Tetrahydro-beta-carboline-3-carboxylic acid compounds in fish and meat: possible precursors of co-mutagenic beta-carbolines norharman and harman in cooked foods

The presence of tetrahydro-beta-carbolines and beta-carbolines was studied in raw, cooked and smoked fish and meat. 1,2,3,4-Tetrahydro-beta-carboline-3-carboxylic acid (THCA) usually was the major beta-carboline found, whereas 1-methyl-1,2,3,4-tetrahydro-beta-carboline-3-carboxylic acid (MTCA) appeared in smoked and 'well done' cooked samples. THCA was detected in raw fish (nd-2.52 micrograms/g), cooked fish (nd-6.43 micrograms/g), cooked meats (nd-0.036 microgram/g), smoked fish (0.19-0.67 microgram/g) and smoked meats (0.02-1.1 micrograms/g). Smoked and cooked samples contained higher amounts of THCA and MTCA than raw products. Deep cooking of fish and meat increased both THCA and MTCA, and this was accompanied by the formation of more beta-carbolines, norharman and harman. The tetrahydro-beta-carbolines THCA and MTCA were chemical precursors of the co-mutagens norharman and harman during cooking. These and previous results confirm that foods are an important source of beta-carbolines in humans.     

Occult maternal exposure to environmental tobacco smoke exposure

Background

Environmental tobacco smoke (ETS) is a recognised air pollutant. Its harmful effects have been found to be implicated in health disorders, including unfavourable pregnancy outcomes. The discrepancy between self‐reported emvironmental tobacco smoke exposure and cotinine levels in pregnant non‐smokers in France was examined.

Method

Plasma cotinine was determined by a CPG‐SM method on women who had answered a self‐questionnaire describing their habits and environment during pregnancy.

Results

Of 698 pregnant women reported as non‐smokers, 305 (43.7%) claimed not to be exposed to ETS, yet 196 of these (64.3%) had plasma cotinine levels above the limit of detection.

Conclusion

Self‐reported data on ETS exposure in pregnant women therefore underestimate actual exposure. However, cotinine assay cab rectify this misclassification. An accurate identification of this risk factore will help to change attitudes towards ETS and avert its adverse effects on mother and fetus.Although environmental tobacco smoke (ETS) has not yet been monitored in France, it is probably, as in the United States National Health and Nutrition Examination Survey (1999–2002), a major source of indoor air pollution. Low levels of ETS exposure can result in unfavourable pregnancy outcomes,^1,2 and many pregnant women still believe that not smoking is sufficient to protect their fetus from ETS. Moreover, far less attention has been paid to perinatal ETS exposure. A better appraisal of these non‐maternal sources and measurement of corresponding prenatal exposure will provide a useful basis for further work and discussion on its effects.     

Hair as a biomarker for exposure to tobacco smoke

This article provides an overview of the hair nicotine biomarker for assessment of exposure to tobacco smoke, with emphasis on environmental tobacco smoke (ETS). Measurement of nicotine in hair can be an informative tool for research looking at ETS and related illnesses. There are still unresolved issues in relation to this biomarker such as influence of hair treatment, hair colour, and growth rate on nicotine levels in hair, which need to be addressed in order to further refine this biomarker for exposure assessment. Nevertheless, hair nicotine promises to be a valid and reliable measure of longer term exposure that can be readily applied in epidemiological studies of exposure to tobacco smoke, and more specifically ETS, and its risk to health.     

Environmental tobacco smoke exposure among Korean American nonsmokers in California.

Information about the extent and patterns of environmental tobacco smoke (ETS) exposure among Korean Americans is sparse, despite the population's having one of the highest male smoking rates. This paper estimates the prevalence of ETS exposure among Korean American nonsmokers in California, and identifies demographic and other characteristics associated with exposure. Data were collected during 2001-2002 from telephone interviews (in English or Korean) with 2,328 nonsmoking Korean American adults. ETS was encountered by 31% of respondents during a typical day. Exposure was most common in "other locations," where 24% of respondents were exposed, compared with 6% at home and 9% at work. Among those exposed, the greatest dose of exposure occurred at work (6 cigarettes/day) and at home (5 cigarettes/day). Women were four times more likely than men to be exposed to ETS at home (8% vs. 2%, respectively). For both men and women, the odds of exposure were greater among those who were younger, who were unmarried, and whose friends smoked. Additionally, traditional men and bicultural women had greater odds of ETS exposure than those who were more acculturated. Women who were married to smokers, had no children at home, consumed more alcohol, and had no home smoking ban also had greater likelihood of exposure. The results indicate the need for a complete ban of smoking in workplaces and in private homes to prevent exposure, particularly for women whose husbands smoke.     

