Nicotine in hair of bar and restaurant workers

AIM: To measure the relation between workplace smoking policies and exposures to Environmental Tobacco Smoke (ETS) of workers in bars and restaurants. METHODS: 114 workers in Wellington and Auckland were questioned about sources of exposure to ETS and smoking habits, and details of the smoke-free policy in their work place were recorded. A hair sample was collected from each participant and tested for nicotine. RESULTS: Among non-smoking workers, hair nicotine levels varied strongly according to the smoke free policy at their place of work (Kruskall-Wallis, chi2 = 26.38, p < 0.0001). Those working in 100% smoke free restaurants had much lower levels than staff working in bars with no restrictions on smoking, and levels were intermediate for staff working in places with a partial smoking ban. These findings were not changed when adjustments were made for other sources of ETS exposure. Hair nicotine levels among nonsmokers working in places with no restriction on smoking were similar to hair nicotine levels of active smokers. CONCLUSION: The present New Zealand Smoke Free Environment Act does not protect workers in the hospitality industry from exposure to ETS. The findings from this study highlight the substantial levels of exposure of bar and restaurant staff from patrons' smoking.     

Exposure to secondhand smoke at home and in public places in Syria: a developing country's perspective

This study employs sensitive methods to address the issue of exposure to secondhand smoke among children and women in an understudied developing country setting (Syria). The study combines data collected by the Syrian Center for Tobacco Studies as part of two international studies conducted in 2006: the Secondhand Smoke Exposure among Women and Children study (Johns Hopkins) and the Global Air Monitoring Study (Roswell Park Cancer Institute). We employed objective measures (hair nicotine, and ambient household nicotine assessed by passive monitors) to assess children's and mothers' exposure to secondhand smoke at home, and used the TSI SidePak personal aerosol monitor to sample respirable suspended particles less than 2.5 microm diameter (PM(2.5)) in the air in public places (40 restaurants/cafés in Aleppo). In homes, the mean ambient nicotine level (+/- standard deviation, SD) was 2.24 +/- 2.77 microg/m(3). Mean level of hair nicotine was 11.8 ng/mg among children (n = 54), and was higher if the mother was a smoker (19.4 +/- 23.6 ng/mg) than nonsmoker (5.2 +/- 6.9 ng/mg) (p < .05). Mean hair nicotine among nonsmoking mothers (n = 23) was 1.17 +/- 1.56 ng/mg. Children's hair nicotine level was strongly correlated with ambient household nicotine and number of cigarettes smoked daily in the house (r = .54 and r = .50, respectively, p < .001), and also was related to having a father who smoked in the children's presence. In public places, average PM(2.5) in the monitored 40 hospitality venues was 464 microg/m(3) and correlated with smoker density measured as cigarettes-waterpipes/100 m(3) (r = .31, p = 0.049). Thus, children in Syria are exposed to high levels of secondhand smoke at home, in which mothers' smoking plays a major role. Also, levels of respirable hazardous particles are high in public hospitality venues, putting customers and workers at serious health risks. Efforts to limit exposure of children and women at home and to adopt clean air policies should become a public health priority in Syria and the Arab region.     

Selective hair analysis of nicotine by molecular imprinted solid-phase extraction: an application for evaluating tobacco smoke exposure.

A method using a molecularly imprinted polymer (MIP) as the selective sorbent for solid-phase extraction (SPE) has been developed. Its application to the assay of hairy nicotine level among smokers and non-smokers with high-performance liquid chromatography (HPLC) and evaluation of exposures to the environmental tobacco smoke (ETS) were validated. The MIP was synthesized using nicotine as the template molecule and methacrylic acid (MAA) as the functional monomer. This MIP-SPE method provided inherent selectivity and a sensitive response to nicotine with a detection limit of 0.2 ng/ml hair at a signal-to-noise ratio of 3:1 and the limit of quantification was 0.5 ng/ml. The linearity was assessed in the range of 0.5-80 ng/ml hair, with a coefficient (r(2)) greater than 0.987. The amounts of nicotine determined in smokers and non-smokers hair were in the range of 5.1-69.5 ng/mg hair and 0.50-9.3 ng/mg hair, respectively. The reported measures of ETS exposure were significantly associated with hairy nicotine levels. This assay of nicotine in hair using MISPE provided a very selective and reliable method for the evaluation of the exposure to tobacco smoke.     

