Child Exposure to environmental tobacco smoke

http://www.bmj.com/cgi/content/short/335/7619/545
BMJ 2007;335:545 (15 September), doi:10.1136/bmj.39311.550197.AE (published 9 September 2007)
Research
Changes in child exposure to environmental tobacco smoke (CHETS) study after implementation of smoke-free legislation in Scotland: national cross sectional survey
Patricia C Akhtar, research fellow1, Dorothy B Currie, senior statistician1, Candace E Currie, director1, Sally J Haw, principal public health adviser2
1 Child and Adolescent Health Research Unit (CAHRU), University of Edinburgh, Edinburgh EH8 8AQ, 2 NHS Health Scotland, Edinburgh EH12 5EZ
Correspondence to: P C Akhtar patricia.akhtar@ed.ac.uk

Objective To detect any change in exposure to secondhand smoke among primary schoolchildren after implementation of smoke-free legislation in Scotland in March 2006.
Design Comparison of nationally representative, cross sectional, class based surveys carried out in the same schools before and after legislation.
Setting Scotland.
Participants 2559 primary schoolchildren (primary 7; mean age 11.4 years) surveyed in January 2006 (before smoke-free legislation) and 2424 in January 2007 (after legislation).
Outcome measures Salivary cotinine concentrations, reports of parental smoking, and exposure to tobacco smoke in public and private places before and after legislation.
Results The geometric mean salivary cotinine concentration in non-smoking children fell from 0.36 (95% confidence interval 0.32 to 0.40) ng/ml to 0.22 (0.19 to 0.25) ng/ml after the introduction of smoke-free legislation in Scotland—a 39% reduction. The extent of the fall in cotinine concentration varied according to the number of parent figures in the home who smoked but was statistically significant only among pupils living in households in which neither parent figure smoked (51% fall, from 0.14 (0.13 to 0.16) ng/ml to 0.07 (0.06 to 0.08) ng/ml) and among pupils living in households in which only the father figure smoked (44% fall, from 0.57 (0.47 to 0.70) ng/ml to 0.32 (0.25 to 0.42) ng/ml). Little change occurred in reported exposure to secondhand smoke in pupils' own homes or in cars, but a small decrease in exposure in other people's homes was reported. Pupils reported lower exposure in cafes and restaurants and in public transport after legislation.
Conclusions The Scottish smoke-free legislation has reduced exposure to secondhand smoke among young people in Scotland, particularly among groups with lower exposure in the home. We found no evidence of increased secondhand smoke exposure in young people associated with displacement of parental smoking into the home. The Scottish smoke-free legislation has thus had a positive short term impact on young people's health, but further efforts are needed to promote both smoke-free homes and smoking cessation.

Some Gene damage: Permanent

Some gene damage from smoking is permanent: study

Aug. 30, 2007
Courtesy BioMed Central
and World Science staff

A new study may help ex­plain why form­er smok­ers are still more prone to lung can­cer than those who have nev­er smoked. It found that smok­ing causes some per­ma­nent ge­ne­tic da­mage.

Quit­ting still of­fers huge health ben­e­fits, re­search­ers stressed, as the risk to form­er smok­ers is much low­er than for cur­rent smok­ers.

A team led by Wan Lam and Ste­phen Lam from the BC Can­cer Agen­cy in Van­cou­ver, Can­a­da, took sam­ples from the lungs of 24 cur­rent and form­er smok­ers, as well as from peo­ple who have nev­er smoked.

They used the sam­ples to cre­ate li­brar­ies us­ing a tech­nique called se­ri­al anal­y­sis of gene ex­pres­sion, which helps to iden­ti­fy pat­terns of gene ac­ti­vity.

Only about a fifth of the genes in a cell are switched on at any giv­en time, but smok­ing leads to changes in gene ac­ti­vity. The re­search­ers found that some of these changes, though not all, per­sisted even years af­ter quit­ting smok­ing.

The re­vers­i­ble genes were par­tic­u­larly in­volved in “xeno­bi­otic” func­tion­s—ma­nag­ing chem­i­cals not pro­duced in the body—and me­tab­o­lism of ge­net­ic ma­te­ri­al and mu­cus se­cre­tion, sci­en­tists found. The irre­vers­i­ble dam­age was to some DNA re­pair genes, and to the ac­ti­vity of genes that help fight lung can­cer de­vel­op­ment.

“Those genes and func­tions which do not re­vert to nor­mal lev­els up­on smok­ing cessa­t­ion may pro­vide in­sight in­to why form­er smok­ers still main­tain a risk of de­vel­op­ing lung can­cer,” said Raj Cha­ri, first au­thor of the stu­dy. To­bac­co smok­ing ac­counts for 85 per­cent of lung can­cers, and form­er smok­ers ac­count for half of those newly di­ag­nosed with the dis­ease.

The gene find­ings are pub­lished in the Aug. 29 is­sue of the on­line re­search jour­nal BMC Ge­nomics.