Effect of passive smoking on frequency of respiratory illnesses and serum immunoglobulin-E (IgE) and interleukin-4 (IL-4) concentrations in exposed children

Abstract

We studied the relationship of serum immunoglobulin-E (Ig-E) and interleukin-4 (IL-4) concentrations, eosinophil counts, and frequency of respiratory illness with passive smoking in 70 randomly selected children of smoking parents. Fifty randomly selected age-matched children of non-smoking parents served as controls. Children of smoking parents had higher frequency of respiratory illnesses per year (P < 0.01), significantly higher total leucocytic and eosinophil counts, higher percentage of eosinophils (P < 0.01), and higher serum IgE and IL-4 concentrations (P < 0.05) compared to the control group. Serum IgE level was correlated positively with the average number of smoked cigarettes/day, number of siblings, and total leucocytic count. Interleukin-4 concentrations were significantly correlated with the number of smoked cigarettes and IgE levels. Although IgE levels were higher in children of smoking parents (587 +/- 359 IU/ml) compared to controls (189 +/- 21 IU/ml), they did not differ significantly between children with and those without frequent respiratory illness (605 +/- 365 and 557 +/- 354 IU/ml, respectively). Interleukin-4 concentrations were significantly higher in children of smoking parents with frequent respiratory illness (1.8 +/- 0.5 pg/ml) v. those without frequent respiratory illness (1.3 +/- 0.45 pg/ml). Multiple logistic regression analysis revealed that the overall positivity of the risk factors predisposing to respiratory diseases in the study children was 79 percent, and the highest odds ratio was that for IL-4 (OR = 5.15). In conclusion, there is a significant increase in IL-4 and Ig-E concentrations, high eosinophil count and frequent respiratory symptoms in children of smoking parents. It remains that the current state of knowledge on health risks associated with passive smoking warrants that strong preventive action be promoted.

Second‐Hand Smoke Increases Bronchial Hyperreactivity and Eosinophilia in a Murine Model of Allergic Aspergillosis

“…The immunomodulatory effect of tobacco smoke and its components have been well documented (Thomas et al, 1975;Ronchetti et al, 1990;Stone, 1992;Sopori et al, 1993;Abrams, 1995;Geng et al, 1995;El-Nawawy et al, 1996;Geng et al, 1996;Oryszczyn et al, 2000;Gilliland et al, 2001). In our previous studies we showed that prolonged exposure of OVA sensitized mice to ETS resulted in enhanced levels of serum IgE, IgG1, and blood eosinophils .…”

“…Epidemiological studies have concluded that exposure to ETS is responsible for some forms of cancer, respiratory disease and may also exacerbate the allergic response (Martinez et al, 1988;Stone, 1992;El-Nawawy et al, 1996;Gilliland et al, 2001). Studies on human subjects are rarely able to focus on ETS alone due to concurrent exposure to other environmental pollutants (such as ozone, diesel exhaust) which may also modulate the immune response.…”

Environmental tobacco smoke exposure and risk of allergic sensitisation in children: a systematic review and meta-analysis

“…Altogether there were 11 cross-sectional studies, 5 7 19–30 4 prospective cohort studies4 6 31–34 and 4 case-control studies. 10 35–37 The studies were conducted in various regions of the world. The included subjects were aged 0–17 years.…”

“…The limited existing data on passive smoking and its direct effects on immune responses and respiratory health in children seem to confirm these observations 10–12. Therefore, our aim was to systematically review and update data from cross-sectional and cohort studies regarding the effect of ETS on serum total immunoglobulin E (tIgE) and specific IgE (sIgE) and skin-prick tests (SPTs), since they are easily assessable and objective markers of allergic sensitisation in children 13…”

Gender Differences in the Allergic Response of Mice Neonatally Exposed to Environmental Tobacco Smoke

“…In contrast, the role of gender as a factor in the development of allergic asthma and particularly in allergic enhancement by environmental tobacco smoke (ETS) exposure has not been well examined. Although, a genetic predisposition to the development of allergic asthma is recognized (Daniels et al, 1996;Gern et al, 1999) evidence strongly suggests that environmental agents such as ETS increase its phenotypic expression (el-Nawawy et al, 1996;Gilliland et al, 2001). Some studies have shown that males are more likely to be allergic from exposure to ETS or mainstream smoke than females (Ronchetti et al, 1992;Omenaas et al, 1994;Jarvis et al, 1995), while others have reported no sex differences in the prevalence of allergy (Osaka et al, 1985).…”