Behavioral effects of nicotine exposure from secondhand tobacco smoke among bar and restaurant workers

This study explores the behavioral effects of nicotine exposure from secondhand tobacco smoke (SHS) on bar and restaurant workers. Baseline data were obtained from a longitudinal study of 105 bar and restaurant workers. Hair nicotine, self-reported SHS exposure, smoking status, symptoms of nicotine exposure after being exposed to a smoky environment, and nicotine dependence were assessed. Nonsmokers reporting four or more symptoms of nicotine exposure had higher hair nicotine levels than those reporting less than four symptoms. Nonsmokers with higher hair nicotine levels were 2.2 times more likely to report 4 or more behavioral symptoms. Self-reported secondhand tobacco smoke exposure and hair nicotine were not predictive of nicotine dependence among smokers. Nicotine exposure from secondhand tobacco smoke may have important behavioral outcomes in nonsmokers. This study provides further evidence for the importance of prohibiting smoking in hospitality venues to protect the health of workers.     

Occupational exposure of hairdressers to [14C]-para-phenylenediamine-containing oxidative hair dyes: a mass balance study.

We monitored the exposure of hairdressers to oxidative hair dyes for 6 working days under controlled conditions. Eighteen professional hairdressers (3/day) coloured hairdresser's training heads bearing natural human hair (hair length: approximately 30 cm) for 6 h/working day with a dark-shade oxidative hair dye containing 2% [14C]-para-phenylenediamine (PPD). Three separate phases of hair dyeing were monitored: (A) dye preparation/hair dyeing, (B) rinsing/shampooing/conditioning and (C) cutting/drying/styling. Ambient air and personal monitoring samples (vapours and particles), nasal and hand rinses were collected during all study phases. Urine (pre-exposure, quantitative samples for the 0-12, 12-24, 24-48 h periods after start of exposure) and blood samples (blank, 4, 8 or 24 h) were collected from all exposed subjects. Radioactivity was determined in all biological samples and study materials, tools and washing liquids, and a [14C]-mass balance was performed daily. No adverse events were noted during the study. Waste, equipment, gloves and coveralls contained 0.41+/-0.16%, dye mixing bowls 2.88+/-0.54%, hair wash 45.47+/-2.95%, hair+scalp 53.46+/-4.06% of the applied radioactivity, respectively. Plasma levels were below the limit of quantification (10 ng PPDeq/mL). Total urinary 0-48 h excretion of [14C] levels ranged from a total of <2-18 microg PPDeq and was similar in subjects exposed during the different phases of hair dyeing. Minimal air levels at or slightly above the limit of quantification were found in a few personal air monitoring samples during the phases of hair dyeing and hair cutting, but not during the rinsing phase. Air area monitoring samples or nasal rinses contained no measurable radioactivity. Hand residues ranged from 0.006 to 0.15 microg PPDeq/cm2, and were found predominantly after the cutting/drying phase. The mean mass balance of [14C] across the six study days was 102.50+/-2.20%. Overall, the mean, total systemic exposure of hairdressers to oxidative hair dyes during a working day including 6 hair dyeing processes was estimated to be <0.36 microg PPDeq/kg body weight/working day. Our results suggest that (a) current safety precautions for the handling of hair dyes offer sufficient protection against local and systemic exposure and (b) professional exposure to oxidative hair dyes does not pose a risk to human health.     

Low level saliva cotinine determination and its application as a biomarker for environmental tobacco smoke exposure.

