Re: What makes you sneeze the most?

The question of what makes one sneeze the most is interesting.
The question your asking," What targets sneezes the most of these: pollen,
pepper, cold, flowers, dust? " Sounds like a fun science project. It would
be interesting to know your results. 

It might be hard to determine the main cause since people show many
differences in sneezing. Some people are allergic to pollens from some
plants and other people are not. So a person that is sensitive will sneeze
and one that is not probably will not sneeze. Pepper seems to work on many
people. You do have to realize there are many different types of pepper. I
guess you could try normal table black pepper. But then again some people
might have an allergy to it and sneeze a lot while others will not.

I did a quick search on this topic by using a searching place for such
information. This way one can look through medical and scientific research
publications.
I typed in " sneeze mechanisms " in a search engine called PubMed.
You can find this on line at :  http://www.ncbi.nlm.nih.gov/entrez/query.fcgi
or at  http://www.nlm.nih.gov/

Some studies that address parts of your question are shown below.

One article discusses how plant biologists  are looking at your same
question. I could not obtain the copy of the full study but I provided you
with the name and title of the study. 


Australas Nurses J. 1976 Mar;4(9):11.	
Botanists probe mystery of 'sneeze-makers'.

Another article states that having an allergic response to particular
compounds is what causes people to sneeze.

Sneezing. J Otolaryngol. 1994 Apr;23(2):125-9.
Leung AK, Robson WL.
Department of Pediatrics, University of Calgary, Alberta, Canada.
Sneezing is a common symptom with numerous causes. Allergic rhinitis is the
most common cause of persistent or frequent sneezing. The evaluation of a
patient with sneezing should be individualized according to the duration
and severity of the symptom. Laboratory tests are not necessary in the
majority of patients, since the diagnosis is usually obvious from the
history and physical examination. The treatment of persistent or recurring
sneezing should be directed at the cause whenever possible. Firm pressure
on the nose or lip may be helpful to abort an attack of sneezing.

Another article states how sneezing is a defense mechanism to help make
sure your airways are clear so you can breath.

Pulmonary and respiratory tract receptors. J Exp Biol. 1982 Oct;100:41-57.

Widdicombe JG.

Nervous receptors in the lungs and respiratory tract can be grouped into
four general categories. 1. Deep, slowly adapting end-organs, which respond
to stretch of the airway wall and have large-diameter myelinated fibres;
those in the lungs are responsible for the Breuer-Hering reflex. 2. Endings
in and under the epithelium which respond to a variety of chemical and
mechanical stimuli (i.e. are polymodal), usually with a rapidly adapting
discharge, and with small-diameter myelinated fibres; they are responsible
for defensive reflexes such as cough and sneeze, and for the reflex actions
to inhaled irritants and to some respiratory disease processes. 3.
Receptors with nonmyelinated nerve fibres which, being polymodal, are
stimulated by tissue damage and oedema and by the mediators released in
these conditions; these receptors may be similar in function to
'nociceptors' in other viscera, and set up appropriate reflexes as a
reaction to respiratory damage. 4. Specialized receptors such as those for
taste and swallowing, and those around joints and in skeletal muscle.
Stimulation of any group of receptors may cause reflex changes in breathing
(including defensive reflexes), bronchomotor tone, airway mucus secretion,
the cardiovascular system (including the vascular bed of the airways),
laryngeal calibre, spinal reflexes and sensation. The total pattern of
motor responses is unique for each group of receptors, although it is
probably unusual for one type of receptor to be stimulated in isolation.
The variety of patterns of motor responses must reflect the complexity of
brainstem organization of these systems.


I found it interesting that some people sneeze when they talk. 

Intractable sneezing as a conversion symptom. Psychosomatics. 1995
Mar-Apr;36(2):103-12.

Fochtmann LJ.
Department of Psychiatry and Behavioral Sciences, State University of New
York at Stony Brook 11794-8101.

A literature review of reported cases of intractable sneezing reveals that
intractable sneezing typically occurs in children or adolescents and is a
manifestation of conversion disorder. Analysis of these cases demonstrates
a number of features that are helpful in differentiating psychogenic from
organic sneezing. Also discussed are aspects of patient management once a
diagnosis of conversion disorder is established.

