Increased abdominal mass in obesity should enhance normal gravitational effects on supine respiratory mechanics. We have examined respiratory impedance (forced oscillation over 4-26 Hz applied at the mouth during tidal breathing), maximum inspiratory and expiratory mouth pressures (MIP and MEP), and maximum effort flow-volume curves seated and supine in seven obese subjects (O) (mean age 51 yr, body mass index 43.6 kg/m2) and seven control subjects (C) (mean age 50 yr, body mass index 21.8 kg/m2). Seated mean total lung capacity was smaller in O than in C (82 vs. 100% of predicted); ratio of functional residual capacity (FRC) to total lung capacity averaged 43% in O and 61% in C (P < 0.01). Total respiratory resistance (Rrs) at 6 Hz seated was higher in O (4.6 cmH2O.l-1.s) than in C (2.2 cmH2O.l-1.s; P < 0.001); total respiratory reactance (Xrs) at 6 Hz was lower in O than in C. In C, on changing to the supine posture, mean Rrs at 6 Hz rose to 2.9 cmH2O.l-1.s, FRC fell by 0.68 liter, and Xrs at 6 Hz showed a small fall. In O, despite no further fall in FRC, supine Rrs at 6 Hz increased to 7.3 cmH2O.l-1.s, and marked frequency dependency of Rrs and falls in Xrs developed. Seated, MIP and MEP in C and O were similar; supine there were small falls in MEP and maximum expiratory flow in O. The site and mechanism of the increase in supine Rrs and reduction in supine Xrs and the mechanism maintaining supine FRC in obesity all need further investigation.

The mechanisms of orthopnea and the role of changes in respiratory mechanics in left ventricular failure (LVF) are poorly understood. We have measured total respiratory airflow resistance (Rrs) using forced oscillation in the sitting and supine positions in 10 patients with chronic LVF (NYHA II-III) shortly after recovery from acute LVF and in 10 matched control subjects (CON). Seated, the patients with LVF had small lung volumes but no evidence of airway obstruction (mean FEV(1)/FVC, 81%). Mean Rrs at 6 Hz was only slightly higher in LVF (3.4 cm H(2)O. L(-1). s) than in CON (2.6 cm H(2)O. L(-1). s). After 5 min supine, breathlessness in LVF increased. Despite much smaller mean falls in mid-tidal lung volume (MTLV) in LVF than in CON, the supine rise in Rrs was 80.5% in LVF and 37.6% in CON; mean increases in specific Rrs (SRrs = Rrs.MTLV) were 75.8% in LVF and 16.6% in CON (p 0.001). Five minutes after resuming the sitting position all values had reverted almost to the original sitting values. In 5 LVF patients, nebulized ipratropium, a muscarinic antagonist, only slightly attenuated the supine rise in SRrs. We conclude that patients with chronic LVF, who had little evidence of airways obstruction when seated, showed a large rise in airflow resistance after lying supine for 5 min. This cannot be attributed to reduction in lung volume when supine and no evidence was found of vagally-induced bronchoconstriction. Further experiments are required to establish the cause of the rapid supine rise in airflow resistance in LVF.

Polyvinylchloride (PVC) resins are widely used in industry. Asthma due to the thermal degradation products of PVC are well documented. In this first case of occupational asthma due to unheated PVC resin dust the patient was exposed to PVC resin dust during the mixing of chemicals used for making plastic seals for bottle caps.Meatwrappers' asthma and asthma due to the thermal degradation products of polyvinylchloride (PVC) are well documented.'4 Pneumoconiosis'9 and interstitial pneumonitis'°among workers exposed to PVC dust have been reported. Respiratory symptoms and abnormalities of lung function and of the chest radiograph have been described in surveys of workers exposed to PVC dust." 12 We report the first case of asthma induced by occupational exposure to unheated PVC resin dust. Case reportA 32 year old man worked for 14 years in a factory manufacturing bottle caps. Each metal cap was lined with a plastic seal on its inner surface. Both the fabrication of the metal caps and the injection moulding process of making plastic seals were carried out in the main production hall ofthe factory. The PVC resin mixture for the injection moulding process was prepared in a fairly large air conditioned room that was separated from the main production hall. For the past eight years the patient worked in this mixing room where he was exposed to PVC resin dust and other chemicals during mixing.He started to have episodes ofcough and breathlessness about five years after working in the mixing room. Initially, the frequency of symptoms was once in three to four months. During the past year, however, his symptoms had occurred almost daily and he had to depend on a ventolin inhaler for relief. He worked a five day week from 0730 to 1630. His symptoms usually started at about 0200 or 0300. Symptoms improved on weekends and holidays. Accepted 22 December 1988 There was no associated rhinitis. He had no history ofasthma or atopy. His sister had a history ofasthma. OCCUPATIONAL EXPOSUREThe preparation of PVC resin mixture in the mixing room was observed and the exposure dust concentration monitored. Three types ofchemicals were blended together to form the mixture: (i) PVC resin, a white powder, (ii) dioctylphthalate or Di-2-ethylhexylphthalate(DOP), a plasticiser in the form of a clear oily liquid, and (iii) a paste containing azodicarbonamide (a plastics blowing or foaming agent), colouring agent, and stabilisers. The PVC resin itself was a mixture of three grades of PVC resin: types A, B, and C. Type A was an emulsion resin with no stabilisers added, type B an emulsion resin that had been stabilised against heat, and type C a suspension resin with no stabilisers added. The ratio of A:B:C was 3:1:0-7. The paste containing azodicarbonamide and the liquid DOP were first placed in a tank, then five bags (120 kg) of PVC resins were manually poured into the tank. The pouring process was visibly dusty and took about 10 minutes. No local exhaust ventilation was provided.A quartz crystal microbalance cascade impactor was u...

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Hypoxaemia and breathing irregularities have been shown to occur during haemodialysis in patients with chronic renal failure. This study examined the role of hypoxia in the genesis of the irregular breathing during haemodialysis. The ventilatory patterns using respiratory inductance plethysmography and arterial blood gases were studied in seven males with chronic renal failure on long-term haemodialysis. The study was carried out before and during dialysis on one day without (D1) and another day with intranasal oxygen at 4 L x min(-1) (D2). On D1, mean (SD) arterial oxygen tension (Pa,O2) fell 1.9 (0.9) kPa (p<0.001) and mean minute ventilation (V'E) fell 1.9 (1.1) L x min(-1) (p<0.01) during dialysis. The arterial carbon dioxide tension (Pa,CO2) did not show a significant decrease (4.7 (0.2) kPa before and 4.6 (0.2) kPa during dialysis). Cumulative number of apnoeas was 64 and the coefficients of variation (COV) of respiratory frequency (fR) and tidal volume (VT) were 29.6 (11.9) and 38.2 (11.9)%, respectively. On D2, mean Pa,O2 remained stable (20.4 (4.1) kPa before, 21.3 (4.1) kPa during dialysis). There was no significant change in mean V'E (6.4 (0.9) L x min(-1) before, 5.5 (0.5) L x min(-1) during dialysis). Pa,CO2 decrease was not significant but the fall was greater (4.8 (0.1) kPa before, 45 (0.5) kPa during dialysis). Cumulative number of apnoeas was 94 and the COVs offR and VT were 35.8 (5.1) and 40.5 (11.3)%, respectively. Oxygen administration did not significantly affect the haemodialysis-induced changes in ventilation and breathing pattern, despite a significant protective effect from the fall in arterial oxygen tension. It was concluded that the fall in arterial oxygen tension is not the main determinant of breathing irregularities during haemodialysis.