1. The determination of personal exposures to environmental tobacco smoke (ETS) and respirable suspended particles (RSP) for housewives, and fixed site monitoring of their homes, have been undertaken by these authors throughout Europe, South East Asia and Australia. Median 24 h time weighted average (TWA) concentrations for ETS particles and nicotine were found to be significantly higher for housewives living in smoking households compared with those living in nonsmoking households. For Europe, median TWA concentrations of 4.1 and <0.26 microg/ml for ETS particles and 0.63 and < 0.08 microg/m3 for nicotine were found for housewives living in smoking and nonsmoking households respectively. 2. In addition to the measurement of RSP, ETS particles and nicotine, saliva cotinine concentrations were determined using a radioimmunoassay method with a limit of quantitation of 1 ng/ml. Median saliva cotinine concentrations of 1.4 and <1 ng/ml were determined for European housewives living in smoking and nonsmoking households respectively, which reflected the poor limit of quantitation of this methodology. A chromatographic method utilising tandem mass-spectrometric detection was developed and validated for the determination of both cotinine and 3-hydroxycotinine, two of the main metabolites of nicotine, with lower limits of quantitation of 0.05 and 0.10 ng/ml respectively. This method was applied to samples collected from subjects with a known ETS exposure history and median cotinine concentrations of <0.05 ng/ml for self-reported unexposed nonsmokers, 0.65 ng/ml for nonsmokers reporting some ETS exposure and 1.28 ng/ml for nonsmokers living with smokers were found. 3. In conclusion, the measurement of RSP and ETS concentrations derived from personal or fixed site monitors for housewives may provide some indication of potential exposures to dependent children. The recent development and application of a highly sensitive assay for the determination of cotinine in saliva has provided evidence to suggest that concentrations determined at sub-nanogram levels may be used as a biomarker for ETS exposure. This improved methodology, coupled with non-invasive sampling for saliva, may be of significance when considering the application of cotinine as a biomarker for ETS exposure in children.     

Comparison of environmental tobacco smoke (ETS) concentrations generated by an electrically heated cigarette smoking system and a conventional cigarette

Smoking conventional lit-end cigarettes results in exposure of nonsmokers to potentially harmful cigarette smoke constituents present in environmental tobacco smoke (ETS) generated by sidestream smoke emissions and exhaled mainstream smoke. ETS constituent concentrations generated by a conventional lit-end cigarette and a newly developed electrically heated cigarette smoking system (EHCSS) that produces only mainstream smoke and no sidestream smoke emissions were investigated in simulated "office" and "hospitality" environments with different levels of baseline indoor air quality. Smoking the EHCSS (International Organisation for Standardization yields: 5 mg tar, 0.3 mg nicotine, and 0.6 mg carbon monoxide) in simulated indoor environments resulted in significant reductions in ETS constituent concentrations compared to when smoking a representative lit-end cigarette (Marlboro: 6 mg tar, 0.5 mg nicotine, and 7 mg carbon monoxide). In direct comparisons, 24 of 29 measured smoke constituents (83%) showed mean reductions of greater than 90%, and 5 smoke constituents (17%) showed mean reductions between 80% and 90%. Gas-vapor phase ETS markers (nicotine and 3-ethenylpyridine) were reduced by an average of 97% (range 94-99%). Total respirable suspended particles, determined by online particle measurements and as gravimetric respirable suspended particles, were reduced by 90% (range 82-100%). The mean and standard deviation of the reduction of all constituents was 94 +/- 4%, indicating that smoking the new EHCSS in simulated "office" and "hospitality" indoor environments resulted in substantial reductions of ETS constituents in indoor air.     

Assessment of the exposure of children to environmental tobacco smoke (ETS) by different methods.

1. In order to elucidate the role of exposure to environmental tobacco smoke (ETS) in various acute and chronic illnesses in children, it is important to assess the degree of exposure by suitable methods. For this purpose, we determined the exposure to ETS in 39 children (4-15 years) and 43 adults (16+ years) by questionnaires, personal diffusion samplers for nicotine, and cotinine measurements in saliva and urine. In addition, the influence of the smoking status and the location of the home (urban or suburban) on the benzene exposure of the children was investigated. 2. On average, the 24 children living in homes with at least one smoker were exposed to ETS for 3.1 h/d. This is significantly longer (P<0.001) than the daily exposure time of the 15 children from nonsmoking homes (0.3 h/d). The nicotine concentrations on the personal samplers worn over 7 days were 0.615 and 0.046 microg/m3 for children from smoking and nonsmoking homes, respectively (P<0.001). Average salivary cotinine levels were 1.95 ng/ml in children from smoking homes and 0.11 ng/ml in children from nonsmoking homes (P< 0.01). The corresponding urinary cotinine levels were 29.4 and 4.5 ng/mg creatinine (P< 0.001). There was no difference in the extent of ETS exposure between children and adults from smoking households. Adults from nonsmoking homes tended to have higher ETS exposure than children from nonsmoking homes. 3. Exposure to benzene, which was determined by means of personal samplers, measurements of benzene in exhaled air and of the urinary benzene metabolite trans, trans-muconic acid, was not significantly related to the smoking status of the home but primarily dependent on the location of the home.     

