Anosmia after exposure to a pyrethrin-based insecticide: a case report fabriziomaria gobba

506

C A S E   R E P O R T S

International Journal of Occupational Medicine and Environmental Health 2012;25(4):506 – 512

DOI 10.2478/S13382-012-0060-4

ANOSMIA AFTER EXPOSURE TO A PYRETHRIN-BASED 

INSECTICIDE: A CASE REPORT

FABRIZIOMARIA GOBBA and CARLOTTA ABBACCHINI

University of Modena and Reggio Emilia, Modena, Italy  

Chair of Occupational Medicine, Department of Diagnostic, Clinical and Public Health Medicine

Abstract

We present the case of a subject developing anosmia, preceded by nasal transient irritation and short lasting phantosmia and 

torqosmia, upon re-entrance into a room treated with a pyrethrin-based insecticide. The concentration of the insecticide in the 

room is unknown, but relatively high levels are predicted basing upon the modality of exposure and by the irritation symptoms 

in the subject. Despite corticosteroids therapy, anosmia has persisted unmodified for more than three years; according to, 

and based on evidence in the literature on olfactory disturbance prognosis, anosmia in this patient is likely to be permanent. 

The significance of this case report is related to the current wide use of insecticides containing pyrethrin and pyrethroids and 

highlights the need for more adequate attention to lowering airborne concentrations of pyrethrins and pyrethroids prior to 

re-entering the treated rooms. In particular, in a closed space sprayed with pyrethrins and pyrethroids insecticide, any irritant 

symptoms and/or dysosmia should be immediately considered relevant warning signs, and must be avoided. 

Key words:

Insecticides exposure, Adverse effects, Pyrethrins, Irritant symptoms, Anosmia

Received: January 12, 2012. Accepted: September 26, 2012.

Address reprint request to F. Gobba, Chair of Occupational Medicine, Department of Diagnostic, Clinical and Public Health Medicine, Via Campi 287-41125 Modena, 

Italy (e-mail: [e-mail]).

BACKGROUND 

Olfactory impairment has historically been overlooked 

as a problem of public health, and has been frequently 

relegated to the status of a mere annoyance, rather than 

a medical disability. However, olfaction is a critical physio-

logic function in humans: normal perception is fundamen-

tal for detection of many warning signals of life-threa-

tening situations, such as smoke, spoiled food, dangerous 

chemicals, gas leaks, etc.: in some studies a relation was 

observed between the degree of olfactory loss and the risk 

of hazardous events [1,2]. Furthermore, nutritional status 

and many other topics related to the quality of life may 

be affected by the impairment of olfactory function [3], 

and loss of smell is accompanied by an increased risk of 

depression [4]. In addition, it is present in up to the 90% 

of Parkinson’s Disease patients, and is considered one 

of the most prevalent troublesome nonmotor problems 

in this disease [5].

The prevalence of subjects with the impairment of olfac-

tory perception in the general population ranges from 

1 up to 20% [6–8]. However, this is likely an underesti-

mation, especially considering the fact that many people 

with a reduced olfactory sensitivity are unaware of their 

situation [3]. 

The terms ‘anosmia’ and ‘hyposmia’ are usually applied 

to describe the absence or diminished smell function, 

respectively (even if, apparently, ‘anosmia’ has been occa-

sionally used in a broad sense, to include both conditions). 

‘Dysosmia’ is an altered perception of smell and includes 

‘cacosmia’ (altered perception of a stimulus present) and 

Nofer Institute of Occupational Medicine, Łódź, Poland

ANOSMIA ANd PYRETHRIN-BASEd INSECTICIdE EXPOSURE

           C A S E   R E P O R T S

IJOMEH 2012;25(4)

507

Furthermore, in a large proportion of olfactory disorders 

no  specific  cause  is  identified.  Approximately  10–25% 

of all smell impairments in the general population are cur-

rently classified as ‘idiopathic’ [6,9,21]; some of these idio-

pathic olfactory losses are likely to be related to unnoticed 

chemical exposure. 

