Environmental tobacco smoke exposure and eye disease

Aim: To undertake a systematic review of the literature on the effect of environmental tobacco smoke (ETS) and eye disease. Methods: Medline (1950-January Week 2 2007), EMBASE (1980 to 2007 Week 07), SCOPUS and Science Direct were searched on ETS exposure and eye disease using various combinations of the following terms: passive smoking, environmental tobacco smoke, sidestream smoke, involuntary smoking, secondhand smoke; with eye, conjunctiva, sclera, episclera, cornea, lens, iris, retina, choroid, uvea, optic nerve, uveitis, iritis, blindness, visual loss, cataract, thyroid eye disease, conjunctivitis, age-related macular degeneration, dry eye, tears. The above terms were also used to search abstracts published on The Association for Research in Vision and Ophthalmology Annual Meeting abstracts, from 1995 to 2006, and the grey literature, including PhD and MSc theses/dissertations. A search was further conducted specifically on eye diseases where active smoking has been proposed to be a risk factor, including age-related macular degeneration, Graves ophthalmology, glaucoma, uveitis, refractive errors, strabismus, tobacco-alcohol amblyopia, non-arteritic ischaemic optic neuropathy, Leber optic neuropathy and diabetic retinopathy. Given the scarce number of studies found through the above search, all articles found on ETS and eye disease were included in this review. Results: Seven studies evaluated the possible relationship between ETS and an eye disease. These studies referred to refractive errors in children (n = 2), cataract (n = 1), age-related macular degeneration (n = 3) and Grave ophthalmopathy (n = 1). The data available were insufficient to establish conclusive relationships between ETS and these eye diseases. Conclusion: Very scarce data exist in the literature on the effect of ETS on diseases of the eye. It seems appropriate that ETS should be included in future studies addressing the effect of smoking on eye disease.

Occupational exposure to environmental tobacco smoke in hospitality venues: are genetic- or proteomics-based biomarkers predictive of respiratory diseases?

Environmental tobacco smoke (ETS) is recognized as an occupational hazard in the hospitality industry. Although Portuguese legislation banned smoking in most indoor public spaces, it is still allowed in some restaurants/bars, representing a potential risk to the workers’ health, particularly for chronic respiratory diseases. The aims of this work were to characterize biomarkers of early genetic effects and to disclose proteomic signatures associated to occupational exposure to ETS and with potential to predict respiratory diseases development. A detailed lifestyle survey and clinical evaluation (including spirometry) were performed in 81 workers from Lisbon restaurants. ETS exposure was assessed through the level of PM 2.5 in indoor air and the urinary level of cotinine. The plasma samples were immunodepleted and analysed by 2D-SDSPAGE followed by in-gel digestion and LC-MS/MS. DNA lesions and chromosome damage were analysed innlymphocytes and in exfoliated buccal cells from 19 cigarette smokers, 29 involuntary smokers, and 33 non-smokers not exposed to tobacco smoke. Also, the DNA repair capacity was evaluated using an ex vivo challenge comet assay with an alkylating agent (EMS). All workers were considered healthy and recorded normal lung function. Interestingly, following 2D-DIGE-MS (MALDI-TOF/TOF), 61 plasma proteins were found differentially expressed in ETS-exposed subjects, including 38 involved in metabolism, acute-phase respiratory inflammation, and immune or vascular functions. On the other hand, the involuntary smokers showed neither an increased level of DNA/chromosome damage on lymphocytes nor an increased number of micronuclei in buccal cells, when compared to non-exposed non-smokers. Noteworthy, lymphocytes challenge with EMS resulted in a significantly lower level of DNA breaks in ETS-exposed as compared to non-exposed workers (P<0.0001) suggestive of an adaptive response elicited by the previous exposure to low levels of ETS. Overall, changes in proteome may be promising early biomarkers of exposure to ETS. Likewise, alterations of the DNA repair competence observed upon ETS exposure deserves to be further understood. Work supported by Fundação Calouste Gulbenkian, ACSS and FCT/Polyannual Funding Program.

Exposure to environmental oestrogenic chemicals and breast cancer.

The human population is now exposed on a daily basis to a multitude of environmental pollutant chemicals that would not have been present a century ago, and many of these chemicals have been detected in the human breast. The fatty nature of human breast tissue makes it a particular target for lipophilic as well as hydrophilic pollutant chemicals, which may enter the human body through oral, respiratory, or dermal routes. These chemicals possess a range of endocrine-disrupting properties and genotoxic activity, but from a breast cancer perspective the greatest concern has centered around their ability to mimic or interfere with the action of estrogen. The breast is an endocrine target organ and exposure to estrogen is a known risk factor for breast cancer.

