Genotoxicity of environmental tobacco smoke: a review

Husgafvel‐Pursiainen, Kirsti

doi:10.1016/j.mrrev.2004.06.004

Cited by 161 publications

(109 citation statements)

References 123 publications

Supporting

Mentioning

104

Contrasting

Unclassified

Order By: Relevance

“…These results appear to contrast with previous reports of significant increases in MN-RETs after exposure to STS (reviewed in ref. 7). However, we are aware of only one previous study that investigated the induction of MN in the bone marrow of mice exposed to STS in inhalation chambers (25).…”

Section: Resultsmentioning

confidence: 99%

“…Much less is known about the health effects of second-hand (or passive) smoking, although evidence is rapidly accumulating that exposure to second-hand smoke can be as harmful and hazardous to human health as active smoking (6,7), and that there may be no risk-free level of exposure (8). Sidestream tobacco smoke (STS), the main component of secondhand smoke, is a complex mixture of more than 4,000 chemicals, including at least 50 known carcinogens (8).…”

mentioning

confidence: 99%

See 1 more Smart Citation

Sidestream tobacco smoke is a male germ cell mutagen

Marchetti

Rowan-Carroll

Williams

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

Active cigarette smoking increases oxidative damage, DNA adducts, DNA strand breaks, chromosomal aberrations, and heritable mutations in sperm. However, little is known regarding the effects of second-hand smoke on the male germ line. We show here that short-term exposure to mainstream tobacco smoke or sidestream tobacco smoke (STS), the main component of secondhand smoke, induces mutations at an expanded simple tandem repeat locus (Ms6-hm) in mouse sperm. We further show that the response to STS is not linear and that, for both mainstream tobacco smoke and STS, doses that induced significant increases in expanded simple tandem repeat mutations in sperm did not increase the frequencies of micronucleated reticulocytes and erythrocytes in the bone marrow and blood of exposed mice. These data show that passive exposure to cigarette smoke can cause tandem repeat mutations in sperm under conditions that may not induce genetic damage in somatic cells. Although the relationship between noncoding tandem repeat instability and mutations in functional regions of the genome is unclear, our data suggest that paternal exposure to second-hand smoke may have reproductive consequences that go beyond the passive smoker.DNA mutation | micronuclei | germline | spermatogenesis D espite years of intense public campaigns to limit and reduce tobacco consumption, smoking is still widespread, and its health effects remain a significant public concern. Approximately 35% of men of reproductive age in the United States smoke cigarettes (1), and there is extensive evidence to suggest that tobacco smoking can result in abnormal reproductive outcomes such as spontaneous abortions and birth defects (2). Men who smoke are at high risk for several semen abnormalities, including reduced motility, sperm DNA damage such as DNA breaks and adducts, and chromosomal abnormalities (3). In mice, exposure to mainstream tobacco smoke (MTS) induces germ-line mutations in expanded simple tandem repeats (ESTR) that can be transmitted to the progeny, causing irreversible modifications in the genome of the offspring (4). Recently, the International Agency for Research on Cancer concluded that there is enough evidence to link paternal smoking in humans with increased risk of childhood cancer, suggesting that tobacco smoking causes heritable germ cell mutation in humans (5).Exposure to second-hand smoke also remains widespread, with an estimated 40% of nonsmokers being exposed to secondhand smoke (6). Much less is known about the health effects of second-hand (or passive) smoking, although evidence is rapidly accumulating that exposure to second-hand smoke can be as harmful and hazardous to human health as active smoking (6, 7), and that there may be no risk-free level of exposure (8). Sidestream tobacco smoke (STS), the main component of secondhand smoke, is a complex mixture of more than 4,000 chemicals, including at least 50 known carcinogens (8). Qualitative differences between MTS-the smoke inhaled by active smokers-and STS are small; however, some toxicants...