Accordingly, more attention is needed to airborne chemi-

cals as a cause of olfactory dysfunction [1,20]. 

As there is no particular test for environmental toxins as 

a source of olfactory loss, the causative agent is commonly 

based on a detailed history: a significant exposure history 

in an absence of other common causes of olfactory loss 

strengthens an argument for environmental toxins as the 

etiology of the smell loss.

We describe here a case of anosmia following an acute 

exposure to a pyrethrin-based insecticide. 

CASE PRESENTATION AND DISCUSSION 

In May 2008, in a large Hospital in North Italy a wall and 

a part of the examining room used by a 50-year-old male 

physician was infested by parasites coming from the out-

side through the windows. To disinfest the parasites, an 

exterminating company sprayed the room with an insecti-

cide composed of a mixture of pyrethrin, 2-butoxiethanol 

and 2-etil 6-propilpiperonil ether dissolved in water. The 

quantity of the insecticide sprayed is unknown, as are its 

airborne concentrations. After the treatment, the door 

and the 3 windows of the room were left shut, as requested 

by the exterminating company.

The subject, as indicated, returned to work in the 

room 24 hours after the treatment, but no forced exchange 

of air was provided prior to the work. For practical reasons, 

only one of the windows could be left open; it was a ‘vasistas’ 

type window, i.e. a small secondary window opening in the 

window. Thus the flow of indoor air was limited. 

Upon entering the room, the subject immediately per-

ceived an intense disagreeable odour, qualitatively 

‘phantosmia’ (odour perception without stimulus). The sen-

sation of the smell of burnt or metallic smell in the absence 

of the stimulus is sometimes defined as ‘torqosmia’ [9]. 

In a large Swedish study, overall prevalence of hypos-

mia and anosmia in the general population were 13.3% 

and 5.8%, respectively [6], and similar proportions were 

reported in Germany [8]. 

One of the main factors related to olfactory dysfunction is 

aging [11], but several other causes are also known. Among 

the most important are: head trauma [12], infections of the 

upper respiratory tract, nasal and paranasal sinus diseas-

es [13] and tumours [14]. Loss of olfactory function can 

be also related to neurodegenerative disease [15], and, in 

fact, it is an early sign of Parkinson’s disease [5,16,17] and 

Alzheimer’s disease [18], and can also be associated with 

several psychiatric diseases, such as schizophrenia [14].

Other uncommon possible causes, including endocrine 

conditions, immune disorders, pharmaceutical drugs con-

sumption, cocaine addiction and congenital causes have 

also been reported [1,9].

Smell dysfunction is a common outcome of exposure to 

some airborne chemicals. This is not unexpected, as recep-

tors of the olfactory neurons are relatively unprotected. 

A comprehensive list, including more than 120 substances, 

including drugs, possibly affecting the olfactory function 

was published several years ago by Amoore [19], however 

several new chemicals have been recently added [1]. 

A relevant limit in the current knowledge on the effect 

of chemicals on olfactory function is that, up to now, 

it is mainly based on animal studies, on occasional case 

reports and on the relatively few epidemiological studies 

in workers [1,20]. Accordingly, the prevalence of olfactory 

dysfunction caused by airborne exposure to chemicals is 

difficult to estimate; values ranging 0.5 up 5% of all ol-

factory disorders have been proposed [21–23], but these 

data may be an underestimation. In effect, one theory for 

age-related loss of olfaction invokes cumulative damage 

to the epithelium from the lifetime toxic exposures [23]. 

C A S E   R E P O R T S            

F. GOBBA and C. ABBACCHINI

IJOMEH 2012;25(4)

508

otolaryngologist and seek medical assistance. According 

to medical history, findings of the visit, including rhinos-

copy, did not reveal overt significant clinical picture; ac-

cordingly symptom was regarded as the consequence 

of  a  non-specific  irritation  related  to  inhalation  of  the 

insecticide; due to the informal circumstances no written 

medical report including a description of the conditions 

of the mucosa was prepared. The patient was prescribed 

per os corticosteroids, nasal spray corticosteroids and na-

sal washing cycles.

