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The level of nickel in smoker's blood and urine

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General population is exposed to nickel from various sources. Smoking presents a significant form of exposure. The research was conducted in period 2000--2003 in Institute of Public Health in Nis. The samples of tobacco and cigarettes (127 samples) were both domestic and imported, and samples of biological material (123 blood samples and 147 urine samples) were taken from occupationally unexposed persons (smokers and non-smokers). The analyses were performed by electrothermal atomization technique, by Perkin Elmer AAS M-1100. The results obtained, revealed a high content of nickel in cigarettes (2.32-4.20 mg/kg) and in tobacco (2.20-4.91 mg/kg) regardless of the kind and the origin of tobacco. Nickel content in the blood of smokers (0.01-0.42 microg/l, median 0.07 microg/l) was higher than in the blood of non-smokers (0.01-0.26 microg/l, median 0.06 microg/l) although this difference was not statistically significant (p>0.05). In the urine of smokers (<0.01-8.20 microg/l, median 1.20 microg/l) there was a significantly higher concentration of nickel than in the urine of non-smokers (<0.01-4.60 microg/l, median 0.50 microg/l), p<0.05. The exposure of smokers to nickel through tobacco smoke was high regardless of the kind and the origin of tobacco and cigarettes. The content of nickel in tissue fluids established by biomonitoring shows that smokers can be far more exposed to this carcinogenic substance than non-smokers and that health risks for smokers are higher in this context.
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187
INTRODUCTION
Nickel comes into environment both from natural sources and
as a product of human activity (anthropogenic nickel sources).
It is found in all spheres (atmosphere, lithosphere, hydrosphere
and biosphere) in small concentrations. It influences physical and
chemical processes in outer environment biological processes in
living organisms.
Natural sources of nickel in air are volcanic eruptions and
earth dust; with other natural sources have significantly lower
participation. Man himself is the greatest polluter by means of
combustion of oil and its derivates, primary processing of nickel
ores and incinerator operation (1).
A significant source of nickel exposure for occupationally
unexposed population is the inhalation of tobacco smoke. Nickel
in tobacco smoke is present in form of gaseous phase or partic
-
les. A special toxicological significance is attributed to nickel
carbonyl, a compound found in tobacco smoke, which passes
through alveolar barrier very quickly after inhalation. Since al
-
veolar membranes contain phospholipids, fat solubility of nickel
carbonyl is of great importance for its good penetration through
the membrane.
After the absorption, nickel enters the blood, attaches itself to
protein carriers and reaches by means of bloodstream all organs
and tissues (2). The existence of trans-placental transfer of nickel
is confirmed and it represents the very beginning of exposure
which is continued after birth due to environmental factors (3).
THE LEVEL OF NICKEL IN SMOKER’S BLOOD
AND URINE
Stojanović D., Nikić D., Lazarević K.
Medical Faculty of Nis, Institute of Public Health Nis, Nis, Serbia and Montenegro
SUMMARY
General population is exposed to nickel from various sources. Smoking presents a significant form of exposure. The research was conducted
in period 2000–2003 in Institute of Public Health in Nis. The samples of tobacco and cigarettes (127 samples) were both domestic and imported,
and samples of biological material (123 blood samples and 147 urine samples) were taken from occupationally unexposed persons (smokers and
non-smokers). The analyses were performed by electrothermal atomization technique, by Perkin Elmer AAS M-1100.
The results obtained, revealed a high content of nickel in cigarettes (2.32–4.20 mg/kg) and in tobacco (2.20–4.91 mg/kg) regardless of the kind
and the origin of tobacco. Nickel content in the blood of smokers (0.01–0.42 μg/l, median 0.07 μg/l) was higher than in the blood of non-smokers
(0.01–0.26 μg/l, median 0.06 μg/l) although this difference was not statistically significant (p>0.05). In the urine of smokers (<0.01–8.20 μg/l, median
1.20 μg/l) there was a significantly higher concentration of nickel than in the urine of non-smokers (<0.01–4.60 μg/l, median 0.50 μg/l), p<0.05.
The exposure of smokers to nickel through tobacco smoke was high regardless of the kind and the origin of tobacco and cigarettes. The
content of nickel in tissue fluids established by biomonitoring shows that smokers can be far more exposed to this carcinogenic substance than
non-smokers and that health risks for smokers are higher in this context.
Key words: nickel, cigarettes, exposure, blood, urine
Address for correspondence: D. Stojanović, Medical Faculty of Nis, Institute of Public Health Nis, B. Tasković 50, 18 000 Nis, Serbia and Mon-
tenegro. E-mail: dusicas@eunet.yu.