Family and carer smoking control programmes for reducing children's exposure to environmental tobacco smoke

Background: Exposure to other people’s cigarette smoke (environmental tobacco smoke, or ETS) is an important child health issue.
Objectives: To determine the effectiveness of interventions aiming to reduce exposure of children to ETS.
Search strategy: The Tobacco Addiction Group register of studies was searched.MEDLINE, EMBASE and four other health and psychology databases were searched electronically, bibliographies of retrieved primary studies were checked and specialists in the area consulted.
Selection criteria: Controlled trials with or without random allocation were included in this review if they addressed participants (parents and other family members, child care workers and teachers) involved with the care and education of infants and young children (aged 0-12 years). All mechanisms for reduction of children’s environmental tobacco smoke exposure, and smoking prevention, cessation, and control programmes targeting these participants are included. These include smoke free policies and legislation, health promotion, social behavioural therapies, technology, education and clinical interventions.
Data collection and analysis: Two reviewers independently assessed studies and extracted data. Due to heterogeneity of methodologies and outcomes, no summary measures were possible and results were synthesised using narrative summaries.
Main results: Nineteen studies met the inclusion criteria, one of which was subsequently excluded. Three interventions were targeted at populations or community settings, seven studies were conducted in the well child health care setting and eight in the ill child health care setting. Twelve of these studies are from North America. In 12 of the 18 studies there was reduction of ETS exposure for children in both intervention and comparison groups. In only four of the 18 studies was there a statistically significant intervention effect. Three of these successful studies employed intensive counselling interventions targeted to smoking parents. There is little difference between the well infant, child respiratory illness and other child illness settings as contexts for parental smoking cessation interventions. The fourth successful intervention was in the school setting targeting the ETS exposure of children from smoking fathers.
Authors’ conclusions: Brief counselling interventions, successful in the adult health setting when coming from physicians, cannot be extrapolated to adults in the setting of child health. There is limited support for more intensive counselling interventions. There is no clear evidence for differences between the respiratory, non-respiratory ill child, well child and peripartum settings as contexts for reduction of children’s ETS exposure.

Environmental cadmium exposure and metabolic responses of the Nile tilapia, Oreochromis niloticus

The contamination of water by metal compounds is a worldwide environmental problem. This study was undertaken to evaluate the impact of short-term cadmium exposure on metabolic patterns of the freshwater fish Oreochromis niloticus. The fish were exposed to 320, 640, 1280 and 2560 mug/l sublethal concentrations of Cd++ (CdCl2) in water for 7 days. The specific activities of the enzymes phosphofructo kinase (PFK-E.C.2.7.1.11.), lactate dehydrogenase (LDH-E.C.1.1.1.27.) and creatine kinase (CK-E.C.2.7.3.2.) were decreased in white muscle after cadmium treatments, indicating decreases in the capacity of glycolysis in this tissue. Cadmium exposure induced increased glucose concentration in white muscle of fish. on the other hand, cadmium exposure at sublethal concentrations increased phosphofructo kinase and LDH in red muscle of fish. Cadmium significantly decreased total protein concentrations in liver and white muscle regardless of tissue glycogen levels. The data suggest that cadmium acts as a stressor, leading to metabolic alterations similar to those observed in starvation. (C) 2001 Elsevier B.V. Ltd. All rights reserved.

SUPEROXIDE RADICAL AND TOXICITY OF ENVIRONMENTAL NICKEL EXPOSURE

Three nickel compounds were tested for pancreatic, hepatic and osteogenic damage in rats by a single i.m. injection Ni++ (7 mg kg(-1)). The nickel induced biochemical alterations included significantly increased levels of serum alkaline phosphatase in rats with NiS (75%) and NiO (50%). Amylase and aspartate transaminase were also increased, and lipoperoxide was increased in rats with NiO (5.6-fold) and NiS (3.4-fold). No serum changes were observed with NiCl2. Daily injection of Cu-Zn superoxide dismutase (SOD) conjugated with polyethylene glycol prevented the serum level changes, indicating that superoxide radical is an important intermediate in toxicity of nickel insoluble compounds.

