Contains naphtha benzoyl

Naphthalene / naphthols and human biomonitoring
- Opinion of the Commission "Human Biomonitoring" of the Environment Agency -

(Federal Health Gazette No. 10/2007 p. 1357)


As a combustion product of organic materials (among other things as a component of tobacco smoke), naphthalene is ubiquitous in the human environment. For a long time, naphthalene, unlike other polycyclic aromatic hydrocarbons (PAH), was not considered to be carcinogenic. On the basis of new findings from animal experiments, the Senate Commission for the Examination of Harmful Working Materials of the German Research Foundation carried out a reassessment in 2001 and classified naphthalene in Category 2 as a substance that is to be regarded as carcinogenic for humans [1]. When characterizing the risk, the EU also comes to the conclusion that carcinogenic effects are possible, but classifies naphthalene in category 3 because it does not consider the data situation to be sufficient for classification in category 2 [2].

It is currently unclear whether there is a relevant health risk from naphthalene for the general population. Knowledge of the exposure is a prerequisite for assessing a risk.

Naphthalene (chemical molecular formula: C10 H8) consists of 2 condensed benzene rings and is thus the smallest representative of the PAH. Its colorless crystals are only slightly soluble in water (30 mg / l) and are subject to slow sublimation at room temperature (vapor pressure at 25 ° C: 10.5 Pa). The melting point is 80.2 ° C, the boiling point 218 ° C [2, 3].

Naphthalene is metabolized in the human body to form 1- and 2-naphthol (1- and 2-hydroxynaphthalene), among other things, which are excreted conjugated in the urine. These metabolites are suitable for human biomonitoring. As sensitive test methods are now available for the quantitative determination of naphthols in urine, the internal exposure of the person can be determined in this way.

Due to the available data, reference values ​​cannot yet be derived. The Human Biomonitoring Commission has therefore compiled the available data in order to enable an orienting assessment of event-related measurement results.

Use and distribution

PAHs result from incomplete combustion of organic material. A large number of polycyclic aromatics are formed by pyrolysis. This applies to industrial processes (e.g. energy supply, waste incineration, petrochemicals, steel production, hard coal coking) as well as traffic, private households (e.g. food preparation, heating, tobacco smoke) and natural processes such as forest fires [4, 5].

In the processes mentioned, naphthalene is also formed; it is also a component of diesel and aircraft fuels [6, 7] and tar-containing paints [3] such as Creosot - a coal tar distillate that is used as a wood preservative for railway sleepers and wooden masts.

Coal tar, which contains naphthalene, is an active ingredient in some pharmaceuticals for the treatment of skin diseases [2, 8]. As a repellent against clothes moths, naphthalene is only used sporadically in Germany; it is even more widespread in the US [9].

Naphthalene is mainly produced industrially by distilling coal tar or from crude oil. The annual production volume in the EU is around 200,000 tonnes [2,10]. It is used in the chemical industry (in addition to o-xylene) for the synthesis of phthalic anhydride, which is further converted to phthalates (e.g. DEHP or diisononyl phthalate) [11]. Phthalates are widely used as plasticizers for plastic products made from PVC.

In addition, naphthalene is required as a raw material for the production of azo paints and naphthalene sulfonic acid, which is processed into aggregates for cement and plasterboard, into dispersants and into tannins.

1- and z-naphthol are manufactured as industrial intermediates. Finally, among other things, carbaryl (i-naphthyl-N-methylcarbamate), a carbamate insecticide, is synthesized.

Entry into the environment and sources of human exposure PAH are ubiquitous in the environment. Limit and guide values ​​generally relate to benzo [a] pyrene, which is often used as a key component in PAH mixtures.

Naphthalene is mainly introduced into the environment through traffic emissions [2]. Naphthalene concentrations in the air are usually lower in rural areas than in cities and densely populated regions. In the open air, the concentrations are usually below 1 µg / m3 [10, 12], but higher values ​​are also possible at traffic hotspots [13].

