The health effects of passive smoking

Oulun Yliopiston Ympäristöterveyden ja Keuhkosairauksien Tutkimuskeskus ja Oulun Yliopiston Kliinien Lääketeiteen Laitoksen Keuhkosairauksien Yksikkö ja OYS:n Medisiinisen Tulosalueen Keuhkosairauksien Yksikkö.
Duodecim; lääketieteellinen aikakauskirja 06/2012; 128(10):1097-106.
Source: PubMed


Passive smoking leads to exposure to carcinogenic, teratogenic, irritant and toxic substances of tobacco smoke as a consequence of other people's smoking. There is strong evidence that passive smoking causes several diseases of major public health importance as well as leads to exacerbations of many diseases. Among children passive smoking increases the risk of middle ear infections, lower respiratory infections, asthma and sudden infant death syndrome, and among adults asthma, COPD, lung cancer and cardiovascular diseases. Passive smoking by pregnant mothers leads to impaired fetal growth and may lead to organ system developmental disturbances. Asking about passive smoking and giving professional advice about stopping such exposure should be part of evidence-based medicine for these diseases. Health care workers have a central role in the prevention of passive smoking in clinical practice and health education.

Download full-text


Available from: Jouni J.K. Jaakkola,
  • [Show abstract] [Hide abstract]
    ABSTRACT: Cigarette smoke exposure is associated with increased risk of different disorders. Immunological dysfunction especially in macrophages is one of important reasons in the initiation, progression and exacerbation of smoke-related pulmonary illnesses. However, it is still obscure how cigarette smoke impacts the vitality and functions of macrophages. In the present study, we examined the effects of cigarette smoke extract (CSE) on mouse Ana-1 macrophages and tried to elucidate the involved mechanism. The results showed CSE induced cell apoptosis accompanied by increased releasing of lactate dehydrogenase (LDH), mitochondrial injury and oxidative stress. It also inhibited anti-apoptosis protein Bcl-2 expression and promoted pro-apoptosis protein Bax and Bad expressions. Moreover, low-dose CSE increased nuclear NF-κB levels of macrophages; on the contrary, high-dose CSE or long-time treatment decreased it. These observations were in correspondence with changes of intracellular ROS level and antioxidant enzymes' activity. Furthermore, pretreatment with 10μM of NF-κB inhibitor pyrrolidine dithiocarbamate (PDTC) for 1h significantly enhanced macrophage apoptosis. Taken together, these data implied that mitochondrial dysfunction and oxidative stress played important roles in the injury of Ana-1 cells caused by CSE, which was related to NF-κB pathway; an anti-apoptotic program played a dominant role at low doses/short-term exposure to CSE, whereas a pro-apoptotic program was initiated at high doses/long-term exposure.
    Experimental and toxicologic pathology: official journal of the Gesellschaft fur Toxikologische Pathologie 03/2013; 65(7-8). DOI:10.1016/j.etp.2013.02.004 · 1.86 Impact Factor