1 There is evidence that community tobacco interventions are effective in reducing uptake of tobacco use in young people.2 The effectiveness is less clear for interventions for adults. In one large trial conducted in the United States, the Community Intervention Trial for Smoking Cessation (COMMIT), a large-scale multicomponent community intervention was assessed to ascertain the effect on the prevalence of smoking. Eleven matched pairs of communities were randomly assigned to either a control or intervention group, with the intervention group exposed to a multicomponent intervention delivered through the media, by health care providers, at worksites and through cessation programs. A cohort of smokers followed over the trial showed a signifi cant increase in the cessation rate among light-moderate smokers in intervention communities compared with that in control communities (31% vs. 28%, p≤0.01) and a non-signifi cant decrease in the cessation rate in heavy smokers in the intervention communities compared with that in the control communities (18% vs. 19%).3 COMMIT demonstrated an overall drop in the prevalence of smoking of 3.5% in intervention communities and a 3.2% drop in control communities, a non-signifi cant difference. 4 In a randomised controlled trial of a community action intervention to address smoking behaviour in rural towns in New South Wales, adults in towns participating in the intervention showed mainly nonsignifi cant increases in quit rate and nonsignifi cant decreases in uptake rate compared with control towns.5 Signifi cantly more male smokers (7%) quit in towns participating in the intervention than in the control towns.

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Very little is known about lipid function during wound healing, and much less during impaired healing. Such understanding will help identify what roles lipid signaling plays in the development of impaired/chronic wounds. We took a lipidomics approach to study the alterations in lipid profile in the LIGHT−/− mouse model of impaired healing which has characteristics that resemble those of impaired/chronic wounds in humans, including high levels of oxidative stress, excess inflammation, increased extracellular matrix degradation and blood vessels with fibrin cuffs. The latter suggests excess coagulation and potentially increased platelet aggregation. We show here that in these impaired wounds there is an imbalance in the arachidonic acid (AA) derived eicosonoids that mediate or modulate inflammatory reactions and platelet aggregation. In the LIGHT−/− impaired wounds there is a significant increase in enzymatically derived breakdown products of AA. We found that early after injury there was a significant increase in the eicosanoids 11-, 12-, and 15-hydroxyeicosa-tetranoic acid, and the proinflammatory leukotrienes (LTD4 and LTE) and prostaglandins (PGE2 and PGF2α). Some of these eicosanoids also promote platelet aggregation. This led us to examine the levels of other eicosanoids known to be involved in the latter process. We found that thromboxane (TXA2/B2), and prostacyclins 6kPGF1α are elevated shortly after wounding and in some cases during healing. To determine whether they have an impact in platelet aggregation and hemostasis, we tested LIGHT−/− mouse wounds for these two parameters and found that, indeed, platelet aggregation and hemostasis are enhanced in these mice when compared with the control C57BL/6 mice. Understanding lipid signaling in impaired wounds can potentially lead to development of new therapeutics or in using existing nonsteroidal anti-inflammatory agents to help correct the course of healing.

Third hand smoke (THS) is the accumulation of second hand smoke (SHS) toxins on surfaces in homes, cars, clothing and hair of smokers. It is known that 88M US nonsmokers ≥3 years old living in homes of smokers are exposed to THS toxicants and show blood cotinine levels of ≥0.05 ng/ml, indicating that the toxins are circulating in their circulatory systems. The goal of the present study is to investigate the mechanisms by which THS causes impaired wound healing. We show that mice living under conditions that mimic THS exposure in humans display delayed wound closure, impaired collagen deposition, altered inflammatory response, decreased angiogenesis, microvessels with fibrin cuffs and a highly proteolytic wound environment. Moreover, THS-exposed mouse wounds have high levels of oxidative stress and significantly lower levels of antioxidant activity leading to molecular damage, including protein nitration, lipid peroxidation and DNA damage that contribute to tissue dysfunction. Furthermore, we show that elastase is elevated, suggesting that elastin is degraded and the plasticity of the wound tissue is decreased. Taken together, our results lead us to conclude that THS toxicants delay and impair wound healing by disrupting the sequential processes that lead to normal healing. In addition, the lack of elastin results in loss of wound plasticity, which may be responsible for reopening of wounds.

Recall of anti-tobacco television advertising was high in these remote Aboriginal communities; more Aboriginal people recalled exposure to anti-tobacco television advertising than to any other cessation intervention. Although the overall cessation rate was low, a small number of smokers had given up as a result of seeing these television advertisements.