The representative environmental survey in Germany in the mid-1980s showed a geometric mean indoor value of 2.0 ug / m3 (maximum value: 14 ug / m3) for measurements in 479 living rooms [14]. In more recent studies, somewhat lower concentrations in indoor air were found in the western federal states [3].

The use of naphthalene-containing moth repellants and tobacco smoke increase the concentrations in indoor air. With values ​​of up to 46 µg naphthalene per cigarette, larger quantities were measured in sidestream smoke than in mainstream smoke [15]. Naphthalene can also be emitted from moisture barriers or from leaks from mineral oil tanks in basement rooms. Joints in the parquet floor, which was laid with old tar glue, are also conceivable as sources [3,16].

The US Environmental Protection Agency (EPa) has an average concentration of 5.2 µg / m3 Estimated air to which humans are exposed [17]. According to their statements, this results in an average daily naphthalene uptake through respiration of 1.1 µg / kg body weight (BW) for adults and 4.5 µg / kg for children. In addition, a reference concentration (RfC) of 3 µg / m3 which, however, does not take into account the carcinogenic potential of naphthalene [17]. The RfC describes the daily inhalation exposure at which a life-long exposure to human health is considered unlikely.

Food is particularly contaminated with PAHs if it has been smoked or cooked on an open fire (grilling). Details for

Naphthalene range from <1 to 176 µg / kg [10]. The EPa estimates the average daily naphthalene intake from food to be 0.04-0.24 µg / kg body weight (children: 0.20-0.94 µg / kg) [17].

The concentration of naphthalene in drinking water is generally well below 1 µg / l [2,10].

In addition to the sources mentioned, there is also absorption via dust, especially in small children. Because of the volatility of naphthalene, this route of absorption is likely to play less of a role than with PAHs with a larger ring system. The EPa estimate shows a daily intake of 0.24 µg / kg body weight for adults and 3.3 µg / kg body weight for children [17].

In addition, naphthalene can be found in household products and consumer goods. For example, tests carried out on behalf of the Öko-Test magazine (07/2003) found naphthalene in concentrations of up to 129 mg / kg in swimming aids made of PVC. It is conceivable that other PVC products also contain naphthalene as an impurity in the phthalates used. Systematic scientific work on this problem is not yet available. It is currently not known to what extent such residues are released when these products are used and to what extent they make a relevant contribution to the exposure of the general population to naphthalene.

At certain workplaces where raw materials containing PAHs such as tar or pitch are used or PAHs are released through pyrolysis processes, PAH concentrations are significantly higher than in the environment. Industries with a significant naphthalene load are in particular: the impregnation with Creosot, the production of mothballs from naphthalene as well as the naphthalene production in general as well as the coal tar distillation and coking. With considerable fluctuations within the same branch, naphthalene concentrations of a few µg to several mg per m3 can be reached at the workplace [10]. In a current study at various workplaces in Germany, a maximum of 0.7 mg / m3 measured [18].


In animal experiments, the target tissues of the eye, the hematopoietic system and the respiratory tract were identified [19, 20, 21]. Mice and rats reacted differently to the tissue in the lungs and nose [22]. This species difference is attributed to different metabolic rates in the tissues of the two animal species. In humans, cataract formation and haemolytic anemia, among other things, have been observed [4].

A two-year inhalation study in rats found naphthalene concentrations of 0, 50, 160 and 320 mg / m, respectively3 were exposed in male rats in all concentration levels and in females from 160 mg / m3 a significantly increased incidence of adenomas of the respiratory epithelium of the nose. The incidence of neuroblastomas in the olfactory epithelium was also dose-dependently increased [4]. In addition, there was chronic inflammation of the nasal mucous membrane. On the basis of these new findings, various scientific committees have rated naphthalene as potentially carcinogenic for humans [1, 2, 17, 23].

