Annoyance and irritation by passive smoking

doi:10.1016/S0091-7435(84)80012-2

Preventive Medicine

Volume 13, Issue 6, November 1984, Pages 618-625

https://doi.org/10.1016/S0091-7435(84)80012-2 Get rights and content

The acute irritating and annoying effects of smoke have been investigated in field and laboratory studies by examining the concentration of some smoke components in air. In the workplace, 30 to 70% of the indoor carbon monoxide, nitrogen oxide, and particulate concentrations are due to tobacco smoke; 25–40% of the employees are disturbed and/or annoyed by smoke and 25% suffer from eye irritation at work. Subjective eye, nose, and throat irritations and eye blink rate increase with increasing smoke concentration and increasing exposure duration. Irritation is due mainly to the particulate phase of environmental tobacco smoke, whereas the gas phase is, to a large extent, responsible for annoyance. It is concluded that healthy individuals can tolerate an environmental tobacco smoke level that corresponds to a carbon monoxide concentration of 1.5 to 2.0 ppm. Above these limits, countermeasures to protect passive smokers are necessary. In order not to exceed the upper tolerable threshold limit of 2.0 ppm carbon monoxide, it is necesary to have a fresh air supply of 33 m³ per hour per cigarette smoked. Special attention should be paid to groups of people with increased sensitivity to environmental tobacco smoke, e.g., asthmatics, allergic individuals, chronic bronchitis sufferers, and children.

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Cited by (39)