Coronary events and exposure to environmental tobacco smoke: a case-control study from Australia and New Zealand

OBJECTIVES—To estimate the relative risk of coronary heart disease (CHD) associated with exposure to environmental tobacco smoke (ETS).
DESIGN—Population-based case-control study.
SUBJECTS—Cases were 953 people identified in a population register of coronary events, and controls were 3189 participants in independent community-based risk factor prevalence surveys from the same study populations.
SETTING—Newcastle, Australia and Auckland, New Zealand.
MAIN OUTCOME MEASURES—Acute myocardial infarction or coronary death.
RESULTS—After adjusting for the effects of age, education, history of heart disease, and body mass index, women had a statistically significant increased risk of a coronary event associated with exposure to ETS (relative risk (RR) = 1.99; 95% confidence interval (CI) = 1.40-2.81). There was little statistical evidence of increased risk found in men (RR = 1.02, 95% CI = 0.81-1.28).
CONCLUSION—Our study found evidence for the adverse effects of exposure to ETS on risk of coronary heart disease among women, especially at home. For men the issue is unclear according to the data from our study. Additional studies with detailed information on possible confounders and adequate statistical power are needed. Most importantly, they should use methods for measuring exposure to ETS that are sufficiently accurate to permit the investigation of dose-response relationships.


Keywords: coronary heart disease; environmental tobacco smoke; World Health Organisation MONICA project     

Reducing children's exposure to environmental tobacco smoke in homes: issues and strategies

It is now well established that children's exposure to environmental tobacco smoke (ETS) results in substantial public health and economic impacts. Children are more likely than adults to suffer health effects from ETS exposure, and the home is the most important site of such exposure.
  Although the responsibility and authority of the community and health professionals to protect children from harm are entrenched in North American society, social, economic, legal, and political factors contribute to a lower level of support for ETS control measures in homes compared with workplaces and public places. It is now clear that ETS control in home environments must be a priority on the public health agenda. Programme and policy options and strategies for ETS control in home environments are outlined. We conclude that the current research base is inadequate to fully support programme and policy development in this area and priorities for research are identified.


Keywords: environmental tobacco smoke; homes; children     

Environmental tobacco smoke exposure in public places of European cities

Background: Exposure to environmental tobacco smoke (ETS) has important public health implications. The results of the first European multi-centre study that measured ETS exposure in a range of public places (transport, educational settings, and leisure facilities such as bars and restaurants) are presented.     

Identification and occurrence of the bioactive β-carbolines norharman and harman in coffee brews

Norharman and harman, two heterocyclic β-carboline alkaloids with biological activity, were found in brewed coffee. Identification and analysis were carried out by HPLC-MS and RP-HPLC-fluorescence, respectively. All tested samples of brewed coffee including ground coffee, decaffeinated coffee, instant coffee and espresso contained both norharman and harman in variable amounts. Norharman was the major β-carboline alkaloid in brewed coffee at levels up to 9.34 μg g^-1 in instant ground coffee compared with harman, which had levels up to 1.67 μg g^-1. The two β-carbolines appeared to be formed during roasting of the coffee beans. It is concluded that drinking coffee is a major exogenous dietary source of these bioactive β-carboline alkaloids previously reported as mild psychoactive compounds in animal studies and in vitro co-mutagens. These results support our previous conclusion that foods containing β-carbolines are an important exogenous source of these alkaloids in humans.     

Estimates of per capita exposure to substances migrating from canned foods and beverages.

A study was undertaken by European industry to estimate the consumption of canned beverages and foodstuffs. European can production data were used with adjustments for imports into and out of the EU. It was further assumed that can production, with adjustments, equalled consumption. Owing to the lack of actual consumption country-by-country or household-by-household data throughout Europe, only per capita estimates of consumption were possible. Data were compiled country-by-country for seven major can-producing EU Member States and for eight different types of canned food and two types of canned beverage (beer and soft drinks). The per capita consumption of canned foods was 1.1 cans/person/week, and consumption of canned fish was estimated as 2.2 kg/person/year. The estimate of per capita consumption of canned food was 62 g/person/day or 22.6 kg/person/year. Canned beverages account for about 60% of the consumption of canned foodstuffs. The usefulness of per capita consumption of beverages is questionable because consumption habits may vary more widely than those for canned foods. However, as the migration into beverages is insignificant, these data were added for completeness. Per capita consumption of canned beverages is 67 cans/person/year or 61 g/person/day. From the average can sizes, the surface area of the cans consumed was estimated. The per capita surface area exposure was 0.55 dm(2)/person/day for canned foods and 0.55 dm(2)/person/day for canned beverages, giving 1.1 dm(2)/person/day. Migration of a substance at 0.02 mg dm(2) gives an exposure of 0.01 mg/person/day assuming a per capita consumption, using a surface area model. Migration at 0.12 mg kg(-1) in food gives an exposure of 0.007 mg/person/day using a weight model. Both models assumed migration into all food types at the same level, which is highly unrealistic. Exposure to BADGE from canned foods has been used as a case study. The best estimate for a worst case per capita exposure to BADGE and relevant derivatives was between 6 and 10 micro g/person/day, depending upon the approach and assumptions used.     

