The path forward is fairly simple, though the execution of it is not. A statistically significant sample of SBS sufferers would be secured, sufferers whose environment had remained essentially unaltered from the point of their symptoms' onset, and where the environmental factors suggested the presence of mold (ie, dampness). An AChEi 'inventory' of each subject's environment is then required, with a key factor in this being a complete environmental analysis to determine both the specific agents present, their concentrations, and their AChEi values. Testing the subjects to determine low PON-activity levels and concentration would then further clarify the results. This PON testing would be particularly significant in cases where a number of individuals experienced similar exposures which resulted in markedly differing outcomes. A 'control' environment would also need to be 'inventoried', one where the environmental quality is known to be 'high'. Then, pursuing an examination of the correlation between environmental AChEi levels and their components, individual PON levels, and subject outcomes, should highlight the validity of this paper's hypothesis.
1. Golomb BA. Acetylcholinesterase inhibitors and Gulf War illnesses. 2008, PNAS, vol. 105 no. 11, 4295-4300
2. Research Advisory Committee on Gulf War Veterans' Illnesses Gulf War Illness and the Health of Gulf War Veterans. Research Advisory Committee on Gulf War Veterans' Illnesses Home. November 2008. http://www1.va.gov/RAC-GWVI/
3. Redlich CA, Sparer J, Cullen MR. Sick-building syndrome. Lancet 1997; 349: 1013-16
4. World Health Organization Indoor Air Quality: Biological Contaminants, 4-9, Report on a WHO Meeting, Rautavaara, 29 August-2 September 1988
5. Chen JW, Luo YL, Hwang MJ, Peng FC, Ling KH. Territrem B, a tremorgenic mycotoxin that inhibits acetylcholinesterase with a noncovalent yet irreversible binding mechanism. 1999 J Biol Chem Dec 3; 274(49):34916-23
6. Shiomi K, Tomoda H, Otoguro K, Omura S. Meroterpenoids with various biological activities produced by fungi. 1999 Pure Appl. Chem., Vol. 71, No. 6, pp. 1059-1064
7. Schwab CJ, Straus DC. The roles of Penicillium and Aspergillus in sick
building syndrome. Adv Appl Microbiol 2004; 55:215-38
8. Edvardsson B, Stenberg B, Bergdahl J, Eriksson N, Linden G, Widman L. Medical and social prognosis of non-specific building-related symptoms (Sick Building Syndrome): a follow-up study of patients previously referred to hospital. Int Arch Occup Environ Health 2008 Jul; 81(7):805-12
9. Gorny RL, Reponen T, Willeke K, Schmechel D, Robine E, Boissier M,
Grinshpun S. Fungal Fragments as Indoor Air Biocontaminants. Appl Environ Microbiol. 2002 July; 68(7): 3522-3531
10. Bloom E, Bal K, Nyman E, Must A, Larsson L. Mass Spectrometry-Based Strategy for Direct Detection and Quantification of Some Mycotoxins Produced by Stachybotrys and Aspergillus spp. in Indoor Environments. Appl Environ Microbiol. 2007 July; p. 4211-4217, Vol. 73, No. 13
11. Haley RW, Billecke S, La Du BN. Association of Low PON1 Type Q
(Type A) Arylesterase Activity with Neurologic Symptom Complexes in Gulf War Veterans. Toxicol Appl Pharmacol 1999 Jun 15;157(3):227-33.
12. McKeown-Eyssen G, Baines C, Cole DEC, Riley N, Tyndale RF, Marshall L, Jazmaji V. Case-control study of genotypes in multiple chemical sensitivity: CYP2D6, NAT1, NAT2, PON1, PON2 and MTHFR. Int J Epidemiol 2004 Oct;33(5):971-8.
13. Rainwater DL, Mahaney MC, Wang XL, Rogers J, Cox LA, Vandeberg JL Determinants of variation in serum paraoxonase enzyme activity in baboons. 2005 Jul;46(7):1450-6. Epub 2005 Apr 16.
14. Gouedard C, Koum-Besson N, Barouki R, Morel Y. Opposite regulation of the human paraoxonase-1 gene PON-1 by fenofibrate and statins. Mol Pharmacol, 2003 Apr;63(4):945-56.
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