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African dust-laden atmospheric conditions activate the
trigeminovascular system

H Doganay1,D Akcali2,T Goktaş3,K Çaglar4,D Erbas3,C Saydam5,H Bolay1,*

Article first published online: 13 MAR 2009 DOI: 10.1111/j.1468-2982.2008.01839.x




Volume 29, Issue 10, pages 1059–1068, October 2009


  • Atmosphere;
  • Saharan desert dust;
  • headache;
  • nitric oxide;
  • trigeminovascular system

It has been recently noticed that dust originating from deserts can be
transported to other continents by the atmosphere and has an adverse effect on
public health, such as increased asthma attacks. Dust originating from the
Saharan Desert could initiate a series of reactions upon contact with cloud
water and results in the formation of reduced iron (Fe2+), oxalate
and various basic amino acids. We aimed to evaluate whether the simulation of
Saharan dust-containing atmospheric conditions could trigger the
trigeminovascular system. Freely moving rats incubated within simulated
atmospheric conditions containing (i) Saharan dust, (ii) Co60 gamma
ray-treated Saharan dust (sterilized) and (iii) dust-free air, were investigated
for the presence of c-fos expression in trigeminal nucleus caudalis (TNC) and
for NOx (nitrate+nitrite) levels in blood samples. Atmospheric samples were
analysed for microorganisms. Saharan dust-containing atmospheric conditions
induced c-fos expression in nociceptive neurons within TNC. The number of c-fos+
neurons in superficial lamina of TNC was significantly higher in the Saharan
dust group (32.9 ± 5.3, P = 0.0001) compared with dust-free air
(11.02 ± 2.7) or Co60-treated Saharan dust groups (15.01 ± 2.4). An
increase in NOx levels was detected in blood samples of rats exposed to Saharan
dust-containing atmosphere. This study has revealed an unknown environmental
factor as a possible trigger for headache. It is the first time that transport
of Saharan dust with the atmospheric air stream has been documented to be able
to trigger the trigeminovascular system in animals. Further studies are needed
to explore the mechanisms and molecules that mediate the nociceptive effect and
to guide new treatment strategies.