Certain amounts of nickel are introduced to infants by means of
mothers milk (4).
Nickel elimination from an organism can be performed in
several manners (sweat, biliary system, feces, hair, nails, and
elimination through nursing, umbilical cord and placenta), but
urinary excretion is considered the most important. People ex-
posed to nickel in various ways are found to have increased nickel
content in their urine.
Nickel is classified as a carcinogenic substance and its toxic
effect on most organs and tissues is established without any
doubt (5, 6).
Objective: The purpose of this paper is to establish the ex-
posure of smokers to tobacco smoke nickel and to ascertain, by
biomonitoring nickel concentration in body fluids (the blood and
the urine) and to estimate the health risk for smokers.
METHODS
This research has been conducted in the Institute for Public
Health, Nis, in period 2000-2003. We obtained and analyzed 127
samples of cigarettes and tobacco derivates, 123 blood samples
and 147 urine samples. The sampling was done by means of po
-
lyethylene plastic vessels which had been previously washed by
deionized water and dried. Tobacco and cigarette samples were
both domestic and imported, while body fluids samples were
taken from healthy, occupationally unexposed persons (18–54
Cent Eur J Publ Health 2004; 12 (4): 187–189
188
-year-old). Until the analyses they were kept in the freezer under
–20 ºC temperature.
Samples of urine and blood were collected in acid-washed
polyethylene containers. Persons who handled samples used talc
-
-free gloves to avoid nickel contamination from sweat. Prior to the
determination of nickel in samples of urine these were oxidized
by nitric acid at temperatures under 80 °C to remove organic
constituents which interfere during analysis. Samples of blood,
tobacco and cigarettes were treated at high temperature (400 °C)
and residues were dissolved in nitric acid. The analyses were
performed, by electrothermal atomization technique, by Perkin
Elmer AAS M-1100. The validity of the procedure was checked
by the 3x repetitive analysis.
Results of the examinations were processed by mathematical
and statistical methods. Percentiles were calculated (C25 = 25th
percentile, C50 = 50th percentile or median, C75 = 75th percen
-
tile) and Mann-Whitney Rank Sum Test was used to compare the
variables, because they were not normally distributed. Statistical
significance was set at p value <0.05. The analysis was performed
using statistical software SPSS
®
for Windows
TM
, release 8.0 (SPSS
Inc., Chicago, IL, USA).
RESULTS
We established that nickel concentrations in tobacco and cigarettes
are high regardless of the brand and the origin (Table 1). Nickel
concentrations ranged from 2.20 mg/kg to 4.91 mg/kg in tobacco
and 2.32 mg/kg to 4.20 mg/kg in cigarettes. The median of nickel
content in tobacco (4.51 mg/kg) was higher than the median of
nickel concentration in cigarettes (3.40 mg/kg), but this difference
was not statistically significant (p>0.05). It is obvious that tobacco
processing during cigarettes manufacture does not significantly
reduces nickel content in the final product.
Nickel in the form of nickel carbonyl remains in the lung
parenchyma for only a short time and very quickly enters general
circulation. The established nickel content (Table 2) in the blood of
smokers was higher (the median was 0.07 μg/l) than in the blood
of non-smokers (the median was 0.06 μg/l), but this difference
was not statistically significant (p>0.05).
Nickel content in urine, established during this research (Table
3) ranged in smokers from undetectable values under 0.01 μg/l
to 8.20 μg/l (the median was 1.20 μg/l) and in non-smokers from
undetectable levels to 4.60 μg/l (the median was 0.50 μg/l). There
Table 1. Concentration of nickel in cigarettes and in tobacco
Number of
samples
Percentiles Mann-Whitney
Rank Sum Test
Min C25 C50 C75 Max
mg/kg
Tobacco
56 2.20 3.30 4.51 4.80 4.91
n.s.*
Cigarettes 71 2.32 3.15 3.40 3.96 4.20
*not differ significantly
(p<0.05 was considered as the criterion of statistical significance)
Table 2.
Concentration of nickel in the blood of smokers and non-smokers
Number of
samples
Percentiles Mann-Whitney
Rank Sum Test
Min C25 C50 C75 Max
µg/l
Smokers 57 0.01 0.02 0.07 0.13 0.42 n.s.*
Non-smokers 66 0.01 0.03 0.06 0.12 0.26
*not differ significantly
(p<0.05 was considered as the criterion of statistical significance)
Table 3.