Despite the treatment, anosmia and hypogeusia per-

sisted for several months. The corticosteroids therapy 

was  repeated,  but  without  significant  improvement.  In 

Autumn 2010, 20 months after the exposure, the subject 

once again contacted the otorhinolaryngologist. The lat-

ter explained to the patient that he suspected a permanent 

nervous damage and advised further medical examinations. 

In October 2010, a neuropsychological evaluation was per-

formed: no neurodegenerative diseases (as amyotrophic 

lateral sclerosis, Alzheimer’s or Parkinson’s diseases) 

or  psychiatric  diseases  were  identified.  During  the  visit, 

a clinical odour identification test, based on recognition 

of solutions of 15 substances of common use (lavender, 

sage, rosemary, mint, mandarin, rose, aniseed, coconut, 

coffee, ammonia, strawberry, almond, banana and vanilla) 

was performed, revealing anosmia (0/15 substances identi-

fied); the test was not aimed at an evaluation of thresh-

olds, so suprathreshold concentrations of the odorants 

were tested. No other significant signs or symptoms were 

observed during neuropsychological evaluation. Based on 

these finding, the diagnosis was “anosmia probably related 

to a nervous receptorial damage”. 

In  November  2010,  a  rhinofibroscopia  failed  to  identify 

anatomical alterations which could explain anosmia. The 

morphology of nasal sinus was normal, and significant in-

flammatory aspects were absent.

In December 2010, a head magnetic resonance im-

aging (MRI) showed normality of the dimension 

described as ‘sweetish’. Within a few minutes, subjective 

nasal irritation, but no nasal discharge, appeared. In the 

meantime the subject also noted a progressive reduction 

in odour perception. Despite the symptoms, the subject 

worked for about 6 hours in the room. According to the 

medical history, the subject had never smoked, and had 

no upper respiratory tract infections, allergies or known 

nasal sinus diseases ongoing, or in the previous weeks. The 

presence of potential allergens or irritants in the examin-

ing room can be ruled out as medical visit to outpatients, 

but not medical treatments, were performed. Obviously, 

smoking was strictly forbidden in the whole area.

Some of the patients examined by the physician during the 

day, in the course of the visit spontaneously referred the 

perception of an intense odour, but none complained of 

adverse effects, possibly due to the very limited time they 

spent in the room. 

The subjective intense nasal irritation experienced by the 

physician persisted also at home, after work and remained 

substantially unmodified next morning, when the subject 

went to work.

Over the next few days, the physician carried on his duties 

in the same examining room for approximately 6 hours/

day. The subjective nasal irritation was progressively 

reduced, but phantosmia persisted, with progressive ap-

pearance of torqosmia (described as a subjective percep-

tion of an intense, unpleasant smell of burnt). At the same 

time, the perception of odour progressively decreased, 

and, within a few days, complete anosmia appeared. Con-

comitantly, taste was also largely compromised. 

At the anamnesis, no upper respiratory infections devel-

oped, or head trauma occurred at the time of inhalational 

exposure to the insecticide, or in the weeks before.

Over the next few days the subject considered the symp-

toms  as  nonspecific,  transitory  effect  of  irritation.  Ac-

cordingly, no medical advice was requested. Approxi-

mately one month after the exposure the persistence of 

anosmia convinced the physician to contact a colleague 

ANOSMIA ANd PYRETHRIN-BASEd INSECTICIdE EXPOSURE

           C A S E   R E P O R T S

IJOMEH 2012;25(4)

509

course, suggest a role of insecticide inhalation as the prin-

cipal cause of his olfactory dysfunction.

The main active components of the insecticide were py-

rethrins. In the formulation, 2-etil 6-propilpiperonil ether 

and 2-butoxiethanol were also present, but these com-

pounds can be considered less relevant from the toxico-

logical point of view, even if butoxiethanol is moderately 

irritant following inhalational exposure [25].