Determination of arsenic in urine by atomic absorption spectrophotometry for biological monitoring of occupational exposure to arsenic.

An atomic absorption spectrophotometric (AAS) method was successfully applied to analysis of urine for arsenic (As) as a measure of biological monitoring of occupational exposure to As in Vietnam. The application of the method to urine samples from 75 non-exposed control urbanites (after 2-day abstinence from sea foods) gave a reference level of 62.4 +/- 11.6 microg/l (as mean +/- S.D.), from which the upper limit of the normal value (74 microg/l as mean +/- 1 S.D.) and the acceptable limit (100 microg/l as mean +/- 3S.D.) were deduced. Further application to urine samples from 147 workers occupationally exposed to As in Bacthai Non-ferrous Metallurgic Corporation showed significantly elevated levels of As in urine, with mean +/- S.D. of 78.5 +/- 20.2 microg/l. Improvement of working conditions to reduce As exposure resulted in substantial reduction in the ratio of those with urinary As at the level in excess of the acceptable limit. The practical importance of total arsenic determination in urine after 2-day sea food abstinence is discussed in connection with current conditions in analytical laboratories in Vietnam.     

Time course of nicotine and cotinine incorporation into samples of nonsmokers' beard hair following a single dose of nicotine polacrilex

Hair nicotine and cotinine have been proposed as longer-term markers of exposure to secondhand smoke. In this study, we evaluated the rate and extent of nicotine and cotinine deposition into beard hair among six male nonsmokers following a single exposure to 4 mg of nicotine in Nicorette(?) (nicotine polacrilex) gum. We collected beard hair samples daily for 12 days following exposure and urine samples for 6 days after exposure. Using liquid chromatographic-tandem mass spectrometric analysis, we found that both nicotine and cotinine could be detected in beard samples within 24 h of the exposure and reached a maximum of about 71 pg nicotine and 47 pg cotinine/mg hair, respectively, within 1-2 days, followed by a gradual decline. Compared to beard hair concentrations, nicotine, cotinine, and hydroxycotinine were excreted in urine at much higher levels and also peaked on the day after exposure (mean ± SD urine cotinine = 300 ± 183 ng/mL). Our results confirmed that both nicotine and cotinine can be measured in beard hair samples following a single dose of nicotine. However, both the time-course and extent of deposition of these analytes in beard hair in this study differed from the results reported previously from a similar evaluation.     

Assessment of DNA damage in peripheral blood lymphocytes of individuals susceptible to arsenic induced toxicity in West Bengal, India

Assessment of DNA damage was carried out using alkaline comet assay in lymphocytes of 30 individuals exposed to high levels of arsenic (247.12+/-18.93 microg/l) through contaminated groundwater in North 24 Parganas district, West Bengal, India. All of them exhibited high arsenic contents in nail (4.20+/-0.67 microg/g), hair (2.06+/-0.20 microg/g) and urine (259.75+/-33.89 microg/l) samples and manifested various arsenical skin lesions. Unexposed samples were collected from 30 residents of the unaffected East Midnapur district with very little or no exposure to arsenic (7.69+/-0.49 microg/l) in drinking water. The results were evaluated principally by manual analysis of comets and partly by computerized image analysis. Both the analytical methods exhibited a high degree of agreement in results. The exposed participants expressed significantly higher DNA damage (p < 0.01) in their lymphocytes than the unexposed participants. Alkaline comet assay was also combined with formamidopyrimidine-DNA glycosylase enzyme digestion to confirm that arsenic induced oxidative base damage in the lymphocytes. Significant positive trend effects of comet lengths in relation to arsenic levels in water prove that DNA damage can be used as a sensitive biomarker of arsenic exposure. This study demonstrates that arsenic induced significant DNA damage in the exposed participants, which could correspond to a higher susceptibility to arsenic induced toxicity and carcinogenicity.     