Uptake, metabolism and carcinogenicity of naphthalene

As a highly volatile PAH, naphthalene is mainly absorbed by inhalation. However, absorption into the body is also possible dermally and orally [4, 24, 25]. In test animals, naphthalene is initially metabolically activated in analogy to the other PAHs. Cytochrome P45o forms naphthalene-1,2-epoxide (2 stereoisomers), the half-life of which is a few minutes [22]. The epoxide can be partially converted into glutathione conjugates, which are ultimately eliminated renally as naphthyl mercapturic acids [26, 27, 28].

1- and 2-naphthol and 1,2-dihydro-1,2-dihydroxynaphthalene are also formed from the epoxide. Other metabolites are 1,2- and 1,4-dihydroxynaphthalene and 1,2- and 1,4-naphthoquinone. To date, a total of 30 naphthalene metabolites have been identified in the urine of mammals [4].

There are considerable differences between rats, mice and humans in terms of the enzymes and naphthalene metabolism in tissue [22]. This could explain why, after inhalation, with the same naphthalene concentrations in the breath, the concentration of toxic metabolites in human tissues is lower than in rodents. For details, please refer to the statement of the adhoc working group "Indoor reference values" [3].

In humans, r- and 2-naphthol and 1,2- and 1,4-dihydroxynaphthalene have been described as metabolites in the urine [29], as well as 1,4-naphthoquinone [30]. The excretion of i-naphthol occurs biphasic with half-lives of 1-2 h and 14-46 h. After inhalation, 6.3-8.5% of the naphthalene was excreted as i-naphthol in the 24-hour urine [31]. Bieniek [32] gives a half-life of 4 hours. Metabolic pathways can also be induced by PAHs and cigarette smoke [33, 34].

In contrast to the PAHs with more rings in the molecule, according to the current state of the art it can be assumed that the actual carcinogenic agents are not the epoxide or a diol epoxide, but rather a. the naphthoquinones [35, 36].

There are currently two main hypotheses regarding the mechanism of the carcinogenic effects of naphthalene: On the one hand, the naphthoquinones could increase the concentration of reactive oxygen species via a redox cycle, which damage the DNA by oxidation [37]. On the other hand, naphthoquinones form covalent bonds with nucleophilic functional groups. Protein adducts have been found in workers exposed to naphthalene [38] and suggest that DNA adducts can also be formed.

The Adhoc Working Group of the Indoor Air Hygiene Commission of the Federal Environment Agency and the Supreme State Health Authorities (Adhoc AG IRK / AOLG) have derived guideline values ​​for naphthalene for indoor air based on the toxicological endpoint "inflammation of the nasal mucosa". In animal experiments, long-term inhalation of naphthalene resulted in chronic inflammation of the nasal and lung mucosa, as well as hyperplasias, neuroblastomas and adenomas in the same organs. In contrast, inflammation and cancer caused by naphthalene in humans have not yet been identified. The main reasons for this could be seen in the different anatomy and physiology of the nasal and pharynx in experimental animals compared to humans. Rats and mice are mandatory nasal breathers. Other possible reasons are the lower respiratory volume relative to the body mass and a lower sensitivity of humans to naphthalene due to metabolic differences. In the opinion of the adhoc working group, sufficient protection against the carcinogenic effects of naphthalene can be assumed if the occurrence of signs of inflammation is avoided. Under these conditions, a guideline value II (hazard value) of 20 µg naphthalene / m was established3 and a guideline value of 1 of 2 µg naphthalene / m3 derived [3]. The guideline values ​​of the US-EPa and the ATSDR (Agency for Toxic Substances and Disease Registry) as RfC of 3 µg / m are of the same order of magnitude3 or as a minimum risk level (MRL) of 4 pg / rn3 [39]