Pyrethrins, the active insecticidal compounds of pyrethrum 

derived from the flowers of Chrysanthemum cinerariaefolium 

and Chrysanthemum cineum, and their synthetic analogues 

and derivatives, the pyrethroids, are commonly used due 

to their rapid paralyzing activity in insects, but low environ-

mental persistence and low general toxicity to mammals. 

In humans they are considered to be one of the least poison-

ous insecticides [26]. A few cases of systemic poisoning due 

to pyrethrins and pyrethroids have been reported, almost all 

related to their effect on the nervous system [27]. The main 

mechanisms of toxicity of pyrethrin and pyrethroids in mam-

mals are well documented, affecting sodium channels and 

cellular depolarization [28,29]. The effect on sodium chan-

nel is related to the loss of olfaction in insects [30]; a critical 

role for sodium channels in olfactory function has also been 

recently documented in humans [31].

In reported cases of inhalational exposure in humans, re-

spiratory irritation is the most common effect, but hyper-

sensitivity pneumonitis have also been described [26]. The 

signs of respiratory irritation, such as shortness of breath, 

cough,  and  congestion,  were  reported  among  office 

workers, commencing upon entry into a building that had 

been 2 days previously treated for termites with a cyper-

methrin based insecticide [32].

A problem in our study is that the environmental concentra-

tion of pyrethrins (and of 2-butoxiethanol and 2-etil 6-pro-

pilpiperonil ether) in the subject’s inhaled air is unknown, 

nor it is possible to reliably estimate it. Concentrations in 

the μg/m

3

 range can be expected after treatment analogous 

to the one carried out in the case described herein [33] 

and morphology of the ventricular system, regular sub-

aracnoidal spaces over and undertentorial, and normal 

signal from cerebral parenchyma; a mild hypertrophy of 

inferior turbinates was observed. 

In January 2011, a revised diagnosis was issued. As no 

known common causes of anosmia were noted at the an-

amnesis and physical examination, and the results of neu-

ropsychological and ear, nose and throat (ENT) specialist 

visits and MRI did not show specific pathological condi-

tions inducing anosmia, the final diagnosis was “anosmia 

probably related to a nervous receptorial damage”. 

The significant acute exposure and the evolution of the 

symptoms, in an absence of other common causes of olfac-

tory loss, support the role of insecticide inhalation in the 

etiology. The mild hypertrophy of inferior turbinates ob-

served at MRI may represent an unspecific consequence 

of an inflammatory response to the insecticide exposure.

Currently (September 2011), the symptoms are un-

changed: due to their long persistence (more than two 

years), and based on data from the literature on progno-

sis of patients with olfactory disturbances [24], anosmia in 

the subject is likely to remain permanent. No symptoms 

or signs of any other disease are currently present. 

In the case presented here, we describe a subject develop-

ing permanent anosmia, preceded by nasal irritation and 

short lasting phantosmia and torqosmia, after working 

several hours in a room treated with an insecticide sprayed 

to control infestation of parasites. 

The results of medical examinations, including ENT spe-

cialist repeated visits, neuropsychological evaluation and 

head MRI, failed to illuminate the presence of any of the 

principal known causes of anosmia, including head trau-

ma, upper respiratory infections, tumours, neurodegen-

erative (e.g. Parkinson’s or Alzheimer’s disease) or psy-

chiatric diseases, endocrine conditions, immune disorders, 

and use of pharmaceutical drugs inducing olfactory loss. 

Consistent with the course of the patient’s clinical pre-

sentation, the time sequence of symptoms and the clinical 

C A S E   R E P O R T S            

F. GOBBA and C. ABBACCHINI

IJOMEH 2012;25(4)

510

cells of human nasal mucosa has been observed [37]. These 

studies lend support to the hypothesis of the insecticide 

exposure as the primary cause for the permanent anosmia 

observed.