New experimental model of exposure to environmental tobacco smoke

PURPOSE: To describe a new model to passive smoking for rodents. METHODS: Twenty rats were distributed into two study groups (N=10): control group (CG), that was not exposed to tobacco smoke and used as normal standard for biochemical and histological analysis; Experimental Group (EG), that Animals were exposed to the passive smoking; Euthanasia was performed after 14 days of exposure. The serum level of nicotine and histological analysis were performed. RESULTS: There was a statistical difference on the nicotine serum levels between Experimental and Control group, with level of 286 ±23 nanograma/mL in the EG and undetectable on CG (p<0.01). The histological study suggested the model efficacy producing alveolar destruction and emphysema in the EG compared with the insignificant lesions in the CG's lung. CONCLUSION: The model of exposure to environmental tobacco smoke for rodents induced easily the changes related to secondhand smoke.

Exposure to environmental microorganisms and childhood asthma

Children who grow up in environments that afford them a wide range of microbial exposures, such as traditional farms, are protected from childhood asthma and atopy. In previous studies, markers of microbial exposure have been inversely related to these conditions.

Transient exposure to environmental estrogen affects embryonic development of brown trout (Salmo trutta fario).

Transient exposure of brown trout embryos from fertilization until hatch (70 days) to 17β-estradiol (E2) was investigated. Embryos were exposed to 3.8 and 38.0 ng/L E2 for 2h, respectively, under four scenarios: (A) exposure once at the day of fertilization (0 days post-fertilization, dpf), (B) once at eyeing stage (38 dpf), (C) weekly exposure until hatch or (D) bi-weekly exposure until hatch. Endpoints to assess estrogen impact on embryo development were fertilization success, chronological sequence of developmental events, hatching process, larval malformations, heart rate, body length and mortality. Concentration-dependent acceleration of development until median hatch was observed in all exposure scenarios with the strongest effect observed for embryos exposed once at 0 dpf. In addition, the hatching period was significantly prolonged by 4-5 days in groups receiving single estrogen exposures (scenarios A and B). Heart rate on hatching day was significantly depressed with increasing E2 concentrations, with the strongest effect observed for embryos exposed at eyeing stage. Estrogenic exposure at 0 dpf significantly reduced body length at hatch, not depending on whether this was a single exposure or the first of a series (scenarios A and D). The key finding is that even a single, transient E2 exposure during embryogenesis had significant effects on brown trout development. Median hatch, hatching period, heart rate and body length at hatch were found to be highly sensitive biomarkers responsive to estrogenic exposure during embryogenesis. Treatment effects were observable only at the post-hatch stage.

Smoke free restaurant ordinance, compliance with the regulation to reduce exposure to environmental tobacco smoke while dining at local restaurants in San Antonio, Texas

This study is a secondary analysis of a survey developed by Dr. Jimmy Perkins and administered by San Antonio/Bexar County Metropolitan Health District. The survey was developed subsequent to the implementation of the city smoking ordinance effective January 1, 2004. The survey had a multi-purpose plan to establish the number of restaurants having smoke free status prior to and following the ordinance, determine compliance as it relates to a necessary smoking section and proper signage, and expose the rationale for restaurants to become smoke free. The data resulting from the survey was presented to the San Antonio/Bexar County Metropolitan Health District. The summary presented the types of establishments surveyed, smoking status of the establishment, reasons for the establishment becoming smoke free, compliance with smoking sections, compliance with signage requirements, awareness of ordinance, and chain status of the establishment. ^ The results of this study display the relationships among the variables previously mentioned. The following relationships have been examined and the outcomes have determined whether each is significant. After careful analysis, knowledge translates into compliance with signage regulations, which then translate into ordinance compliance. Size does matter as it relates to an establishment's number of employees and seating capacity. The smaller the establishment the more likely the establishment is to have become smoke free before the ordinance went into effect. Restaurants, rather than fast food establishments most commonly cited their reason for becoming smoke free was to comply with the ordinance and only ten percent of restaurants gave policy as the main reason for becoming smoke free. ^ This study is important for public health because the negative health effects of environmental tobacco smoke (ETS) are still an overwhelming problem in the United States (3). ETS is a Known Human Group A Carcinogen (5). The Environmental Protection Agency (EPA) has estimated that around 3,000 non-smoking Americans die every year from lung cancer caused by ETS (6). This information illustrates the importance of providing smoke free establishments, especially to non-smoking patrons. ^

Environmental tobacco smoke exposure, respiratory and cardiovascular health in restaurant and bar workers in Mexico