Analytical determination of naphthols in urine

The parameters 1- and 2-naphthol in urine have proven themselves in numerous occupational and environmental medical studies [10]. In the published analytical methods, the conjugates are usually first enzymatically cleaved. In earlier studies, however, hydrochloric acid was used for the hydrolysis of sulfates and glucuronides. However, this can lead to analytical problems due to undesired side reactions. Hill et al. [40] reported that the internal standard used due to acid13 C.6-1-naphthol was degraded. Yang et al. [41] found a lower naphthol yield compared to conjugate cleavage by enzymatic hydrolysis. These analytical problems with acid hydrolysis have been confirmed by current comparative studies [42]. In order to obtain comparable results, the uniform application of the gentler enzymatic hydrolysis with beta-glucuronidase / aryl sulfatase is therefore recommended.

The quantification of 1- and 2-naphthol can then be carried out by means of high pressure liquid chromatography (HPLC) with fluorescence detection or, alternatively, by coupling capillary gas chromatography to mass spectrometry. An overview of the analytical methods is given in Table 1. For routine analysis, a method should be selected with which 1- and 2-naphthol can be determined in parallel with a limit of quantification of a maximum of 5 µg / l each. This makes it possible to detect increased concentrations of just one naphthol. This is important because, in addition to exposure to naphthalene, the following sources can also contribute to the excretion of just one naphthol isomer.

Exposure to carbaryl causes increased excretion of 1-naphthol [43]. The insecticide is not approved for agricultural use in Germany. However, imported fruit can contain carbaryl. For example, residues of up to 1.9 mg / kg were found in pears from Argentina and Chile [44].

Another possible disruptive factor for the detection of naphthalene exposure via the quantitative determination of naphthols in urine is possible exposure to naphthols. For example, 1-naphthol is used in various chemical hair colors. In addition, contact with residues of 2-naphthol is conceivable, which is used as a chemical intermediate for azo dyes, tanning agents and as a preservative for glue, wood and leather. It is excreted in the urine of humans both unchanged and conjugated [45]. The significance of exposure to naphthols compared to naphthalene exposure for the general population cannot yet be conclusively assessed.

Table 1: Analytical methods for the determination of 1- and 2-naphthol in urine

Authors [literature]hydrolysisAnalytesInt. defaultmethodDerivatizationNWG / BG
Preuss, Angerer [57]enzyme1-N and 2-NwithoutHPLC-FD 1.5 µg / l
0.5 µg / l
Kuusimäki et al. [58]enzyme2-NwithoutHPLC-FD 1 µg / l BG
Andreoli et al. [59]without1-N
1-N-glucuronide and 2-N-sulfate
withoutLC-MS 0.1 mg / l
Elovaara, et al. [60]enzyme1-N and 2-NwithoutHPLC-FD 4 µg / l BG
1.5 µg / l BG
Hansen et al. [61]enzyme1-NwithoutHPLC-FD 5.5 µg / l
Kim et al. [62]enzyme2-NwithoutHPLC-FD 0.13 µg / l BG
Heikkiläetal. [31]HCI1-NwithoutGC-ECDPentafluorobenzyl bromide10 µg / l
Bieniek [63]HCI1-N and 2-NwithoutGC-FIDwithout100 µg / l
Bouchard et al. [64]enzyme1-N and 2-NwithoutGC-MS-SIMAcetic anhydride / K2 CO30.1 µg / l
Hill et al. [40]enzyme1-N and 2-N13C6-IN
GC-MS-MSChloriodopropane1 µg / l
Jansen et al. [65]Enzyme and acid1-N and 2-N2H7-1 NGC-MS-SIMBenzoyl chloride0.7 µg / l
Keimig, Morgan [66]HCI1-N and 2-NwithoutGC-ECDPentafluorobenzyl bromide / K2 CO310 µg / l
Serdar et al. [7]enzyme1-N and 2-N2H7-1 NGC-MS-SIMSilylation0.3 µg / l
Smith et al. [67]enzyme1-N and 2-N7306-1 NGC-HRMS according toSilylation0.016 µg / l
0.011 µg / l
Petropoulou et al. [68]enzyme1-N and 2-N and carbarylN-ethyl-p-methyl-3-carboxamideSPME GC-MS / MSTrifluoroacetic anhydride / triethylamine0.2 µg / l BG
Hardt et al. [50]enzyme1-N and 2-N2H7-1 NGC-MS-SIMAcetic anhydride / K2CO30.5 µg / l BG
Yang et al. [41]Enzyme> HCI1-N and 2-N2H10 anthraceneGC-MS-SIMPentafluorobenzyl bromide / K2CO30.27 µg / l

