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- Ralf Clauss, Julian Mayes, Paul Hilton, and Ross Lawrenson.
- Nuclear Medicine, Royal Surrey County Hospital, Egerton Road, Guildford, Surrey GU27XX, UK. rclauss@royalsurrey.nhs.uk
- Med. Hypotheses. 2005 Jan 1;64(6):1198-201.
AbstractPrevious publications have highlighted seasonal variations in the incidence of thrombosis and pulmonary embolism, and that weather patterns can influence these. While medical risk factors for pulmonary thrombo-embolism such as age, obesity, hypercoagulable states, cancer, previous thrombo-embolism, immobility, limb paralysis, surgery, major illness, trauma, hypotension, tachypnoea and right ventricular hypokinesis are not directly implicated regarding environmental factors such as weather, they could be influenced indirectly by these. This would be especially relevant in polluted areas that are associated with a higher pulmonary embolism risk. Routine nuclear medicine lung ventilation/perfusion studies (V/Q scans) of 2071 adult patients referred to the nuclear medicine department of the Royal Surrey County Hospital in Guildford, UK, between January 1998 and October 2002 were reviewed and 316 of these patients were classified as positive for pulmonary embolism with high probability scan on PIOPED criteria. The occurrence of positive scans was compared to environmental factors such as temperature, humidity, vapour pressure, air pressure and rainfall. Multiple linear regression was used to establish the significance of these relations. The incidence of pulmonary embolism was positively related to vapour pressure and rainfall. The most significant relation was to vapour pressure (p=0.010) while rainfall was less significant (p=0.017). There was no significant relation between pulmonary embolism and air pressure, humidity or temperature. It is postulated that rainfall and water vapour may be contributary factors in thrombosis and pulmonary embolism by way of pollutants that are carried as condensation nuclei in micro-droplets of water. In particular, fossil fuel pollutants are implicated as these condensation nuclei. Pollutants may be inhaled by populations exposed to windborne vapour droplets in cities or airports. Polluted vapour droplets may be absorbed by the lung to hasten coagulation cascades in the blood. This may lead to thrombosis and increased pulmonary embolism under high vapour pressure conditions. With combined factors such as pre-existing ill health or immobility on long flights, the risk of thrombosis and consequent embolism might increase substantially.
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