As no particular test is available to confirm the role of en-

vironmental toxins as a source of olfactory loss, the diag-

nosis is mainly based on an accurate history showing a sig-

nificant exposure, a coherent time course and the lack of 

other common causes: all these criteria have been met in 

this case report. Accordingly, we conclude that the anos-

mia observed in the physician is very likely related to the 

exposure to inhalation of relatively high concentrations of 

pyrethrins, even if the role of 2-butoxiethanol, 2-etil 6-pro-

pilpiperonil ether, or a synergistic effect of co-exposure 

cannot be totally discarded.

CONCLUSIONS 

The case discussed herein shows the possibility that 

an acute inhalational exposure to a pyrethrin-based insec-

ticide can induce permanent anosmia. The environmental 

concentration of the insecticide is unknown, but relatively 

high levels are suggested by exposure modality (spraying 

for parasites disinfestations, no forced exchange of air be-

fore re-entering the room and limited exchange of indoor 

air), and by the irritant effect reported by the subject. 

This case report is of significance, as pyrethrins and py-

rethroids are ubiquitously applied in many commercial 

products used to control insects, including household 

insecticides, pet sprays and shampoos, potentially involv-

ing an exposure in both, workers and general popula-

tion. Our case report emphasizes the need for focused 

attention on lowering pyrethrins’ concentrations in the 

air to safe levels as well as the importance of adequate 

exchange of air, prior to re-entering the rooms sprayed 

with the insecticide, and for considering the appearance 

of any subjective irritant symptoms after re-entrance as 

a relevant warning sign. 

but higher concentrations, related e.g. to a wrong or in-

adequate spraying procedure are possible, and the strong 

nasal irritation referred by the subject is coherent with this 

hypothesis. It is also difficult to evaluate the real duration 

of the inhalation exposure; in any case a significant 6-hour 

exposure during the first day is likely, especially considering 

the irritant symptoms in the patient, as well as complaints 

by other patients about the presence of odour. Exposure 

to significant concentrations over the next few days is less 

likely, but the persistence of undegraded active compounds 

of the insecticide on the walls, furniture, door handles and 

other objects, may have contributed to its persistence in the 

atmosphere of the room. Nevertheless, the possible risk 

cannot be reliably evaluated. 

To our knowledge, at least one case of permanent anosmia 

following inhalation of a spray insecticide containing py-

rethrum has been previously reported. Analogous to the 

case reported herein, the symptoms appeared immediate-

ly after the first use of the insecticide. An allergic rhinitis 

was diagnosed based on positive skin test, but the conclu-

sion of the Author was that “It would seem probable that 

the pyrethrum has damaged the olfactory nerve endings 

in the nasal mucosa” [34]. In the case described here, the 

skin test was not available, but symptoms do not suggest 

an allergic rhinitis. 

A large collection of literature suggest that the olfactory 

neuroepithelium is susceptible to environmental expo-

sures to several chemicals [20], and acute and chronic ex-

posures can induce both temporary as well as permanent 

olfactory loss [19]. Changes in the olfactory mucosa were 

described in many experimental studies in animals, includ-

ing degeneration and necrosis of olfactory neurons and 

other neurotoxic effects [35].

The capacity for cellular reconstitution after lesion of the 

olfactory system is remarkable, but recovery can fail in 

severely injured areas, which subsequently reconstitute 

as aneuronal respiratory epithelium [36]. Furthermore, 

a strong genotoxic effect of pyrethrins on the epithelial 

ANOSMIA ANd PYRETHRIN-BASEd INSECTICIdE EXPOSURE

           C A S E   R E P O R T S

IJOMEH 2012;25(4)

511

11.  Murphy C, Schubert CR, Cruickshanks KJ, Klein BE, 

Klein R, Nondahl DM. Prevalence of olfactory impairment in 

older adults. JAMA 2002;288:2307–12. 

12.  Ottaviano G, Marioni G, Marchese Ragona R, Trevisan CP, 

de Filippis C, Staffieri A. Anosmia associated with hearing 

loss and benign positional vertigo after head trauma.  Acta 

Otorhinolaryngol Ital 2009;29:270–3.

13.  Wang JH, Kwon HJ, Jang YJ. Detection of Parainfluenza Vi-

rus 3 in Turbinate Epithelial Cells of Postviral Olfactory Dys-

function Patients. Laryngoscope 2007;117:1445–9.