1-N: 1-naphthol, 2-N: 2-naphthol BG: limit of quantification, ECD: electron capture detector, FD: fluorescence detector, FID: flame ionization detector, GC: gas chromatography, (HP) LC: (high pressure) liquid chromatography, HR: high resolution, MS: mass spectrometry, NWG: detection limit, SIM: selected ion monitoring, SPME: solid phase microextraction.

The parallel determination of i- and 2-naphthol, however, ensures the specificity of these parameters for naphthalene exposure, since the two metabolites correlate well [9]. After occupational exposure (n = 277), the concentration of 1-naphthol was approximately 1.2 times that of 2-naphthol [18]. Serdar et al. [46] also found slightly higher 1- than 2-naphthol values ​​in workers exposed to naphthalene, and a concentration ratio of approximately one in control persons. According to Yang et al. [41] tobacco smoke influences the ratio of 1- to 2-naphthol: the quotient was approx. 1.2 for smokers and 1.5 for non-smokers. The specified concentration ratios were derived on the basis of the collective investigations; deviations are possible on an individual basis [9, 47]

For the sake of completeness, it should be pointed out that in addition to the naphthols in urine, other metabolites can in principle be used for human biomonitoring of naphthalene. For example, 1,2- and 1,4-dihydroxynaphthalene have been determined in the urine of occupationally exposed persons. The measured concentrations correlated with those of the naphthols [29]. Unmetabolized naphthalene was also measured in the urine of workers exposed to PAH [48].

However, only 3- and 2-naphthol have so far been determined on a larger scale and have also proven to be suitable for environmental medicine issues.

Internal exposure of the general population

The concentrations of i- and 2-naphthol in the urine of people who were not exposed to naphthalene at work are shown in Table 2. It must be pointed out that the compiled values, with the exception of those from the USA, which do not come from representative collectives.