Environmental tobacco smoke (ETS) is a well established health hazard, being causally associated to lung cancer and cardiovascular disease. ETS regulations have been developed worldwide to reduce or eliminate exposure in most public places. Restaurants and bars constitute an exception. Restaurants and bar workers experience the highest ETS exposure levels across several occupations, with correspondingly increased health risks. In Mexico, previous exposure assessment in restaurants and bars showed concentrations in bars and restaurants to be the highest across different public and workplaces. Recently, Mexico developed at the federal level the General Law for Tobacco Control restricting indoors smoking to separated areas. AT the local level Mexico City developed the Law for the Protection of Non-smokers Health, completely banning smoking in restaurants and bars. Studies to assess ETS exposure in restaurants and bars, along with potential health effects were required to evaluate the impact of these legislative changes and to set a baseline measurement for future evaluations.^ A large cross-sectional study conducted in restaurants and bars from four Mexican cities was conducted from July to October 2008, to evaluate the following aims: Aim 1) Explore the potential impact of the Mexico City ban on ETS concentrations through comparison of Mexico City with other cities. Aim 2). Explore the association between ETS exposure, respiratory function indicators and respiratory symptoms. Aim 3). Explore the association between ETS exposure and blood pressure and heart rate.^ Three cities with no smoking ban were selected: Colima (11.5% smoking prevalence), Cuernavaca (21.5% smoking prevalence) and Toluca (27.8% smoking prevalence). Mexico City (27.9% smoking prevalence), the only city with a ban at the time of the study, was also selected. Restaurants and bars were randomly selected from municipal records. A goal of 26 restaurants and 26 bars per city was set, 50% of them under 100 m2. Each establishment was visited during the highest occupancy shift, and managers and workers answered to a questionnaire. Vapor-phase nicotine was measured using passive monitors, that were activated at the beginning and deactivated at the end of the shift. Also, workers participated at the beginning and end of the shift in a short physical evaluation, comprising the measurement of Forced Expiratory Volume in the first second (FEV1) and Peak Expiratory Flow (PEF), as well as blood pressure and heart rate.^ A total of 371 establishments were invited, 219 agreed to participate for a 60.1% participation rate. In them, 828 workers were invited, 633 agreed to participate for a 76% participation rate. Mexico City had at least 4 times less nicotine compared to any of the other cities. Differences between Mexico City and other cities were not explained by establishment characteristics, such as ventilation or air extraction. However, differences between cities disappeared when ban mechanisms, such as policy towards costumer's smoking, were considered in the models. An association between ETS exposure and respiratory symptoms (cough OR=1.27, 95%CI=1.04, 1.55) and respiratory illness (asthma OR=1.97, 95%CI=1.20, 3.24; respiratory illness OR=1.79, 95%CI=1.10, 2.94) was observed. No association between ETS and phlegm, wheezing or respiratory infections was observed. No association between ETS and any of the spirometric indicators was observed. An association between ETS exposure and increased systolic and diastolic blood pressure at the end of the shift was observed among non-smokers (systolic blood pressure beta=1.51, 95%CI=0.44, 2.58; diastolic blood pressure beta=1.50, 95%CI=0.72, 2.28). The opposite effect was observed in heavy smokers, were increased ETS exposure was associated with lower blood pressure at the end of the shift (systolic blood pressure beta=1.90, 95%CI=-3.57, -0.23; diastolic blood pressure beta=-1.46, 95%CI=-2.72, -0.02). No association in light smokers was observed. No association for heart rate was observed. ^ Results from this dissertation suggest Mexico City's smoking ban has had a larger impact on ETS exposure. Ventilation or air extraction, mechanisms of ETS control suggested frequently by tobacco companies to avoid smoking bans were not associated with ETS exposure. This dissertation suggests ETS exposure could be linked to changes in blood pressure and to increased respiratory symptoms. Evidence derived from this dissertation points to the potential negative health effects of ETS exposure in restaurants and bars, and provides support for the development of total smoking bans in this economic sector. ^

Environmental carcinogens and human cancer : estimation of exposure to carcinogens in the ambient air /

Sponsored by Health Effects Research Laboratory, Research Triangle Park, N.C.

Development of a sensitive bioassay to detect exposure to environmental estrogens /

"RR-86"

The gender differences in health effects of environmental cadmium exposure and potential mechanisms

On a viewpoint of gender differences in Cd body burden and its health effects, we reviewed the population- based research including our own which conducted in Japan, Thailand, Australia, Poland, Belgium and Sweden to assess health effects of human exposure to environmental cadmium and their potential mechanisms. As a result, six risk factors in Cd health effects in women have been identified; ( 1) more serious type of renal tubular dysfunction, ( 2) difference in calcium metabolism and its regulatory hormones, ( 3) kidney sensitivity; difference in P450 phenotype, ( 4) pregnancy, ( 5) body iron store status, and ( 6) genetic factors. Further studies of Cd toxicity targeted to women would now appear necessary.