Concentration of nickel in the urine of smokers and non-smokers
Number of
samples
Percentiles Mann-Whitney
Rank Sum Test
Min C25 C50 C75 Max
µg/l
Smokers 69 < 0.01 0.50 1.20 3.50 8.20 p<0.05*
Non-smokers 78 < 0.01 0.05 0.50 1.45 4.60
*differ significantly
(p<0.05 was considered as the criterion of statistical significance)
189
is a significant difference in nickel urine content of smokers
and non-smokers (p<0.05) which shows that smokers are more
exposed to the effects of this carcinogenic substance than non
-
-smokers.
DISCUSSION
Similar results concerning nickel content in cigarettes are also
mentioned by other authors in their papers: in USA, nickel was
present in concentration of 2.3 μg per cigarette, the values ran
-
ging from 1.1 to 3.1 μg, while tobacco, cigars and other tobacco
derivatives had similar concentration. In Germany, cigarettes have
average nickel concentrations of 1.2–4.0 mg/kg (1).
In nickel toxicology, a special place is reserved for nickel
carbonyl, a compound soluble in fat phase, which is present
in gaseous form in tobacco smoke. A research revealed that
0.04–0.58 μg of nickel is taken through the consumption of one
cigarette (8). Consumption of two packs of cigarettes per day
includes the intake of 3–15 μg/day, which is 1–5 mg per year (1).
Our results show that smoking increases nickel concentrations in
the blood of smokers, but many other factors (exposure to other
nickel sources, the degree of nickel concentration in other organs,
the degree of elimination...) also has influence on the level of
blood nickel content. The results of the research of other authors
show similar or slightly higher nickel blood concentrations (8, 9,
10). They also concluded that smoking does not have a significant
influence on nickel levels in the blood (9, 10).
What most of the researchers agree on is the fact that there
are very few researches including biomonitoring of occupatio
-
nally unexposed population concerning nickel. The same authors
propose analysis of blood and urine nickel levels as a reliable
and acceptable method of evaluation of environmental nickel
exposure (11–15), and TRACY protocol gives referential nickel
concentration in blood of <0.05–3.8 μg/l (16).
Research results show reveal similar nickel biomonitoring
results in urine of the occupationally unexposed population. In
Italy, the values of percentile distribution of nickel in the urine of
non-sensitized subjects: C25-0.6 μg/l, C50-2.1 μg/l, C75-1.1 μg/l,
which are approximate to the result of our research. Sunderman
et al. obtained similar results (8).
It is known that smoking contributes to an increased exposure
to various noxious agents, including carcinogens, like nickel,
which can have significant negative health effects. Many re
-
searches show greater incidence of malignant diseases in nickel
exposed workers who are smokers for many years (6).
Based on our result we can conclude that the exposure of smo
-
kers to tobacco smoke nickel is high, regardless of the kind and the
origin of tobacco. The content of nickel in tissue fluids established
by biomonitoring shows that smokers can be far more exposed to
this carcinogenic substance than non-smokers and that health risk
of smokers are higher. It is necessary to use all relevant means to
reduce smoking as a bad and health hazardous habit.
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Received March 29, 2004
Received in revised form and accepted July 26, 2004
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Chapter
Hand eczema (or hand dermatitis) is a term used to describe all eczematous skin conditions that affect the hands. Hand eczema is considered an umbrella term that covers both different clinical disease manifestations along with different causations, the most prevalent ones being contact dermatitis and atopic dermatitis, which often makes diagnosis, treatment, and future prevention complex and requires detailed patient-centered dermatological investigations.
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The aim of the research was to determine the degree to which nickel, as a cancerogenic element, is present in the ambiance air of Niš and Niška Banja, to determine what amount of it is inhaled by professionally non-exposed population through the respiratory system and to estimate health risk among smokers and non-smokers. The research was done at the Institute for Health protection in Niš in the period from 1995 to 2000. The examined material included 384 samples of air sediment, 58 samples of tobacco and tobacco derivatives and 227 blood samples of professionally non-exposed population. The presence of nickel in the airsediment of Niš (28,83 + 74,59 mg/m/day) and Niška Banja (20,77 + 41,88 mg/m/day) is evident at all the measuring points during the whole examination period; this represents a health risk for the population living in the area since it is a cancerogenic element. Comparison of the heating and non-heating seasons reveals that there is no statistically important difference regarding nickel content in the air-sediment. The average nickel introduction by inhalation amounts to 0,011 g per day and it is lower with respect to the introduction of this metal among the general population in cities of the developed industrial countries. The presence of nickel in tobacco (4,01 + 1,02 mg/kg) and cigarettes (3,28 + 0,71 mg/kg) is high regardless of the sort and origin of tobacco. The nickel content in people's blood is 0,108 + 0,141 gN/1 and it does not considerably depend upon gender and age. People who live in towns and smoke cigarettes (or are passive smokers) introduce more nickel into their organism than the country people and smokers but this difference is not statistically important.