Table 2: Naphthol concentrations in the urine of the general population

Smoking status + countryAgeN1-naphthol in the urine2-naphthol in the urineAuthors [literature]
NOa Germanyfrom 10y63 MUMd 5.0 µg / l (<1.5-29.4 µg / l)
P95 19.7 µg / l
Md 3.6 µg / l (<0.5-23.6 µg / l)
P95 17.1 µg / L
Preuss et al. [49]
NOa Germany2,5-6,5135 MUMd 3.0 µg / l ≪ 1.5-12.0 µg / l)
P95 10.7 µg / l
Md 2.6 µg / l (<0.5-35.4 µg / l)
P95 9.8 µg / l
Preuss et al. [49]
NOb Germany25-51 J w67 MUMd 3.6 µg / l (<1.5-82.4 µg / l)
P95 29.9 µg / l
Md 2.1 µg / l (<0.5-22.9 µg / l)
P95 16.9 µg / l
Holz and Wilhelm [47]
NOb Germany5-7 y94 MUMd 2.4 µg / l (<1.5- 82.6 µg / l)
P95 20.9 µg / l
Md 1.5 µg / l (<0.5-68.3 µg / l)
P95 6.5 µg / l
Holz and Wilhelm [47]
NOc Germany25-51 J w48 MUMd 2.6 µg / l (<1.5-68.4 µg / l)
P95 24.0 µg / l
Md 2.0 µg / l (<0.5-62.4 µg / l)
P95 21.9 µg / l
Holz and Wilhelm [47]
NOc Germany5-7 y91 MUMd 2.7 µg / l (<1.5-252 µg / l)
P95 12.6 µg / l
Md 2.4 µg / l (<0.5-93.2 µg / l)
P95 12.8 µg / L
Holz and Wilhelm [47]
NOed Germanyfrom 18 y50 MUMd 1.0 µg / l (<0.5-18.3 µg / l)Md 1.0 µ / l (<0.5-28.4 µg / l)Hardt et al. [50]
NR Finland 20GM 1.9 µg / gK (<0.9-4.5 µg / gK)GM 2.2 µg / gK (<0.9-5.4 µg / gK)Väänänen [69]
NR Finland (winter) 46-Md 1.7 µg / gKKuusimäki et al. [58)
NR Finland (summer) 38-Md 2.9 µg / gKKuusimäki et al. [58]
NR Canada 26 MUMd 1.3 µg / gK
P95 8.7 µg / gK
Md 1.2 µg / gK
P95 6.4 µg / gK
Bouchard et al. [64]
NOe Canada30 MUMd 3.4 µg / gK
P95 10.7 µg / gK
Md 2.6 µg / gK
P95 6.3 µg / gK
Bouchard et al. [64]
NR Japan 56 MUGM 3.0 µg / lGM 1.1 µg / lYang et al. [41]
NR Korea12 +/-1 1137 MU Md 2.8 (0.3-74.6) µg / gKKang et al. [70]
NR Korea 62-Md 1.6 (0.4-11.3) µg / gK
P95 7.0 µg / gK
Kim et al. [71]
NR Korea 87 GM 2.0 µg / gKNan et al. [72]
NR China 19GM 3.2 µg / lGM 3.3 µg / lSerdar et al. [46]
R.a Germanyfrom 1019 MUMd 20.61 µg / l (3.6-56.3 µg / l)Md 19.5 µg / l (2.2-48.3 µg / l)Preuss et al. [49]
R.f Germany26-44 J, f35 MUMd 13 µg / l (2-36 µg / l)
P95 32.9 µg / l
Md 17 µg / l (1-92 µg / l)
P95 52.01 µg / L
Holz and Wilhelm [47]
R Japan 63 MUGM 8.3 µg / lGM 7.8 mg / lYang et al. [41]
R Korea67Md 5.1 µg / gK (0.9-16.4 µg / gK)
P95 11.2 µg / gK
Kim et al. [71]
R Korea 41-GM 5.0 µg / gKNan et al. [72]
R, NR USA983Md 4.4 µg / l ≪ 1-2500 µg / l)
P95 43 µg / l
Md 3.4 mg / l (<1-88 µg / l)
P95 30 µg / l
Hill et al. [43]
R, NR USAfrom 20.11626Md 1.9 µg / l
P95 23 µg / l
Md 2.4 µg / l
P95 28 µg / l
CDC [51]
(R), NR USA6-11 y387Md 1.2 µg / l
P95 12 µg / l
Md 1.7 mg / l
P95 7.7 µg / l
CDC [51]
R, NR Denmark 119Md 2.5 µg / gK-Hansen et al. [73]
28 R, 8 NR Poland 36P95 12.1 µg / gK
GM 9.9 µg / gK
GM 5.8 µg / gKBienik [30]
(Range), GM: geometric mean, Y: years, Md: median, MU: morning urine, N: number of samples examined, NR: non-smoker, P95: 95th percentile, R: smoker, µg / gK: µg / g creatinine , w: female
a) includes in-house control collective in a bitumen processing company,
b) unencumbered control collective,
c) residents of a coking plant who did not differ from the unpolluted control collective with regard to 1-naphthol values,
d) patients in an environmental clinic,
e) residents in the vicinity of a Creosot impregnation system,
f) Residents of a coking plant and unpolluted control collective who did not differ with regard to naphthol values.