Chromium status of tannery workers in relation to metabolic disorders.

Chromium (Cr), being an excellent tanning agent, is widely used in the leather industry. In the process of leather production, tannery workers are exposed to either inorganic Cr(III) compounds or Cr bound to proteins (leather dust). The total Cr content in tannery air (1-54 microg m(-3)) is rather high in comparison to ambient air (4-6 ng m(-3)) but the amount of Cr in inhalable particles (<10 microm) is two to three orders of magnitude less (20-60 ng m(-3)). The total daily intake of Cr was estimated by the analysis of diet (24.3 +/- 4.0 microg Cr day(-1)), drinking water (0.3 +/- 0.1 microg Cr dm(-3)) and ambient air. The contribution of the latter was dominant for tannery workers and almost negligible (8%) for the unexposed population. Chromium is an essential nutrient required for sugar and fat metabolism. The normal dietary intake of Cr for the occupationally unexposed population is found to be suboptimal (<30 microg Cr day(-1)) whereas tannery workers receive on average 150-325 microg of supplemental Cr day(-1). Assessment of the Cr status of both populations was made on the basis of the Cr contents of their scalp hair, pre-shift urine and thermally induced sweat. The median Cr contents in these tissues and fluids were significantly higher (P<0.01) in tannery workers (hair: 4 microg Cr g (-1), urine: Cr/creatinine 1.7 microg Cr g(-1), sweat: 25 microg Cr dm(-3)) in comparison with the control group (hair: 0.16 microg Cr g(-1), urine: Cr/creatinine 0.13 microg Cr g (-1), sweat: 0.7 microg Cr dm(-3)). Tannery workers absorbed up to 13 times more Cr in comparison to controls, the amount varying considerably depending on the workplace and duration of exposure. The main route of Cr absorption appears to be through the gastrointestinal tract, where medium to large particles play a dominant role. The absorption of Cr from leather dust may be more efficient in comparison to inorganic Cr(III) compounds. Under normal circumstances sweat Cr losses represent at least 20% of urinary Cr excretion. The incidence of glucose intolerance and disturbed lipid metabolism was compared between the unexposed (control) population (n=150) and a population of tannery workers (n=138) from the same residential area. The percentage of glucose-intolerant subjects was significantly (P<0.01) lower in the older subgroup (age>48 years), who were even more obese, but not in the whole tannery population in comparison to controls. In the group of subjects displaying glucose intolerance, those from the control population showed a significantly higher body mass index (BMI) of 32.3 and a considerably larger proportion of females (86%) in comparison to subjects from the tannery population (28.2 and 60%, respectively). There was no significant difference in total serum cholesterol levels between the groups. Results of other lipid variables, such as high-density lipid (HDL) cholesterol, low-density lipid (LDL) cholesterol and triglycerides, are controversial: namely, the HDL/LDL ratio was higher for the controls, who showed in contrast significantly higher serum triglyceride levels in comparison to the older subgroup of tannery workers. The possible effects of other parameters on serum HDL-cholesterol level are outlined but the influence of Cr on lipid metabolism in tannery workers remains unclear.     

Phenytoin concentration in head hair sections: a method to evaluate the history of drug use

Phenytoin (PHT) levels were determined in sections of head hair taken from 60 patients (34 males and 26 females), aged 5 to 69 years, who were regularly receiving the drug. The hair sectional analysis included dissolution, liquid phase extraction procedures, and immunoassay (Abbott TDx) or high-pressure liquid chromatography (HPLC) analytical techniques. The values of PHT levels in the hair from the first section (close to the hair root) to the fifth section for female patients were 18.0, 15.2, 13.1, 11.6, and 10.7 microg/g, respectively, according to HPLC measurements. There were no significantly different results obtained using the immunoassay technique, according to which the mean values of PHT in the hair sections were 17.9, 15.2, 13.1, 11.9, and 10.9 microg/g, respectively, from the first to the fifth sections. The corresponding mean values for male patients by HPLC and immunoassay techniques, respectively, were 17.9, 15.0, 12.5, 12.1, and 12.3 microg/g and 17.8, 14.9, 12.2, 11.9, and 121 microg/g. Generally, a reduction of drug concentrations in hair from the first to the subsequent segments was observed. The hair PHT concentrations were found to be dependent on the dosage (by fluorescence polarization immunoassay: r = 0.987, p < or = 0.02; by HPLC: r = 0.988, p < or = 0.02). Mean dose and assay outcome values by hair color and correlation between hair PHT mean values, daily mean doses of the drug, and patients' age are presented. The differences among doses according to hair color were significant. PHT hair profiles from female and male patients compared with the mean +/- SD concentrations of the hair sections are discussed. The data indicate the possible use of hair section testing as a marker of the dosage history and the compliance of patients receiving long-term treatment with PHT.     