Legislation reduces exposure to second-hand tobacco smoke in New Zealand bars by about 90%

Aim

To measure exposure to second‐hand smoke (SHS) in New Zealand bars before and after comprehensive smoke‐free legislation enacted on 10 December 2004.

Methods

Cotinine is the main specific metabolite of nicotine and a well‐established biomarker for SHS exposure. We measured cotinine levels in saliva of non‐smoking volunteers before and after a 3 h visit to 30 randomly selected bars in 3 cities across the country. Two measures of cotinine before the smoke‐free law change during winter and spring 2004, and two follow‐up measurements in the same volunteers and venues during winter and spring 2005, were included.

Results

Before the smoke‐free law change, in all bars and in all volunteers, exposure to SHS was evident with an average increase in saliva cotinine of 0.66 ng/ml (SE 0.03 ng/ml). Increases in cotinine correlated strongly with the volunteers'' subjective observation of ventilation, air quality and counts of lit cigarettes. However, even venues that were judged to be “seemingly smoke free” with “good ventilation” produced discernable levels of SHS exposure. After the law change, there remained some exposure to SHS, but at much lower levels (mean saliva cotinine increase of 0.08 ng/ml, SE 0.01 ng/ml). Smoking indoors in bars was almost totally eliminated: in 2005 only one lit cigarette was observed in 30 visits.

Conclusions

Comprehensive smoke‐free legislation in New Zealand seems to have reduced exposure of bar patrons to SHS by about 90%. Residual exposures to SHS in bars do not result from illicit smoking indoors.Before December 2004, smoking was prohibited in most, but not all, workplaces in New Zealand. Bars, restaurants and hotels were not required to be smoke free. This changed on 10 December 2004 when the Smokefree Environments Amendment Act 2003 came into force. Since that time, smoking is not permitted in any indoor place of work. After Ireland, which passed its legislation in March 2004, New Zealand was one of the first countries to introduce national, comprehensive smoke‐free legislation.The purpose of this study was to measure the impact of this legislation on personal exposures to second‐hand smoke (SHS) in New Zealand bars. Previous papers^1,2,3 have described exposures of bar workers in Ireland, New York and Scotland before and after legislation. The effects of reduced exposures to SHS on the respiratory health of employees in this industry have also been documented.^3,4 However, we know of no other study that has examined the effects of smoke‐free laws on exposures of the patrons of bars and hotels. In an earlier publication,⁵ we have described in greater detail the analytical methods and findings at baseline.     

Active and passive tobacco smoke exposure: a comparison of maternal and child hair cotinine levels.

The objective of this study was to compare tobacco smoke exposure in mothers and their healthy children less than 3 years old using hair cotinine (HC) levels as an objective long-term measure of exposure. Hair samples were obtained from mother/child pairs recruited from the Columbus Children's Hospital Primary Care Center, and were analyzed by radioimmunoassay to compare HC levels. Mothers were both self-reported smokers and nonsmokers. Contributing and confounding variables were assessed based on questionnaires completed by participants. Exclusion criteria for children were prematurity and presence of chronic cardiopulmonary disease. Hair samples and questionnaires were obtained from 104 mother/child pairs. Child and maternal HC levels were correlated for both self-reported maternal smokers (R2 = .13, p < .013) and self-reported maternal nonsmokers (R2 = .54, p < 001). Child HC levels were higher than maternal HC levels (1.18 ng/mg vs. .78 ng/mg, p < .001). Children of nonsmokers had higher HC levels than their mothers (.77 ng/mg vs. .35 ng/mg, p < .001), while HC levels of smokers and their children were no different (1.91 ng/mg vs. 1.92 ng/mg, p = .978). The relationship between child and maternal HC did not differ by child age, gender, or race. In conclusion, environmental tobacco smoke exposure in young children as reflected by HC is higher than expected based on prior studies of biomarkers and passive tobacco smoke exposure in adult nonsmokers.