Ocular conditions and dry eye due to traditional and new forms of smoking: A review
2020, Contact Lens and Anterior Eye
Citation Excerpt :
One Japanese study reported that 25–40 % of employees encountered tobacco smoke in their work environment, while 25 % of this group suffered from dry eye disease [9]. Weber, who first reported these percentages in 1984, adds that there is a positive correlation between the concentration and exposure duration to smoke and eye/nose/throat irritation and eye blink rate [74] Environmental exposure to smoke has also been linked further to dry eye symptoms [9,75] as has passive smoking [76,77], even in children [78].
Addiction to cigarette smoking has high prevalence rates recorded worldwide. Smoking has been linked to several life-threatening systemic conditions such as cancer, heart attack and stroke, in addition to a range of ocular pathologies. In recent years, electronic cigarettes (EC) have emerged as alternatives to smoking. ECs are nicotine delivery devices which produce an aerosol by heating, rather than combusting, a liquid which contains nicotine, flavours and preservatives. This review focuses on the association of traditional and new forms of smoking with dry eye disease, contact lens wear and four other common ocular diseases: cataract, age-related macular degeneration, glaucoma and Graves’ ophthalmopathy. It is concluded that smoking and vaping appear as a risk factor for the aforementioned ocular conditions. An evidence-based, clear link between cigarette smoking, or EC vaping and ocular problems is yet to be discovered.
TRPA1: Acrolein meets its target
2017, Toxicology and Applied Pharmacology
The effect of Nrf2 knockout on ocular surface protection from acute tobacco smoke exposure: Evidence from Nrf2 knockout mice
2015, American Journal of Pathology
Ocular surface mucosa is the first-line ocular tissue to be exposed to environmental stress. We evaluated tear functions and keratoconjunctival epithelial alterations after sidestream cigarette smoke (SCS) exposure and tried to clarify the role of the transcription factor nuclear factor erythroid 2–related factor 2 (Nfe2l2, also known as Nrf2), on the ocular surface. In wild-type and Nrf2^−/− mice, tear volume did not change after SCS exposure. Tear film breakup time (tear stability) in Nrf2^−/− mice was significantly shorter than that in wild-type mice after SCS exposure. Vital staining scores, including fluorescein and Rose Bengal staining, showed significantly higher values in Nrf2^−/− mice than in wild-type mice after SCS exposure. Excessive oxidative stress accumulation was detected in Nrf2^−/− mice after SCS exposure using immunohistochemical analysis. Immunohistochemical analysis also revealed decreased mucin 1 (Muc1) and Muc5ac staining in Nrf2^−/− mice after SCS exposure. mRNA expression levels of Muc1, Muc4, and Muc5ac and of SAM-pointed domain epithelial-specific transcription factor in Nrf2^−/− mice were lower than those in wild-type mice after SCS exposure. Mean tear IL-6 concentrations increased significantly in Nrf2^−/− mice after SCS exposure. In conclusion, SCS exposure induced decreased tear stability, ocular surface damage, and altered conjunctival phenotype in Nrf2^−/− mice. Nrf2 could play an important role in protection of the ocular surface against SCS exposure.
Tear cytokine and ocular surface alterations following brief passive cigarette smoke exposure
2008, Cytokine
Purpose: To prospectively investigate the effects of acute passive cigarette smoke exposure on the ocular surface and tear film in healthy non-smokers. Methods: Twelve right eyes of 12 subjects without any ocular diseases were examined before, 5 min, and 24 h after 5 min of passive cigarette smoke exposure in a controlled smoke chamber. Tear samples were obtained before, 5 min and 24 h after smoke exposure to detect tear hexanoyl-lysine (HEL), acrolein and inflammatory cytokine concentrations. Tear evaporation rate, DR-1 tear film lipid layer interferometry, tear film break-up time (TBUT), ocular surface fluorescein staining (FS) and Rose Bengal staining (RB), Schirmer I test were performed before, 5 min, and 24 h after smoke exposure. Conjunctival impression cytology (IC) and brush cytology (BC) were carried out before and 24 h after smoke exposure. Results: Tear evaporation rate, tear lipid spread time, tear film break-up time, and vital staining scores showed significant worsening with passive smoke exposure. Tear HEL and IL-6 concentrations increased significantly 24 h after smoke exposure. Tear acrolein level showed an insignificant increase at 5 min. IC and RT-PCR revealed a significant reduction in goblet cell density, a shift toward higher squamous metaplasia grades and a significant downregulation of MUC5AC mRNA expression at 24 h. Conclusion: Even brief passive exposure to cigarette smoke in healthy non-smoker subjects was associated with adverse effects on the ocular surface health as evidenced by an increase of tear inflammatory cytokines, tear lipid peroxidation products and decrease of mucosal defense resulting in tear instability and damage to the ocular surface epithelia.
Smoking Associated With Damage to the Lipid Layer of the Ocular Surface
2006, American Journal of Ophthalmology
Citation Excerpt :
Because free radical–mediated lipid peroxidation has been associated with the pathogenesis of some diseases like atherosclerosis, placental defense, and age-related macular degeneration, several studies have been performed concerning the relation between smoking and development of these diseases. Demographic surveys have shown that 25% to 40% of employees experience cigarette smoke in their direct environment, and that 25% of them have dry eye–related ocular symptoms.22 The ocular surface is the most environmentally exposed mucosal surface of the body.
To evaluate the effects of smoking on ocular surface.
Prospective, comparative, interventional case series.
setting: Institutional. study population: Sixty smokers (33 men, 27 women) and 34 healthy subjects (18 men, 16 women) were enrolled into this study. Patients with associated ophthalmic or systemic diseases, and history of contact lens use and ocular surgery were excluded. The duration of average smoking was 13.1 years (range 5 to 35 years). intervention:Ocular surface was evaluated by measuring corneal and conjunctival sensitivity, surface staining with fluorescein, tear film breakup time, Schirmer 1 test, and conjunctival impression cytology. Dry eye symptoms were scored by questionnaire. Kinetic analysis of sequential tear interference images obtained by a DR-1 tear lipid layer interferometry was used to investigate the precorneal lipid layer spread. Results were compared with a control group. main outcome measures: Comparison of subjective complaints with objective parameters in cigarette smokers and normal subjects.
In the smoker group, the mean Schirmer 1 test value was 10.8 mm (range 8 to 14 mm). The mean breakup time was 5.3 seconds (range 1 to 10 seconds), the average conjunctival sensitivity was 26.2 mm (range 0 to 45 mm), and the average central corneal sensitivity was 37.6 mm (range 5 to 60 mm). There was no statistically significant difference in goblet cell densities or in Schirmer 1 test values between smokers and controls (P > .05). Higher grades of lipid layer changes were observed in smokers by DR-1 interferometry kinetic analysis.
Smoking has deteriorating effects on the lipid layer of precorneal tear film.
The association betwen cigarette smoking and ocular diseases
1998, Survey of Ophthalmology
Tobacco smoke is composed of as many as 4,000 active compounds, most of them toxic on either acute or long-term exposure. Many of them are also poisonous to ocular tissues, affecting the eye mainly through ischemic or oxidative mechanisms. The list of ophthalmologic disorders associated with cigarette smoking continues to grow. Most chronic ocular diseases, with the possible exception of diabetic retinopathy and primary open-angle glaucoma, appear to be associated with smoking. Both cataract development and age-related macular degeneration, the leading causes of severe visual impairment and blindness, are directly accelerated by smoking. Other common ocular disorders, such as retinal ischemia, anterior ischemic optic neuropathy, and Graves ophthalmopathy, are also significantly linked to this harmful habit. Tobacco smoking is the direct cause of tobacco-alcohol amblyopia, a once common but now rare disease characterized by severe visual loss, which is probably a result of toxic optic nerve damage. Cigarette smoking is highly irritating to the conjunctival mucosa, also affecting the eyes of nonsmokers by passive exposure (secondhand smoking). The dangerous effects of smoking are transmitted through the placenta, and offspring of smoking mothers are prone to develop strabismus. Efforts should be directed toward augmenting the campaign against tobacco smoking by adding the increased risk of blindness to the better-known arguments against smoking. We should urge our patients to quit smoking, and we must make them keenly aware of the afflictions that can develop when smoke gets in our eyes. (Surv Ophthalmol 42:535–547, 1998.

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¹: Presented at the Symposium “Medical Perspectives on Passive Smoking,” April 9–12, 1984, Vienna, Austria.

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Annoyance and irritation by passive smoking1

Chest

Environ. Int.

Environ. Res.

Environ. Res.

Passive smoking in children

Nursing Times

Parental smoking and the risk of childhood asthma

Amer. J. Public Health

Climatic influence on smell and irritation effects from tobacco smoke

Nord. Hyg. T.

Influence of family factors on asthma, wheezing incidence of lower repiratory illness, and ventilation function in children

Brit. J. Prev. Soc. Med.

Experimental study on irritations and annoyance due to passive smoking

Int. Arch. Occup. Environ. Health