Adducts of acrylonitrile with hemoglobin in nonsmokers and in participants in a smoking cessation program.

Hemoglobin adducts have been used to assess exposure to carcinogenic compounds in tobacco smoke. However, because of background levels in nonsmokers, most adducts that have been studied are not useful for monitoring low-level exposure. Bergmark [(1997) Chem. Res. Toxicol. 10, 78-84] showed that the level of adducts of acrylonitrile (AN) with N-terminal valine (ANVal) increases with increasing cigarette consumption, and the increment from 1 cigarette/day was estimated to be 8 pmol/g of globin. The background level of ANVal in nonsmokers was not quantified (<2 pmol/g of globin). The objective of this study was to determine the background level of ANVal in hemoglobin and to study the stability of this adduct in vivo. Globin samples previously analyzed by Bergmark from 17 nonsmokers and 2 smokers were reanalyzed in the study presented here. Globin samples from 7 additional nonsmokers and from 10 participants in a smoking cessation program were also analyzed. Smoking habits and exposure to environmental tobacco smoke (ETS) were assessed by interview. Only two of the participants completed the program. The levels of ANVal in these 2 subjects decreased after quitting and were at background level by 126 days. The time course of the decrease was compatible with removal of stable adducts. The levels of ANVal in the nonsmokers were 0.76 +/- 0.36 (mean +/- SD) (n = 18; reporting no exposure ETS), 1.1 +/- 0.6 (n = 3; reporting exposure to ETS), and 1. 2 +/- 0.5 pmol/g of globin (n = 3; snuff users). Thus, the adduct level in nonsmokers corresponds to the adduct increment from about 0. 1 cigarette/day. Measurements of the level of ANVal could be used to distinguish between nonsmokers and low-level smokers on an individual level, but larger groups of individuals would be required to detect a possible contribution to the background from passive smoking.     

Serum copper levels among quartz stone crushing workers: a cross sectional study

The present cross sectional study was carried out among 134 workers of quartz stone crushing units to assess the serum Cu activity among quartz stone workers without disease. Demographic and occupational details of the subjects were recorded on the predesigned proforma. Standard diagnostic criteria were used for diagnosing silicosis and tuberculosis. The pulmonary functions of the subjects were measured using Spirovit SP-10. The mean age for male was found to be 26.63 +/- 6.28 years while that for female was 21.93 +/- 4.29 years and for the whole group was 26.13 +/- 6.26 years. In the present study only one case of silicosis and seven cases of tuberculosis were found. The mean serum Cu levels of those having respiratory disease was found to be 91.5 +/- 19.8 microg/dl while mean serum Cu level of those free from respiratory disease was 86.8 +/- 21.3 microg/dl The difference was found to be statistically non-significant (t = 0.64, df= 1, P > 0.05). Thus, in the present study, though the elevated level of serum Cu was found in solitary case of silicosis, no association could be established between the silica exposure and serum copper levels as suggested by non-significant effect of duration of exposure (P = 0.53).     