Table 3: Brief overview

Investigation mediumparametermethodLimits of quantification
(Naphthalene metabolites)
HPLC fluorescence or GC-MS<5 Ng / l
Reference values: currently not derivable
Orientation values ​​for non-smokers:
1-naphthol <30 µg / l
2-naphthol <20 µg / l
swellexcretionEffects at high exposure
Tobacco smoke, smoked food and food grilled over an open fire, diesel fuel, small combustion systems, traffic, moth protection containing naphthalene, contaminated consumer goodsElimination in the urine with 2 different half-lives (approx. 1-2 or 14-46 h)Hemolytic anemia, respiratory disease, cancer risk
First repeat measurements, whereby the creatinine concentration of the sample should be in the range of 0.5 to 2.5 µ / l. If necessary, determine 1-hydroxypyrene in the urine, evaluate using reference values. If the naphthol values ​​increase again: initiate a search for sources (see above)

As expected, smokers show higher values ​​than non-smokers. In the German studies, the median values ​​for smokers were about 5 times as high as for non-smokers [47, 49]

The smoking status is the dominant influencing variable in the general population not exposed to occupational stress. A meaningful interpretation of the naphthol concentrations in the urine is therefore only possible for non-smokers. From the compiled data it follows that the following concentrations are generally measured in adults who are not occupationally exposed and who do not smoke:

1-naphthol in the urine below 30 µg / l, 2-naphthol in the urine below 20 µg / l.

Because of the small German collectives, these values ​​are subject to considerable uncertainty [47, 49]. The concentrations mentioned reflect the current state of knowledge and serve as a preliminary orientation. Investigations in patients at an environmental outpatient clinic in southern Germany [50] showed lower median values ​​than the other two German studies mentioned.

The data from the USa [51] indicate that the concentrations related to the urine volume in children (investigated collective: 6-n years old) could be somewhat lower. The currently available data from Germany do not allow any valid statements in this regard.

Measures in the event of abnormal measured values

In those cases in which the stated orientation values ​​are exceeded and tobacco smoke can be excluded as a source, control measurements are indicated. In order to be able to better assess the result of a control measurement, it must be ensured that the creatinine concentration of the urine sample is in the range of 0.5 to 2.5 g / l [52].

If multiple, reliable measurements have confirmed an increased naphthol excretion, the causes of this exposure must be determined within the framework of the proportionality. In addition to tobacco smoke, possible sources include indoor air pollution from building materials, naphthalene-containing moth repellants and open fireplaces, as well as the consumption of grilled and smoked food and contact with consumer goods that are contaminated with naphthalene. The latter are e.g. products made of PVC with phthalate plasticizers, which can be contaminated with naphthalene. Leakage in diesel tanks and the use of tar paints should also be considered as possible sources.

The therapeutic external use of ointments containing tar for certain skin diseases can lead to high naphthol concentrations in the urine [53] and must be subjected to an individual risk assessment in each individual case.

It should be expressly pointed out that a priori toxicological assessment is not possible on the basis of the orientation values ​​mentioned.

If there is a suspicion of additional exposure to other PAHs, the determination of the parameter i-hydroxypyrene in the urine should be considered and assessed using the published reference value [54. 55].

Naphthalene is metabolized to 1- and 2-naphthol, which are usually excreted in comparable amounts. In contrast, carbaryl residues on food lead to an isolated increase in the excretion of i-naphthol [56]. This is also to be expected for the use of certain hair dyes that contain i-naphthol. In

In cases in which the concentration of i-naphthol exceeds that of 2-naphthol blatantly (e.g. by a factor of 4-5), abnormal values ​​can usually not be attributed to exposure to naphthalene. This applies analogously to the opposite constellation with an isolated increased 2-naphthol excretion, the causes of which are still unclear.


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