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Endemic nephropathy (EN) is a disease of unknown etiology, and its occurrence is determined only at the Balkan peninsula. This study started form the assumption that nickel, being a highly toxic and cancerogenous substance, could be a risk factor or precipitating factor in generation of EN and urothelial tumors as well. The aim of the study was to prove the extent to which nickel, as a cancerogenous substance, is present in the urine and kidneys of inhabitants in EN settlements. As a material, 93 samples of urine and 32 samples of autopsy material were used. The urine samples were taken by the random sampling method from inhabitants of endemic and hypo endemic settlements in the valley of South Morava river, as well as from urban population of the municipality of Nis, as the control settlement. The samples of the kidney tissue represented autopsy material taken from cadavers who used to live, almost the whole life, in some of the endemic of hypo endemic settlements (target group), or in the urban zone of municipality of Nis (control group). The nickel presence was determined using method of atomic absorption spectrophotometry. The nickel concentration in the urine is higher in the endemic/hypo endemic settlements population than that in the control settlement group. The difference is not though, statistically significant. The nickel content in the kidney tissue of inhabitants from endemic or hypo endemic settlements is higher then in relevant kidney samples of inhabitants from control settlements, but the difference is not statistically significant either. Further investigations of the nickel content in biological materials are needed, along with the epidemiological study of incidence and prevalence of EN and malignant changes of the urotrackt in the endemic settlement population.
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During the last four decades in all the Central and East European countries it was intended that prevention of the adverse health effects of chemicals in occupational and environmental settings, including the drinking water and food basket of populations, be achieved by determination and compulsory observance of hygienic limit values (MAC, TLV, ADI). The authors have tried to demonstrate some specific features of risk assessment of exposure to chemicals in environmental and occupational settings. Although the approach to risk assessment and management was similar in many respects in the CMEA countries, implementation and hygienic practice was different in the individual countries in terms of many details and effectiveness. Due to long lasting experience with environmental pollution including health impact on humans, such as in the "Dirty Triangle of Europe" and other heavily contaminated areas a considerable knowledge has been gained. The authors recommend to analyse critically and evaluate the knowledge and experience and present it to the international scientific community and international institutions such as UNEP, ILO, IPCS, IRPTC and last but not least, OECD.
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The aim of this article was to summarize the epidemiologic studies on the possible impact of parental occupational exposure to lead or other metals on spontaneous abortion. For paternal exposure, the total number of abortions in the studies with adequate exposure contrast were 340 for lead, 240 for mercury, and 90 for unspecified metals and, correspondingly, for maternal exposure, about 80 for lead, 80 for mercury, 70 for nickel, and 130 for exposure to unspecified metals. Epidemiologic studies indicate that paternal exposure to lead or mercury might be associated with the risk of spontaneous abortion. For maternal exposure, no clear conclusion could be reached. In particular, paternal occupational exposure levels to metals were substantial compared with population values. Even though there are shortcomings in the present knowledge, protective goals for paternal exposure to lead and mercury are warranted. More well-designed studies on metals are needed.
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To investigate the relation between occupational hazards among nickel refinery workers and their exposure to different forms of nickel over time and the interaction between smoking and total exposure to nickel. The cohort consisted of 379 workers with first employment 1916-40 and at least three years of employment and 4385 workers with at least one year of employment 1946-83. Data on smoking (ever or never) were available for almost 95% of the cohort. Two analyses were used, indirect standardisation from observed and expected numbers and Poisson regression. During the follow up 1953-93, 203 new cases of lung cancer were observed v 68 expected (standardised incidence ratio (SIR) 3.0, 95% confidence interval (95% CI) 2.6-3.4) and 32 cases of nasal cancer were observed v 1.8 expected (SIR 18.0, 95% CI 12-25). The Poisson regression analysis showed an excess risk of lung cancer in association with exposure to soluble forms of nickel, with a threefold increase in relative risk (RR) (P < 0.001) and a multiplicative effect of smoking and exposure to nickel. The RRs were 1.1 (95% CI 0.2-5.1) for exposed workers who had never smoked and 5.1 (95% CI 1.3-20.5) for exposed workers who smoked. It is not possible to state with certainty which specific nickel compounds are carcinogenic, but a significant excess risk was found for workers exposed to soluble nickel alone or in combination with other forms of nickel. The present study suggests a multiplicative effect of smoking and nickel exposure.