Reference values for hair cotinine as a biomarker of active and passive smoking in women of reproductive age, pregnant women, children, and neonates: systematic review and meta-analysis

Exposure to environmental tobacco smoke (ETS) is most often estimated using questionnaires, but they are unreliable. Biomarkers can provide valid information on ETS exposure, the preferred biomarker being cotinine. However, no reference range of hair cotinine exists to distinguish among active, passive, and unexposed nonsmokers. This study identifies cutoffs to validate cotinine as a marker for exposure to ETS. Data were obtained from six databases (four US, one Canada, one France). Active smoking and exposure to ETS were measured in the hair of women of reproductive age, pregnant women, their children, and neonates. Subjects were classified into active smokers, passively exposed to ETS, and unexposed nonsmokers. A total of 1746 cases were available for analysis. For active smokers, mean hair cotinine concentrations (95% confidence interval) were 2.3 to 3.1 ng/mg for nonpregnant women and 1.5 to 1.9 ng/mg for pregnant women. In the group of passive smokers, mean hair cotinine concentrations were 0.5 to 0.7 ng/mg for nonpregnant women, 0.04 to 0.09 ng/mg for pregnant women, 0.9 to 1.1 for children, and 1.2 to 1.7 for neonates. Among unexposed nonsmokers, mean hair cotinine was 0.2 to 0.4 ng/mg in nonpregnant women, 0.06 to 0.09 ng/mg in pregnant women, and 0.3 to 0.4 ng/mg in children. Cutoff values for hair cotinine were established to distinguish active smokers from passive or unexposed (0.8 ng/mg for nonpregnant women and 0.2 ng/mg for pregnant women). A cutoff value of 0.2 ng/mg was accurate in discriminating between exposed children and unexposed. These new values should facilitate clinical diagnosis of active and passive exposure to tobacco smoke. Such diagnosis is critical in pregnancy and in a large number of tobacco-induced medical conditions.     

Beta-carotene supplementation attenuates cardiac remodeling induced by one-month tobacco-smoke exposure in rats.

OBJECTIVE: The objectives were to analyze the cardiac effects of exposure to tobacco smoke (ETS), for a period of 30 days, alone and in combination with beta-carotene supplementation (BC). Research methods and procedures: Rats were allocated into: Air (control, n = 13); Air + BC (n = 11); ETS (n = 11); and BC + ETS (n = 9). In Air + BC and BC + ETS, 500 mg of BC were added to the diet. After three months of randomization, cardiac structure and function were assessed by echocardiogram. After that, animals were euthanized and morphological data were analyzed post-mortem. One-way and two-way ANOVA were used to assess the effects of ETS, BC and the interaction between ETS and BC on the variables. RESULTS: ETS presented smaller cardiac output (0.087 +/- 0.001 vs. 0.105 +/- 0.004 l/min; p = 0.007), higher left ventricular diastolic diameter (19.6 +/- 0.5 vs. 18.0 +/- 0.5 mm/kg; p = 0.024), higher left ventricular (2.02 +/- 0.05 vs. 1.70 +/- 0.03 g/kg; p < 0.001) and atrium (0.24 +/- 0.01 vs. 0.19 +/- 0.01 g/kg; p = 0.003) weight, adjusted to body weight of animals, and higher values of hepatic lipid hydroperoxide (5.32 +/- 0.1 vs. 4.84 +/- 0.1 nmol/g tissue; p = 0.031) than Air. However, considering those variables, there were no differences between Air and BC + ETS (0.099 +/- 0.004 l/min; 19.0 +/- 0.5 mm/kg; 1.83 +/- 0.04 g/kg; 0.19 +/- 0.01 g/kg; 4.88 +/- 0.1 nmol/g tissue, respectively; p > 0.05). Ultrastructural alterations were found in ETS: disorganization or loss of myofilaments, plasmatic membrane infolding, sarcoplasm reticulum dilatation, polymorphic mitochondria with swelling and decreased cristae. In BC + ETS, most fibers showed normal morphological aspects. CONCLUSION: One-month tobacco-smoke exposure induces functional and morphological cardiac alterations and BC supplementation attenuates this ventricular remodeling process.     

