Guest guest Posted May 9, 2011 Report Share Posted May 9, 2011 In response to my post (hereinbelow) about carbon monoxide in the home as possibly relevant to autism's time trends per year (1a), a physician commented, " If so, the same mechanism as with smoking cigarettes? " Given that CO is not the only adverse factor implicated in smoking, I found 31 cites via autis*[tw] AND (smoking[tw] OR tobacco[tw]) At least one such cite found " low ventilation rate in the home " to be associated with autism (2a), a finding consistent with the possibility that carbon monoxide is among background factors contributing to the findings of Zerbo et al (1a). */ /* 1a. Month of Conception and Risk of Autism. <http://www.ncbi.nlm.nih.gov/pubmed/21543984> Zerbo O, Iosif AM, Delwiche L, C, Hertz-Picciotto I. Epidemiology. 2011 May 3. " Higher risks for autism among those conceived in winter months suggest the presence of environmental causes of autism that vary by season. " 2a. Associations between indoor environmental factors and parental-reported autistic spectrum disorders in children 6-8 years of age. <http://www.ncbi.nlm.nih.gov/pubmed/19822263> Larsson M, Weiss B, Janson S, Sundell J, Bornehag CG. Neurotoxicology. 2009 Sep;30(5):822-31. An analysis of the associations between indoor environmental variables in 2000 as well as other background factors and the ASD diagnosis indicated five statistically significant variables: (1) maternal smoking; (2) male sex; (3) economic problems in the family; (4) condensation on windows, a proxy for */low ventilation rate in the home/*; (5) PVC flooring, especially in the parents' bedroom. > 2011/5/8 Binstock <binstock@... > > > > Perhaps (along with maternal vaccinations for influenza) /in-home > carbon monoxide/ is a factor (eg, 1-8), as homes would have > windows closed more often, furnaces running more often. > * > About CO standards and CO monitors* > > My CO monitors have been chirping occasionally for weeks. During > that time I've had many conversations with home-heating > specialists - who have devices that can detect and report CO > levels as low as 1 ppm. One day, with a reading of 14 ppm, the > technician said I ought be sensing symptoms such as fatigue, > dizziness. (I was). > > In-home CO detectors are set to sound after hours of 70 ppm, > shorter times for higher levels. The easily available CO detectors > with digital readouts do so at 30 ppm and above but sound after > hours of 70 ppm. However, the technician said I ought be sensing > symptoms in the vicinity of 14 ppm. > > An EPA CO site (here <http://www.epa.gov/iaq/co.html>) offers > diverse guidelines, including concern for 8-hour levels of 55, 35, > or 25 ppm (9). > > *Questions* > > Is the 70 ppm standard for home-detectors an industry-serving > fiction? > > Is in-home carbon monoxide is factor influencing embryonic > development in an autism direction? > > /**/ > > 1-7 via: > " carbon monoxide " [tw] AND embry*[tw] AND (neuron* OR brain OR CNS) > > 1. Evidence for oxidative stress in the developing cerebellum of > the rat after chronic mild carbon monoxide exposure (0.0025% in > air). <http://www.ncbi.nlm.nih.gov/pubmed/19580685> > IA, Acuna D, Beltran-Parrazal L, IE, Amarnani A, > Cortes M, Edmond J. > BMC Neurosci. 2009 May 27;10:53. > > 2. Chronic prenatal exposure to carbon monoxide results in a > reduction in tyrosine hydroxylase-immunoreactivity and an increase > in choline acetyltransferase-immunoreactivity in the fetal > medulla: implications for Sudden Infant Death Syndrome. > <http://www.ncbi.nlm.nih.gov/pubmed/10744060> > Tolcos M, McGregor H, D, Rees S. > J Neuropathol Exp Neurol. 2000 Mar;59(3):218-28. > > 3. Exposure to prenatal carbon monoxide and postnatal > hyperthermia: short and long-term effects on neurochemicals and > neuroglia in the developing brain. > <http://www.ncbi.nlm.nih.gov/pubmed/10739630> > Tolcos M, Mallard C, McGregor H, D, Rees S. > Exp Neurol. 2000 Apr;162(2):235-46. > > 4. A delayed role for nitric oxide-sensitive guanylate cyclases in > a migratory population of embryonic neurons. > <http://www.ncbi.nlm.nih.gov/pubmed/9851840> > JW, Schwinof KM, Snyder MA, Copenhaver PF. > Dev Biol. 1998 Dec 1;204(1):15-33. > > 5. Ornithine decarboxylase activity in fetal and newborn rat > brain: responses to hypoxic and carbon monoxide hypoxia. > <http://www.ncbi.nlm.nih.gov/pubmed/8306425> > Packianathan S, Cain CD, Stagg RB, Longo LD. > Brain Res Dev Brain Res. 1993 Nov 19;76(1):131-40. > > 6. Carbon monoxide and brain development. > <http://www.ncbi.nlm.nih.gov/pubmed/3537859> > Fechter LD, Mactutus CF, Storm JE. > Neurotoxicology. 1986 Summer;7(2):463-73. > > 7. Chronic low level maternal carbon monoxide exposure and fetal > growth and development. <http://www.ncbi.nlm.nih.gov/pubmed/687711> > Garvey DJ, Longo LD. > Biol Reprod. 1978 Aug;19(1):8-14. > > 8. Carbon monoxide and the nervous system. > <http://www.ncbi.nlm.nih.gov/pubmed/12667497> > Raub JA, Benignus VA. > Neurosci Biobehav Rev. 2002 Dec;26(8):925-40. > > 9. EPA > http://www.epa.gov/iaq/co.html > > [OSHA PEL] The current Occupational Safety and Health > Administration (OSHA) permissible exposure limit (PEL) for carbon > monoxide is 50 parts per million (ppm) parts of air (55 milligrams > per cubic meter (mg/m(3))) as an 8-hour time-weighted average > (TWA) concentration [29 CFR Table Z-1]. > > [NIOSH REL] The National Institute for Occupational Safety and > Health (NIOSH) has established a recommended exposure limit (REL) > for carbon monoxide of 35 ppm (40 mg/m(3)) as an 8-hour TWA and > 200 ppm (229 mg/m(3)) as a ceiling [NIOSH 1992]. The NIOSH limit > is based on the risk of cardiovascular effects. > > [ACGIH TLV] The American Conference of Governmental Industrial > Hygienists (ACGIH) has assigned carbon monoxide a threshold limit > value (TLV) of */25 ppm/* (29 mg/m(3)) as a TWA for a normal > 8-hour workday and a 40-hour workweek [ACGIH 1994, p. 15]. The > ACGIH limit is based on the risk of elevated carboxyhemoglobin > levels [ACGIH 1991, p. 229]. > > > > > > Quote Link to comment Share on other sites More sharing options...
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