Releases Saturday 12 February 2000
No 7232 Volume 320
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(1)
FOOD HYGIENE AND DECLINE IN OROFECAL
INFECTIONS
MAY UNDERLIE EPIDEMIC OF
ASTHMA AND
RHINITIS IN DEVELOPED WORLD
(2) RISK
OF LUNG CANCER FROM PASSIVE
SMOKING MAY
HAVE BEEN OVERSTATED
(1) FOOD HYGIENE
AND DECLINE IN OROFECAL
INFECTIONS MAY UNDERLIE EPIDEMIC OF
ASTHMA AND RHINITIS IN DEVELOPED WORLD
(Exposure to foodborne and orofecal
microbes versus
airborne viruses in relation to
atopy and allergic asthma:
epidemiological study)
http://www.bmj.com/cgi/content/full/320/7232/412
A decline in orofecal infections and a
westernised, semisterile
diet may be the root of the epidemic of
allergic asthma and
rhinitis [inflammation of the mucous membrane
that lines the
nose] in developed countries, claim researchers
from Italy in
this week's BMJ.
The theory that some infections in early
childhood may
prevent atopy [a predisposition to allergic
reactions] has been
hotly debated and the type of infections
that may be involved
is still unknown. Dr Paolo Matricardi
and colleagues in Rome
investigated how exposure to foodborne
and orefecal
microbes (such as H pylori and the hepatitis
A virus) as
opposed to airborne viruses (such as measles,
mumps and
chickenpox) was associated with a reduced
prevalence of
atopy and respiratory allergies.
Matricardi et al conducted the research
of Italian Armed
Forces in collaboration with the Consiglio
Nazionale delle
Ricerche and the Istituto Superiore di
Sanit in Rome. They
studied 1659 airforce cadets, aged 17-24
years and
examined in depth 240 atopic and 240 non-atopic
individuals. A history of allergic rhinitis
or asthma and
sensitivity to airborne allergens was
detected. They found that
people who had been more exposed to microbes
transmitted
orally were less likely to suffer from
respiratory allergy.
However, the same association was not
evident in those who
had been infected with airborne viruses.
The authors say that this is the first
comparative study
showing that orofecal and/or foodborne
microbes are better
candidates than airborne respiratory viruses
as determinants
of an atopy "protective" effect. H pylori
and Hepatitis A are
probably not directly involved in protection
from atopy, say
Matricardi et al. Nevertheless, the inverse
association of
atopy with this category of microbes seems
to suggest that
there is a role played by the gut-associated
lymphoid tissue,
where microbial stimulation is required
to develop immune
responses against allergens, they say.
The authors caution that further studies
are required to verify
their findings, however, it is not inconceivable
that we may
soon use certain microbes to prevent atopy
without causing
infectious disease. "We must improve hygiene
to reduce the
impact of infectious diseases," Matricardi
adds, "but at the
same time, we must learn how to safely
'train' our immune
system, especially during infancy, in
order to prevent allergy."
Contact:
Dr Paolo Matricardi, Research Director,
Laboratorio di
Immunologia ed Allegologia, Divisione
Aerea Studi Ricerche
e Sperimentazioni, Rome
Email: matricardi.pm{at}mclink.it
(2) RISK OF LUNG
CANCER FROM PASSIVE
SMOKING MAY HAVE BEEN OVERSTATED
(Reanalysis of epidemiological evidence
on lung cancer and
passive smoking)
http://www.bmj.com/cgi/content/full/320/7232/417
Previous studies examining the effect of
passive smoking on
lung cancer, may have overstated the risk,
say statisticians
from the University of Warwick in this
week's BMJ.
Research analysing the findings of 37 trials
in this field has
previously found that there is an increased
risk of lung cancer
of nearly a quarter (24 per cent) in people
exposed to
passive smoke. Professor John Copas and
Dr Jian Qing Shi
argue that this research may have been
skewed by
"publication bias" and that in reality
the excess risk of lung
cancer in those exposed to passive smoke
is in fact lower.
Publication bias occurs when studies that
have positive
findings are more likely to be written
up, submitted to a
journal and published than those that
have negative results.
This means that when a review of all research
in a certain field
(such as the effect of passive smoke on
lung cancer) is
conducted, the reviewers are only able
to analyse the studies
which are likely to have positive results.
Smaller studies or
those that were never published because
they had negative
findings are therefore not included in
the analysis and so the
overall picture is skewed.
Copas and Shi say that this is what they
believe to have
happened with previous attempts to ascertain
the risk of lung
cancer from passive smoking. In a reanalysis
of the 37 trials
and taking account of publication bias,
they conclude that the
increased risk of lung cancer from passive
smoking is more
likely to be around 15 per cent as opposed
to 24 per cent.
They therefore suggest that previous levels
of risk should be
interpreted with caution.
Contact:
Professor John Copas, Department of Statistics,
University of
Warwick, Coventry
Email: jbc{at}stats.warwick.ac.uk
Or
Dr Jian Qing Shi
Email: shi{at}stats.warwick.ac.uk
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