Commentary on Sims et al. (2010): The decline in passive smoking


The decline in passive smoking is a public health success story. Since the US Surgeon General of the time, Jesse L. Steinfeld, declared in 1971 that ‘Nonsmokers have as much right to clean indoor air . . . as smokers have to their so-called right to smoke’, a great deal has been achieved. Improvements are most evident in the work-place, where many countries have comprehensive restrictions on smoking, with high levels of compliance and substantial reductions in the exposure of non-smokers to second-hand smoke (SHS) [1,2]. Among middle-aged non-smoking men who took part in the British Regional Heart Study, cotinine levels at 20-year follow-up were, on average, one-seventh of the levels recorded in 1978–80 [3].

Changes in homes are more difficult to track, but there have also been significant gains here. In this issue Sims et al.[4] report saliva cotinine levels from nationally representative samples of English children aged 4–15 years, who participated in surveys held between 1996 and 2006. There was a consistent and sizable decline—a 59% drop in the geometric mean cotinine. An earlier English study of secondary schoolchildren reported almost a 50% fall in salivary cotinine levels between 1988 and 1996 [5]. Similar findings come from the United States. Data from the National Health and Nutrition Examination Survey (NHANES) show that cotinine levels for children aged 4–11 dropped by almost 75% during the 1990s [6].

The reductions in exposure to SHS have not been distributed equally. In the United States, for example, cotinine levels of the most heavily exposed 5% of children changed little between 1988–91 and 2001–02 [6]. Sims et al., on the other hand, found a decline across the full range and the largest reductions in absolute terms were observed in children in high exposure groups (for example, children whose both parents smoked). It is encouraging that absolute inequalities in exposure to SHS have declined; but relative inequalities persist, and indeed may have increased. In 1996, the median cotinine level of children of parents with no educational qualification was about four times higher than the level of children whose parents had higher education (Sims et al., fig. 1). In 2006, the difference was approximately 10-fold.

What is responsible for the fall in childhood exposures to SHS? Reductions in smoking prevalence, falls in the amount of tobacco consumed, on average, by each smoker, and changes in where and when people smoke have all contributed. The proportion of families that make their homes smoke-free entirely, or in part, has increased in many countries, along with increasing awareness of the health risks associated with SHS and increasing restrictions on smoking in other settings. One study in the United States found that the proportion of homes that included children under 18, in which no one smoked on any days of the week, increased from 25% in 1992 to 35% in 2000 [7].

This trend has continued with the introduction of comprehensive smoke-free legislation covering bars, restaurants, sports stadia and other public places. Far from displacing smoking into the home, as many were concerned would happen, the legislation appears to have consolidated smoke-free behaviours [1]. In Scotland, cotinine levels among 11-year-olds were 40% lower, on average, a year after legislation than before, and parents reported more frequently that there were partial or complete restrictions at home [8]. How important was the legislation? It is perhaps too soon to tell: evaluations based on before and after measures may be foiled by long-term trends. However, we can draw comfort from the continuing improvements, and await more broadly based studies to distinguish the immediate effects of single point-in-time interventions such as the smoke-free legislation from long-term changes in behaviours and patterns of tobacco consumption.

A final point, on a less positive note, is that there is a dearth of information on the group of children who are most harmed by SHS: infants. The excess risk of nearly all respiratory outcomes is much greater in the first 1–2 years of life than subsequently, and children of this age are particularly prone to interruptions of normal growth and development [9,10], yet we know much less about exposures to SHS in early life. Sims et al. report a decline in cotinine of 3.2% per year from age 4 upwards, and one might infer that children under the age of 4, who are even smaller and less mobile, are likely to be more heavily exposed. However, I am not aware of a comparable time–series that displays biomarkers of exposure to SHS among infants.

Questionnaire-based studies on smoking during and after pregnancy shed some light on the potential, at least, for infant exposure to SHS, and it appears that exposures to SHS may have changed less than for older children. During the 1990s, annual surveys of pregnant women were undertaken in England, and the prevalence of antenatal smoking, which is correlated generally with smoking postnatally, altered little between 1992 and 1997 [11]. In the United States, the Pregnancy Risk Assessment Monitoring System (PRAMS) reports improvements, but they are minor only. In 16 study sites with full data over a 6-year period (2000–05), smoking during pregnancy reduced from 15.2% to 13.8%, and smoking 2–6 months after delivery declined from 18.1% to 16.4% [12].

Declaration of interest