show abstract

Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

Sidestream tobacco smoke is a male germ cell mutagen

Marchetti

Rowan-Carroll

Williams

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

show abstract

“…Milk of smoking mothers contains high levels of nicotine, and urinary cotinine levels in infants may equal those of adult smokers. 29,30 Undoubtedly, many tobacco-derived carcinogens are able to pass to the fetus during pregnancy and to a nursing infant, 31 who has to excrete them through the kidney and the bladder; these rapidly growing organs may be particularly vulnerable.…”

Section: Discussionmentioning

confidence: 99%

“…12 Follow-up was started for each offspring at birth, immigration or January 1, 1958, whichever came latest. Follow-up was terminated on diagnosis of first cancer, death, emigration or the closing date of the study, December 31,2002. In alternative analyses, the follow-up was started on January 1, 1990.…”

Section: Methodsmentioning

confidence: 99%

Parental lung cancer as predictor of cancer risks in offspring: Clues about multiple routes of harmful influence?

Hemminki

Chen

2005

Intl Journal of Cancer

View full text Add to dashboard Cite

The carcinogenic effects of active smoking have been demonstrated for many sites, but the effects of passive smoking and exposures during pregnancy and breastfeeding are less well documented. We examined whether 0–70‐year‐old offspring of parents with lung cancer are at a risk of cancer that cannot be explained by their smoking or familial risk. It was assumed that known target sites for tobacco carcinogenesis would be affected, if any. The nationwide Swedish Family‐Cancer Database with cancers recorded from 1958 to 2002 was used to calculate age‐specific standardized incidence ratios (SIRs). Among offspring of affected mothers, increased risks were observed for upper aerodigestive (SIR 1.45), nasal (2.93), lung (1.71) and bladder (1.52) cancers and for kidney cancer (6.41) in one age group. The risk of bladder cancer was found in younger age groups than that of lung cancer. Cancers at many of these sites, but not the kidney or the bladder, were in excess in offspring of affected fathers. Nasal cancer was even increased when either parent was diagnosed with lung cancer; the highest risk was for nasal adenoid cystic carcinoma (7.73). The data suggest that passive smoking during childhood is associated with an increase risk of nasal cancer. For bladder and kidney cancers, a contribution by tobacco carcinogens is implicated through breastfeeding and in utero exposure. © 2005 Wiley‐Liss, Inc.

show abstract

“…The concentrations of benzol(a)pyrene, toluene, dimethylnitrosamines in SHS is much higher than in MSS, and the smaller particles in SHS are more likely to be deposited in the lung. SHS may induce DNA adducts, sister chromosome exchange (44), oxidative DNA damage (45,46), and increased number of p53 mutations in lung cancer (47,48), suggesting a similar etiologic mechanism for cases exposed to SHS and to MSS. SHS exposure may occur at home (including childhood exposure from parents/other family members and exposure from spouse/family members in adulthood), at work (occupational exposure), and at leisure (exposure at public places other than work).…”

Section: Introductionmentioning

confidence: 99%

Second hand smoke, age of exposure and lung cancer risk

Asomaning¹,

Miller²,

Liu³

et al. 2008

Lung Cancer

View full text Add to dashboard Cite

Background-Exposure to second hand smoke (SHS) has been identified as a risk factor for lung cancer for three decades. It is also known that the lung continues to grow from birth to adulthood, when lung growth stops. We hypothesize that after adjusting for active cigarette smoking, if SHS exposure took place during the period of growth i.e. in the earlier part of life (0 to 25 years of age) the risk of lung cancer is greater compared to an exposure occurring after age 25.

show abstract

Genotoxicity of environmental tobacco smoke: a review

Cited by 161 publications

References 123 publications

Sidestream tobacco smoke is a male germ cell mutagen

Sidestream tobacco smoke is a male germ cell mutagen

Parental lung cancer as predictor of cancer risks in offspring: Clues about multiple routes of harmful influence?

Second hand smoke, age of exposure and lung cancer risk

Contact Info

Product

Resources

About