Lastly I found a more in depth article that discusses a number of factors
related to sneezing. I copied some of the text from this article for you.
Have fun on your science project.
All the best,
Robin

Itch, sneeze and wheeze: the genetics of atopic allergy . J R Soc Med. 2002
Jan;95(1):14-7.
Aziz Sheikh MRCP MRCGP   
Department of Primary Health Care and General Practice, Imperial College of
Science, Technology and Medicine: Charing Cross Campus, St Dunstan's Road,
London W6 8RP, UK 
Introduction
In many developed countries over one-fifth of the population are affected
by one or more atopic allergic disorders. Several time-trend studies
indicate that the prevalence and severity of eczema, rhinitis, and asthma
is rapidly increasing1,2,3; and this observation, coupled with the
widespread geographical variations in disease prevalence noted by the
International Studies of Asthma and Allergies in Childhood, points to the
strong contribution of environment to the aetiology4. However, the tendency
of atopic allergic conditions to cluster both within individuals and within
families suggests that genetic factors are also important. 
Asthma is a condition characterized by reversible airflow obstruction and
lower airway hyper-responsiveness, which results in episodic cough, wheeze
and shortness of breath5. Inflammation of the nasal passages, manifesting
as sneezing, nasal blockage and itchy rhinorrhoea, is the symptom complex
known as rhinitis6. Eczema is the commonest cause of dermatitis in
developed countries and affects approximately 20% of the general
population7. The distribution of eczematous lesions varies with age, the
face and trunk being most affected in infants whereas the flexor aspects of
the limbs are typically affected in older children and adults. Advances in
our understanding of the immunobiology of these disorders have shown them
to have a common pathophysiological basis—an exaggerated and inappropriate
IgE-mediated inflammation in response to allergen exposure—referred to as
atopy8. The absence of objective and reliable criteria for defining either
atopy or the atopic allergic conditions (eczema, rhinitis and asthma) has
been and continues to be a major obstacle to establishing the genetic basis
of atopic disorders. 
This review is based in the main on articles retrieved by searching
Medline, EMBASE and OMIM (Online Mendelian Inheritance in Man) electronic
databases. Key websites of possible relevance were also searched9,
including those of the British Society for Human Genetics10, the European
Society for Human Genetics11, and the Human Mutation Database12. Allergy
and genetic texts were consulted, and the analysis was helped by personal
contacts with several experts on human genetics. 

Evidence for familial clustering
Anecdotal evidence for familial clustering of atopic disorders dates back
to the early twentieth century13. More rigorous evidence emerged in the
latter half of the century, when many studies showed that relatives of
atopic patients had a higher prevalence of atopic allergic disorders than
did relatives of matched non-atopic patients14. Research subsequently
revealed that atopic individuals and couples were substantially more likely
than non-atopics to give birth to children with one or more atopic
disorders15. Although these findings provided strong and consistent
evidence for the importance of shared familial characteristics, they were
in themselves insufficient to prove genetic causation. 
Studies in twins are a good way to disentangle genetic and environmental
factors in families, and early work in small numbers showed that
concordance rates for atopic disorders were higher for monozygotic (MZ)
than for dizygotic (DZ) twins14. These findings were replicated in several
larger studies conducted in various population groups. The most notable was
Edfors-Lubs's study of 7000 Swedish twin pairs, in which the MZ versus DZ
concordance rates were: asthma 19.0% vs 4.8%; rhinitis 21.4% vs 13.6%;
eczema 15.4% vs 4.5%16. Work by Hanson and colleagues, comparing serum IgE
levels in MZ and DZ twins reared together and apart, was another landmark
in familial studies: MZ twins had consistently stronger correlation
coefficients for serum total IgE than did DZ twins17. In addition, MZ twins
showed over 70% concordance for specific IgE response to one or more common
aeroallergens; however, the finding that almost one-third of MZ twins were
discordant indicated that sensitization through environmental exposure was
also aetiologically important. 
Segregation analysis
Segregation analysis, or the study of trait distributions in families, has
often been a key step in elucidating the genetic basis for disease,
allowing testing to see whether the pattern of phenotype distribution
within families is consistent with a known genetic model18. But in common
multifactorial and heterogeneous disorders this can be a hazardous
undertaking. Results to date from such studies have been inconsistent and
confusing. Using complex segregation analysis techniques for studying IgE
concentrations in 173 families, Gerard and colleagues concluded that the
regulatory locus for IgE occupied two alleles, with the dominant allele
suppressing persistently high levels of IgE19. The observation that 90% of
atopic asthmatics in 239 members of forty nuclear families had an atopic
parent led Cookson and Hopkin to suggest a dominant model of inheritance
for propensity to produce an exaggerated IgE response20. Other Mendelian
models proposed have included autosomal recessive inheritance, autosomal
dominant inheritance with incomplete penetrance, codominance, and dominant
inheritance through the maternal line21. Opinion has lately converged on
the view that several genes interact to determine liability to disease
(polygenic inheritance). Empirical support for this suggestion comes from
the findings of Xu and colleagues, who, studying serum total IgE data in 92
Dutch families, found that two-locus segregation analysis gave a better fit
than did a one-locus model22. 
An additional layer of complexity comes from the increasing evidence that
inheritance of atopic disorders is end-organ specific—i.e. for the skin
(eczema), nose (rhinitis) and airways (asthma)23. The possibility is thus
raised that, although inheritance of an exaggerated IgE response may
underlie all these conditions, separate genes predispose to specific
clinical manifestations of the allergic phenotype.