14.   Doty  RL. Studies of Human Olfaction from the Univer-

sity of Pennsylvania Smell and Taste Center.  Chem Sens-

es 1997;22:565-86.

15.   Hawkes  C.  Olfaction in Neurodegenerative Disorder. Mov 

Disord 2003;18:364–72. 

16.  Ponsen MM, Stoffers D, Booij J, van Eck-Smit BLF, 

Wolters EC, Berendse HW.  Idiopathic Hyposmia As a Preclin-

ical Sign of Parkinson’s Disease. Ann Neurol 2004;56:173–81.

17.  Haehner A, Hummel T, Hummel C, Sommer U, Junghanns S, 

Reichmann H. Olfactory Loss May Be a First Sign of Idiopathic 

Parkinson’s Disease. Mov Disord 2007;22:839–42. 

18.  Bacon AW, Bondi MW, Salmon DP, Murphy C. Very  early 

changes  in  olfactory  functioning  due  to  Alzheimer  disease 

and the role of apolipoprotein E in olfaction. Ann N Y Acad 

Sci 1998;855:723–31. 

19.   Amoore  JE.  Effects of chemical exposure on olfaction in hu-

mans. In: Barrow CS, editor. Toxicology of the nasal pas-

sages. Washington, DC, USA: Hemisphere Publishing; 1986. 

p. 155–90.

20.   Gobba  F.  Olfactory toxicity: long-term effects of occupational 

exposures. Int Arch Occup Environ Health 2006;9:322–31.

21.  Mott AE, Leopold DA. Disorders in taste and smell. Med 

Clin North Am 1991;75:1321–53.

22.  Heiser  C, Grupp K, Hörmann K, Stuck BA. Loss of olfac-

tory function after exposure to barbituric acid.  Auris Nasus 

Larynx 2010;37:103–5. 

23.  Upadhyay UD, Holbrook EH. Olfactory loss as a result 

of toxic exposure. Otolaryngol Clin N Am 2004;37:1185–207.

ACKNOWLEDGEMENTS 

We would like to thank Dr. Michael Aschner for his invaluable 

comments and revision of the manuscript, and the Patient, that 

consented the presentation of the case.

REFERENCES

1.   Doty  RL.  Olfactory dysfunction and its measurement 

in the clinic and workplace. Int Arch Occup Environ 

Health 2006;79:268–82.

2.  Santos DV, Reiter ER, DiNardo LJ, Costanzo RM. Haz-

ardous Events Associated With Impaired Olfactory Function. 

Arch Otolaryngol Head Neck Surg 2004;130:317–9.

3.  Frasnelli J, Kummel T. Olfactory dysfunction and daily life. 

Eur Arch Otorhinolaryngol 2005;262:231–5.

4.  Temmel AFP, Quint C, Schickinger-Fischer B, Klimek L, 

Stoller E, Hummel T. Characteristics of Olfactory Disorders in 

Relation to Major Causes of Olfactory Loss. Arch Otolaryngol 

Head Neck Surg 2002;128:635–41.

5.  Haehner A, Hummel T, Reichmann H. Olfactory Loss 

in Parkinson’s disease [cited 2011 Nov 25].  Parkinsons 

Dis 2011;2011:450939.  Epub  21  Apr  2011.  Available  from 

URL: http://www.hindawi.com/journals/pd/2011/450939.

6.  Bramerson A, Johansson L, Ek L, Nordin S, Bende M. Prev-

alence of Olfactory Dysfunction The Skovde Population-Based 

Study. Laryngoscope 2004;114:733–7. 

7.  Hoffman HJ, Ishii EK, MacTurk RH. Age-related changes in 

the prevalence of smell/taste problems among the United States 

adult population. Results of the 1994 disability supplement to 

the National Health Interview Survey (NHIS). Ann NY Acad 

Sci 1998;855:716–22.

8.  Landis BN, Konnerth CG, Hummel T.  A study on the frequen-

cy of olfactory dysfunction. Laryngoscope 2004;114:1764–9.

