attacks weekly. He reported no other respiratory symptoms. He had a sore throat following coughing bouts but denied other upper airway complaints. He was otherwise well with no systemic symptoms. His cough had improved following a 2-week summer holiday, and subsequently deteriorated following his return to work.

A chest X-ray organised in primary care was normal. Three years earlier, his general practitioner increased his lansoprazole from 15 to 30 mg once daily for cough. This had not helped although treatment continued. His past medical history included treated obstructive sleep apnoea and hypertension for which he took bendroflumethiazide and losartan; the latter substituted for his ACE inhibitor 3 years earlier. He recalled no personal or family history of asthma or atopy and was a lifelong non-smoker. He had kept budgerigars until 6 months previously when the last bird died.


He had worked for 12 years as a computer numerical control (CNC) machine setter and operator, machining metal parts used to make tools for woodworking. He machined bronze, brass, leaded mild steel, high-speed steel and aluminium pieces to the desired specification. He operated five machines in a single area of the factory, adjacent to where ash handles were turned. He was the sole CNC operator turning metal components in the factory and was not aware of any colleagues reporting respiratory symptoms.

Water-based metalworking fluids (MWFs) were used on all five machines. Each machine collected and recirculated MWFs via its own sump. For the last 4 years, the fluids had occasionally become ‘foul smelling’ and sometimes changed colour from a translucent blue to a chocolate brown. The worksite did not perform dip-slide fluid analysis or use biocide contrary to agreed industry practice. The patient reported exposure to MWF mist when opening the machine doors and cleaning with compressed air. He wore a non-fit tested disposable paper mask for respiratory protective equipment.

Physical examination of the patient was normal. Spirometry revealed an FEV1 of 3.17 L (83% predicted), FVC of 3.9 L (81%) and a FEV1/FVC ratio of 104%. FENO was 92 parts per billion (ppb). TLCO was 12.4 (116%) mmol/min/kPa and KCO 2.29 (160%) mmol/min/kPa/L. Total IgE was raised at 122 KU/L, peripheral eosinophils normal at 0.13×109/L and specific IgG to aspergillus, budgerigar and pigeon within normal limits. A high resolution CT (HRCT) performed midway through a normal working week revealed mild gas trapping on expiratory views.
Two months later, his OASYS demonstrated minimal diurnal variation (DV) at and away from work (5.6% and 6.5%, respectively), with a maximal DV of 13%. The work-effect index (WEI) was negative at 1.64. As the WEI was negative but DV borderline, a mannitol challenge was requested to look for further evidence of airway hyperresponsiveness.

The test was performed during a routine working week on no inhaled corticosteroids (ICS). The maximum % change in FEV1 was 2.8 following the complete dose of 635 mg osmohale, with a maximum FEV1 change between doses of -1.4%. A repeat FENO taken midway through the working week was 94 ppb. An induced sputum sample done at the same time contained 14% eosinophils. Occupational eosinophilic bronchitis was suspected, and the patient returned following a week off work for a repeat FENO. At this point, FENO had dropped to 11 ppb. A diagnosis of occupational non-asthmatic eosinophilic bronchitis (NAEB) was made and the patient commenced on ICS. He was provided with written confirmation of the diagnosis and recommendations about how to reduce further MWF exposures. Work provided fit-tested half-face disposable masks and the patient reduced his use of compressed air. At his next appointment, a midweek FENO on ICS was 18 ppb and his cough had almost disappeared.

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