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Acute and subacute lung toxicity of nickel fumes was examined by single and repeated intratracheal instillation of nickel fumes and Ni2O3 and NiO powders in the rat. LD50 of nickel fumes was estimated as 38.2 mg/kg body weight (b.w.) according to the method of Litchfield and Wilcoxon. Body weight gain was retarded as in the order of a single dose of 13.0 mg Ni2O3/kg > 14.3 mg nickel fumes/kg > 1.4 mg Ni2O3/kg > 13.0 mg NiO/kg b.w. compared to controls. The histopathological changes in the lungs of the 14.3 mg nickel fumes/kg-dosed rats were milder than those induced by administration of 13.0 mg Ni2O3/kg but severer than those induced by administration of 1.4 mg Ni2O3/kg b.w. A single administration of NiO powder did not produce any histopathological effects on the lungs. The repeated administration of nickel fumes produced persistent edema and proteinosis in the alveoli. The nickel fumes, which were chemically composed of 97% of NiO and 3% of Ni2O3, were very fine particles about 5-10 nm in diameter, partly aggregated into larger particles and spherical particles about 0.6 micron in diameter. Solubility in distilled water and saline was in the order of nickel fumes > Ni2O3 powder > > NiO powder. It was suggested that a toxic Ni2O3 component and very fine particles of nickel fumes are involved in the acute lung toxicity of nickel fumes. The epithelial injury induced by reactive oxygen and hydroxy radicals, which would be produced during the process of conversion of Ni(III) to Ni(II) and phagocytosis of nickel fumes by macrophages and polymorphonuclear cells, are presumed to be involved in the pathogenesis of nickel fumes-induced lung lesion.
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Basis of the intercomparison programs for toxicological analyses in occupational and environmental medicine Intercomparison programs are intended to improve the reliability of laboratory results by objectively testing their accuracy under medical requirements. Such intercomparison programs are regulated in Germany by guidelines of the German Federal Medical Council. According to these guidelines, the supervisors of the intercomparison programs are responsible for the announcement, organization, and implementation of each intercomparison program and for the evaluation of the results. The supervisors are therefore scientifically responsible for the intercomparison programs that they organize and for the selection and testing of the suitability of the samples. Their suitability is tested, e.g., by the determination of reference values. The reference values and their tolerance ranges represent the target values for the participants in the intercomparison program. The supervisor awards the participants a certificate for successful participation in the intercomparison programs for each parameter within the tolerance range. The certificate is valid for 12 months. The guidelines for setting of the tolerance range are based both on the analytical conditions and the medical requirements. The medical requirements in the occupational-medical and environmental-medical range must be oriented to the valid reference intervals, and limits of decisions for medical evaluation and in the area of preventive medicine must be applied more strictly than in curative medicine. At least two intercomparison programs must be carried out per year, and for each analyte, two samples must be analyzed with diÄerent concentration settings. The reference values are determined by reference laboratories [5, 6]. These laboratories are commissioned for toxicological analyses by the supervisor on the basis of their qualifications. These qualifications are apparent, e.g., from the observation that the laboratory or its head has evaluated methods for biological monitoring and published them in the international scientific literature. In addition, the laboratory should have successfully taken part in intercomparison programs organized by other institutions. Our laboratories take part in intercomparison programs in Canada, Finland, and Denmark and in the certification programs of the EU and the assignment programs for manufacturers of control materials (USA, Germany, and Norway). Also, the reference laboratories should routinely carry out toxicological analyses. A description of the requirements for reference laboratories has been published by Lehnert et al. [9] and by Angerer and Lehnert [2]. At present, 10 national and 14 international laboratories are commissioned to determine the reference values in the assurance program supervised by one of us (G.L.).
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In Finland, biomonitoring action levels (BAL) have been set since the 1970s. There are different ways of setting these BALs. The value for blood lead is based on legislation. Exposure limits have been set on the basis of the indicative values for carbon disulfide, ethylene benzene, toluene, and phenol. The number of BALs set by the Finnish Institute of Occupational Health (FIOH) has increased year by year, and we now have BAL values for more than 36 different chemicals or chemical groups. The Institute annually publishes a booklet with the latest information about the biomonitoring tests, sample collection, and limit values. The booklet is also available in English as a web version (http:/(/)www.occuphealth.fi/tt/bio/guide346. htm).