Analysis of toxic metals in commercial moist snuff and Alaskan iqmik

The extent to which smokeless tobacco endangers human health is an ongoing subject of debate. Studies have shown that smokeless tobacco products contain high levels of biologically available nicotine and tobacco-specific nitrosamines. Toxic metals in smokeless tobacco products have been less extensively studied. In this study, concentrations of arsenic, barium, beryllium, cadmium, chromium, cobalt, lead, and nickel were measured in snuff products and iqmik tobacco, a product popular among some Alaska Natives. The average arsenic, cadmium, lead, and nickel concentrations in 17 commercially available brands were 0.23 +/- 0.06 microg/g, 1.40 +/- 0.31 microg/g, 0.45 +/- 0.13 microg/g and 2.28 +/- 0.36 microg/g, respectively. In 17 iqmik tobacco samples, the average arsenic, cadmium, lead, and nickel concentrations were 0.19 +/- 0.06 microg/g, 1.41 +/- 0.56 microg/g, 0.55 +/- 0.19 microg/g, and 2.32 +/- 1.63 microg/g, respectively. Using artificial saliva, the extractable levels of beryllium and lead were relatively low and consistent, whereas barium extracted from tobacco samples ranged from 2 to 21%. The group 1 and 2B carcinogens cadmium, cobalt, and nickel were more efficiently extracted by artificial saliva (30-65% of the cobalt, 20-46% of the nickel, and 21-47% of the cadmium).     

Delayed evoked potentials in children exposed to methylmercury from seafood.

Methylmercury poisoning may cause constriction of visual fields and deafness, especially if exposure occurs prenatally. However, the risks associated with exposure from contaminated seafood is unclear. We examined 149 children attending first grade in a Madeiran fishing community. As maternal dietary habits were relatively unchanged, current maternal hair concentrations were used as indicator of the child's prenatal exposure to methylmercury (geometric average, 9.64 microg/g [48.2 nmol/g]). After adjustment for age and sex, the mean (+/-SD) latency of peak III of the brainstem auditory evoked potentials at 40 Hz was increased by 0.128+/-0.047 ms when maternal hair-mercury concentrations exceeded 10 microg/g (50 nmol/g) (p for association, 0.002), and the increase of the N145 pattern-reversal visual evoked potential latency at 15 minutes of arc was 3.16+/-1.57 ms (p for association, 0.002). No such relationships were seen with the child's own hair-mercury concentration, and other clinical examinations revealed no mercury-associated deficits. Neurophysiological evidence of adverse effects on brain function are relatively independent of confounders, and should be considered in the risk assessment of this seafood pollutant.     

Hubble-bubble (water pipe) smoking: levels of nicotine and cotinine in plasma,saliva and urine

OBJECTIVES: The purpose of the present study was to assess the levels of nicotine and cotinine in biological fluids (plasma, saliva, and urine) following hubble-bubble (HB) smoking. METHODS: Fourteen healthy male volunteers, aged 28 +/- 8 years, body weight of 82.7 +/- 13.53 kg, participated in the study. All volunteers were habitual HB smokers for 3.29 +/- 1.90 years who smoked at least 3 runs per week with an average of 20 g Mua'sel per run. Volunteers were requested to avoid smoking, at least 84 hours prior to the time of the study. After baseline samples were taken, volunteers started smoking 20 g of Mua'sel for a period of 45 minutes. Heparinized blood samples (5 or 10 ml each) were drawn for nicotine and cotinine analysis before, during and after the smoking period. Saliva samples were collected just before smoking (time 0) and at the end of smoking (45 min). Urine also was collected at time 0 and 24-hour urine collection was also taken to measure nicotine and cotinine excretion. Nicotine and cotinine were extracted from samples and assayed by gas chromatography. All data are presented as mean +/- SEM throughout the text, Tables and Figures unless indicated otherwise. RESULTS: Plasma nicotine levels rose from 1.11 +/- 0.62 ng/ml at baseline to a maximum of 60.31 +/- 7.58 ng/ml (p < 0.001) at the end of smoking (45 min). Plasma cotinine levels increased from 0.79 +/- 0.79 ng/ml at baseline to its highest concentration of 51.95 +/- 13.58 ng/ml (p < 0.001) 3 hours following the end of smoking. Saliva nicotine levels significantly rose from 1.05 +/- 0.72 to 624.74 +/- 149.3 ng/ml and also saliva cotinine levels significantly increased from 0.79 +/- 0.79 ng/ml to 283.49 +/- 75.04 ng/ml. Mean amounts of nicotine and cotinine excreted in urine during the 24-hour urine collection following smoking were equal to 73.59 +/- 18.28 and 249 +/- 54.78 microg, respectively. CONCLUSION: Following a single run of HB smoking, plasma, saliva and urinary nicotine and cotinine concentration increased to high values. This observation suggests that HB may not be an innocent habit, as people believe.