9.   Schiffman  SS.  Taste and smell losses in normal aging and dis-

ease. JAMA 1997;278:1357–62.

10.  Cullen MM, Leopold DA. Disorders of smell and taste. Med 

Clin North Am 1999;83:57–74.

C A S E   R E P O R T S            

F. GOBBA and C. ABBACCHINI

IJOMEH 2012;25(4)

512

30.  Kadala A, Charreton M, Jakob I, Le Conte Y, Collet C. 

A use-dependent sodium current modification induced by type 

I pyrethroid insecticides in honeybee antennal olfactory recep-

tor neurons. NeuroToxicology 2011;32:320–30. 

31.  Weiss J, Pyrski M, Jacobi E, Bufe B, Willnecker V, Schick-

et B, et al. Loss-of-function mutations in sodium channel 

Nav1.7 cause anosmia. Nature 2011;472:186–90. 

32.   Lessenger  JE.  Five office workers inadvertently exposed to cy-

permethrin. J Toxicol Environ Health 1992;35:261–7.

33.  Siebers J, Mattusch P. Determination of airborne resi-

dues in greenhouses after application of pesticides. Chemo-

sphere 1996;33:1597–607.

34.  Brain DJ. Toxic insecticides. Br Med J 1965;1(5432):450.

35.  Duncan HJ, Smith DV. Clinical disorders of olfaction. 

In: Doty RL, editor. Handbook of olfaction and gustation. 

New York: Marcel Dekker; 1995. p. 345–65. 

36.  Jang W, Youngentob SL, Schwobje JE. Globose Basal Cells 

Are Required for Reconstitution of Olfactory Epithelium after 

Methyl Bromide Lesion. J Comp Neurol 2003;460:123–40. 

37.  Tisch M, Faulde MK, Maier H. Genotoxic Effects of Penta-

chlorophenol, Lindane, Transfluthrin, Cyfluthrin, and Natural 

Pyrethrum on Human Mucosal Cells of the Inferior and Middle 

Nasal Conchae. Am J Rhinol 2005;19:141–51.

24.  London B, Nabet BA, Fisher AR, White B, Sammel MD, 

Doty RL. Predictors of Prognosis in Patients with Olfactory 

Disturbance. Ann Neurol 2008;63:159–66.

25.  World Health Organization. Concise International Chemi-

cal Assessment Document no.10. 2-Butoxyethanol [cited 2012 

Jan 12]. Geneva: World Health Organization; 1998. Avail-

able from URL: http://www.who.int/ipcs/publications/cicad/

cicad_10_revised.pdf.

26.  U.S. Department Of Health And Human Services. Public 

Health Service. Agency for Toxic Substances and Disease 

Registry (ATSDR). Toxicological  profile  for  pyrethrins  and 

pyrethroids  [cited 2012 Jan 12].  Atlanta, GA, USA: U.S. 

Department of Health and Human Services, Agency for 

Toxic Substances and Disease Registry; 2003. Available from 

URL: http://www.atsdr.cdc.gov/ToxProfiles/tp155.pdf.

27.  Ray D, Fry JR. A reassessment of the neurotoxicity of pyre-

throid insecticides. Pharmacol Ther 2006;111:174–93. 

28.   Soderlund DM. Molecular mechanisms of pyrethroid insec-

ticide neurotoxicity: recent avances [cited 2012 Jan 12]. Arch 

Toxicol 2012;86(2):165–81. Available from URL: http://www.

springerlink.com/content/kx4322m77815h184/fulltext.pdf. 

29.  Du Y, Khambay B, Dong K. An important role of a pyre-

throid-sensing residue. F1519 in the action of the N-alkylamide 

insecticide BTG 502 on the cockroach sodium cannel. Insect 

Biochem Mol Biol 2011;41:446–50. 

This work is available in Open Access model and licensed under a Creative Commons Attribution-NonCommercial 3.0 Poland License – http://creativecommons.org/

licenses/by-nc/3.0/pl/deed.en.