Cigarette smoking as a risk factor for tuberculosis in young adults: A casecontrol study

Alcaide, J.; Altet, M.N.; Plans, Pere; Parrón, I.; Folguera, Ll.; Saltó, Esteve; Domínguez, A; Pardell, Hèlios; Salleras, L.

doi:10.1016/s0962-8479(96)90024-6

Cited by 102 publications

(88 citation statements)

References 10 publications

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“…Studies have also reported that tobacco smoking is a risk factor for pulmonary tuberculosis as seen in the present case, with a dose-response relationship with the number of cigarettes consumed daily 43,44 . This could be attributed to nicotine that turns off the production of Tumor necrosis factor-α by the macrophages in the lungs, making the patient more susceptible to the tuberculosis infection.…”

Section: Chromosomal Aberrationssupporting

confidence: 73%

An overview of the risk factors associated with multiple oral premalignant lesions with a case report of extensive field cancerization in a female patient

Sreedhar¹,

Sumalatha²,

Shukla³

2015

BIOMED PAP

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Background. Field cancerization is a well-known and well-documented process of malignant transformation first coined by Slaughter et al. in 1953. Tobacco chewing was associated with the greatest increase in the risk of multiple oral premalignant lesions and may be the major source of field cancerization of the oral cavity in the Indian population. The field cancerization will probably help clinicians in complementing evaluation of pathologic biopsy specimens. Material and Methods. We present a case report of field cancerization in a 63-year-old Indian female. She presented with an intra-oral generalized hyperkeratotic verruciform type white lesions involving right and left buccal mucosa, lower labial mucosa, upper and lower vestibule, dorsal, ventral and right lateral border of the tongue, hard and soft palate. Microscopic examination revealed features of verrucous carcinoma in one area, squamous cell carcinoma in another and carcinoma in situ in other areas. Based on the overall features in various areas of the oral cavity, the lesion was diagnosed as field cancerization. Conclusion. Reviewing the literature revealed the presence of a field with genetically altered cells appear to be induced by tobacco (smoking/smokeless form). The large number of premalignant cells in the fields may increase cancer risk considerably. Thus screening and monitoring of the field may have serious implications for oral cancer prevention.

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Section: Chromosomal Aberrationssupporting

confidence: 73%

An overview of the risk factors associated with multiple oral premalignant lesions with a case report of extensive field cancerization in a female patient

Sreedhar¹,

Sumalatha²,

Shukla³

2015

BIOMED PAP

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“…The acrolein concentrations used in this study (low micromolar range) may be reached in lung tissue after smoking several cigarettes. This finding may thus provide an explanation for the epidemiological observations that smoking or exposure to tobacco smoke increases the incidence of viral, bacterial, and mycobacterial diseases of the lung [138][139][140][141]. Similarly, cooking in poorly ventilated kitchens has been associated with respiratory illnesses, weakening of the immune system, and lung cancer in rural China [142].…”

Section: Discussionmentioning

confidence: 73%

Acrolein: Sources, metabolism, and biomolecular interactions relevant to human health and disease

Stevens

Maier

2008

Molecular Nutrition Food Res

618

634

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Acrolein (2-propenal) is ubiquitously present in (cooked) foods and in the environment. It is formed from carbohydrates, vegetable oils and animal fats, amino acids during heating of foods, and by combustion of petroleum fuels and biodiesel. Chemical reactions responsible for release of acrolein include heat-induced dehydration of glycerol, retro-aldol cleavage of dehydrated carbohydrates, lipid peroxidation of polyunsaturated fatty acids, and Strecker degradation of methionine and threonine. Smoking of tobacco products equals or exceeds the total human exposure to acrolein from all other sources. The main endogenous sources of acrolein are myeloperoxidase-mediated degradation of threonine and amine oxidase-mediated degradation of spermine and spermidine, which may constitute a significant source of acrolein in situations of oxidative stress and inflammation. Acrolein is metabolized by conjugation with glutathione and excreted in the urine as mercapturic acid metabolites. Acrolein forms Michael adducts with ascorbic acid in vitro, but the biological relevance of this reaction is not clear. The biological effects of acrolein are a consequence of its reactivity towards biological nucleophiles such as guanine in DNA and cysteine, lysine, histidine, and arginine residues in critical regions of nuclear factors, proteases, and other proteins. Acrolein adduction disrupts the function of these biomacromolecules which may result in mutations, altered gene transcription, and modulation of apoptosis.

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“…Smoking is known to increase the risk of tuberculosis approximately three-fold [12]. There was no difference in the frequency or intensity of alcohol consumption 2 yrs before tuberculosis was diagnosed.…”

Section: Discussionmentioning

confidence: 88%

“…Within the developed world, the recent increase has principally been associated with immigration from developing countries [5][6][7], increasing poverty [8][9][10], unemployment [10], overcrowding [11], smoking [12], homelessness [13,14], an ageing indigenous population [15,16] and, particularly within the USA, HIV infection [17,18]. However, other studies, by analysing several geographical measures together, have shown that rates of disease across urban areas of England were geographically more closely associated with the proportion of the population that were of non-White ethnic origin than with economic deprivation indices [19].…”

mentioning

confidence: 99%

A case-control study of lifestyle risk factors associated with tuberculosis in Liverpool, North-West England

Tocque

Bellis²,

Beeching³

et al. 2001

European Respiratory Journal

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A retrospective case-control study (with matching by sex, age, postcode and ethnicity) of all tuberculosis cases notified over a 7-yr period in Liverpool, UK, was carried out.Multiple logistic regression showed that, before diagnosis, cases were 7.4 times more likely to have had visitors from abroad; 4.0 times more likely to have been born abroad; and 3.8 times more likely to have lived with someone with tuberculosis. Subtle socioeconomic factors were also evident with cases 4.0 times less likely to have additional bathrooms. Lifestyle factors emerged with cases 2.3 times more likely to have smoked for at least 30 yrs, 3.8 times less likely to eat dairy products every week and 2.6 times less likely to have had high blood pressure. At interview, these factors were still evident, but cases, unlike controls, had reduced their smoking and alcohol consumption and were less likely to go out of the home or exercise than before their illness.Within individuals, lifestyle consequences of tuberculosis lead to a "healthier" lifestyle on the one hand (less smoking and alcohol consumption), but a reduced quality of life (social activity) on the other. Eur Respir J 2001; 18: 959-964.

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Cigarette smoking as a risk factor for tuberculosis in young adults: A casecontrol study

Cited by 102 publications

References 10 publications

An overview of the risk factors associated with multiple oral premalignant lesions with a case report of extensive field cancerization in a female patient

An overview of the risk factors associated with multiple oral premalignant lesions with a case report of extensive field cancerization in a female patient

Acrolein: Sources, metabolism, and biomolecular interactions relevant to human health and disease

A case-control study of lifestyle risk factors associated with tuberculosis in Liverpool, North-West England

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