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could increase pain in spinal cord injury and worsen MS

A neurotoxin called acrolein found in tobacco smoke that is thought to increase pain in people with spinal cord injury has now been shown to accumulate in mice exposed to the equivalent of 12 cigarettes daily over a short time period.

One implication is that if acrolein is exacerbating pain its concentration in the body could be reduced using the drug hydralazine, which has been approved by the U.S. Food and Drug Administration for hypertension, said Riyi Shi (pronounced Ree Shee), a professor in Purdue University's Department of Basic Medical Sciences, College of Veterinary Medicine, and Weldon School of Biomedical Engineering.......Read More - http://www.ms-uk.org/environmentalfactors

Acrolein is a known carcinogen.

Effect of Carcinogenic Acrolein on DNA Repair and Mutagenic Susceptibility
http://www.jbc.org/content/287/15/12379.full.pdf

• Background: Acrolein is highly reactive and abundant in tobacco smoke.
• Results: Acrolein induces DNA damage, inhibits excision repair and mismatch repair, causes repair protein degradation, andenhances mutagenesis.
• Conclusion: Acrolein induces DNA damage and inhibits DNA repair that causes mutagenesis and initiates carcinogenesis.
• Significance: This is the first demonstration that acrolein inhibits DNA repair pathways by induction of repair protein degradation.

Acrolein (Acr), a ubiquitous environmental contaminant, is a human carcinogen. Acr can react with DNA to form mutagenic alpha- and gamma-hydroxy-1, N²-cyclic propano-2’-deoxyguanosine adducts (alpha-OH-Acr-dG and gamma-OH-Acr-dG). We demonstrate here that Acr-dG adducts can be efficiently repaired by the nucleotide excision repair (NER) pathway in normal human bronchial epithelia (NHBE) and lung fibroblasts (NHLF). However, the same adducts were poorly processed in cell lysates isolated from Acr-treated NHBE and NHLF, suggesting that Acr inhibits NER. In addition, we show that Acr treatment also inhibits base excision repair and mismatch repair. Although Acr does not change the expression ofXPA,XPC,hOGG1,PMS2or MLH1genes, it causes a reduction of XPA, XPC, hOGG1, PMS2, and MLH1 proteins; this effect, however, can be neutralized by the proteasome inhibitor MG132. Acr treatment further enhances both bulky and oxidative DNA damage-induced mutagenesis. These results indicate that Acr not only damages DNA but can also modify DNA repair proteins and further causes degradation of these modified repair proteins. We propose that these two detrimental effects contribute to Acr mutagenicity and carcinogenicity.