Perinatal Exposure to Environmental Tobacco Smoke (ETS) Enhances Susceptibility to Viral and Secondary Bacterial Infections

Abstract

Studies suggest childhood exposure to environmental tobacco smoke (ETS) leads to increased incidence of infections of the lower respiratory tract. The objective of this study was to determine whether perinatal exposure to ETS increases the incidence, morbidity and severity of respiratory influenza infection and whether a secondary bacterial challenge at the peak of a pre-existing viral infection creates an enhanced host-pathogen susceptibility to an opportunistic infection. Timed-pregnant female Balb/c mice were exposed to either ETS for 6 h/day, 7 d/week beginning on gestation day 14 and continuing with the neonates to 6 weeks of age. Control animals were exposed to filtered air (FA). At the end of exposure, mice were intranasally inoculated with a murine-adapted influenza A. One week later, an intranasal inoculation of S. aureus bacteria was administered. The respective treatment groups were: bacteria only, virus only or virus+bacteria for both FA and ETS-exposed animals for a total of six treatment groups. Animal behavior and body weights were documented daily following infection. Mice were necropsied 1-day post-bacterial infection. Bronchoalveolar lavage fluid (BALF) cell analysis demonstrated perinatal exposure to ETS, compared to FA, leads to delayed but enhanced clinical symptoms and enhanced total cell influx into the lungs associated with viral infection followed by bacterial challenge. Viral infection significantly increases the number of neutrophils entering the lungs following bacterial challenge with either FA or ETS exposure, while the influx of lymphocytes and monocytes is significantly enhanced only by perinatal ETS exposure. There is a significant increase in peribronchiolar inflammation following viral infection in pups exposed to ETS compared with pups exposed to FA, but no change is noted in the degree of lung injury between FA and ETS-exposed animals following bacterial challenge. The data suggests perinatal exposure to ETS alters the response of neonates to the timing and severity of infection as well as ETS alters the pattern of inflammation and cellular influx into the lungs due to viral and bacterial infection.

Alterations in DNA methylation and airway hyperreactivity in response toin uteroexposure to environmental tobacco smoke

“…Actual exposure conditions to ETS during pregnancy can be highly variable – increasing the difficulty in extrapolating the effects observed in these mice following in utero ETS exposure to predictions related to children’s health and development. However, several animal studies observed immune responses similar to ours (Avdalovic et al, 2009; Claude et al, 2012). Claude et al (2012) used the same concentration of perinatal exposure to ETS and showed alterations in the pattern of inflammation in mice.…”

“…However, several animal studies observed immune responses similar to ours (Avdalovic et al, 2009; Claude et al, 2012). Claude et al (2012) used the same concentration of perinatal exposure to ETS and showed alterations in the pattern of inflammation in mice. The same amount of ETS exposure during a postnatal period is also associated with altered lung development in infant monkeys (Avdalovic et al, 2009).…”

Modulation of neutrophil NETosis: interplay between infectious agents and underlying host physiology

“…While it is well appreciated that prenatal exposure to maternal smoking or airborne particulate matter is associated with higher rates of pediatric asthma [112], new data indicate that these events may debilitate the neonatal immune response [113], rendering the developing child more susceptible to infections [114]. …”

Exposure to traffic and early life respiratory infection: A cohort study

“…Post‐natal diesel exposure has been found to attenuate the lung's immune response to viral respiratory infection and to augment the inflammatory response, which likely result in a worse course of illness . Perinatal tobacco exposure has also been found to alter the inflammatory response to pulmonary infection …”