Swimming in Allergens?
Pool Use and Asthma
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Pooling data. Regular exposure to chlorine at indoor pools may contribute to atopic asthma.
image: BananaStock/Alamy |
Atopic asthma (inflammation of the airways caused
by exposure to airborne allergens) has become increasingly prevalent
since the 1960s and is now the most common chronic childhood disease
in the United States and many other industrialized countries. The cause
for the rise is unclear, though many hypotheses have been put forth.
Now researchers provide new findings that further support one proposed
reason—increased use of indoor chlorinated swimming pools by children
[EHP 114:1567–1573; Bernard et al.].
The researchers studied 341 children aged 10–13
years who had attended, at varying rates, three indoor pools in Brussels,
Belgium. Ambient levels of a highly reactive chlorine by-product, trichloramine,
ranged from 0.25 to 0.54 mg/m3 at these pools. Trichloramine
is created when chlorine reacts with organic matter such as sweat or
urine. The researchers administered various tests to the participants,
including a questionnaire about health history and pool attendance,
an exercise-induced bronchoconstriction test, and a measurement of total
serum and aeroallergen-specific IgE (a mediator of atopic asthma).
Forty children had asthma, as indicated by previous
doctor diagnosis or the exercise-induced bronchoconstriction test. Cumulative
time spent at swimming pools emerged as one of the most consistent predictors
of asthma, just after family history of asthma or hay fever and atopy
(a genetic tendency toward developing IgE-mediated allergies).
Time spent at pools was associated with increased
incidence of asthma only in children with elevated serum IgE. All the
effects were dose-related and most strongly linked to pool attendance
before the age of about 7 years, suggesting that attendance at indoor
chlorinated pools, especially by young children, interacts with atopic
status to promote the development of childhood atopic asthma.
The scientists suggest a possible mechanism—that
chlorine by-products such as trichloramine disrupt the protective epithelial
barriers of the respiratory tract, allowing allergens to enter the lungs.
This idea is supported by earlier findings from the same team that children
who used an indoor pool showed increased levels of blood markers that
indicated damage to these protective membranes, indeed after as little
as 1 hour of exposure.
The findings suggest that regular attendance at
pools, especially during early life, can promote the development of
atopic asthma. Given that atopic asthma is the form of the disease that
appears largely responsible for the childhood asthma epidemic and is
a chronic disease that greatly affects quality of life, the study points
to the need for preventive measures, the authors state. One option is
that children younger than 7, especially those with allergies, could
avoid strongly chlorinated swimming pools, as identified by a strong
smell of chlorine at the surface of the water (for outdoor pools) or
inside the enclosure (for indoor pools).
Angela Spivey
This Little PBDE Went to Market
Estimating Intake from Grocery Store Foods
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Chemicals in the case. New findings show how PBDEs in dairy products, meats, and other foods contribute to levels in Americans' blood.
image: iStockPhoto |
High concentrations of polybrominated diphenyl ethers
(PBDEs) found in the U.S. population are a cause for concern because
of these compounds' similarity to polychlorinated biphenyls. Unlike
the latter, which have recently decreased in blood levels, PBDEs have
increased substantially in the last two to three decades. A new U.S.
"market basket" survey measuring values of PBDEs in grocery
store foods shows which chemicals within this class are taken in by
eating and adds to a growing body of evidence that food is only part
of how humans are exposed to these chemicals
[EHP 114:1515–1520;
Schecter et al.].
This article is also the first to estimate U.S.
PBDE intake via food from infancy to old age.
PBDEs are flame retardants applied to fabrics, incorporated
into plastics and electronics, and mixed into the foam cushioning used
in furniture. The behavior of PBDE congeners can differ due to variable
physical, chemical, and biological properties. Though human health effects
are not yet well understood, PBDEs' reach in animal studies includes
reproductive and developmental toxicity, endocrine disruption, cancer,
and central nervous system effects. High levels of PBDEs have been found
in human milk, blood, and adipose tissue, as well as in food. U.S. blood
and breast milk samples have shown levels 10 to 20 times higher than
similar samples from Europeans.
The team used high-resolution mass spectrometry
to measure 13 different PBDE congeners in samples of 62 basic foods
including fresh and processed meats, fish, milk products, and eggs.
The foods analyzed were purchased at three large national chain supermarkets
in Dallas in 2003 and 2004.
Of the 13 congeners measured, only about half were
found as major contaminants of the food sampled, a finding that parallels
earlier observations of the relative prevalence of various congeners
in human blood. Although levels of PBDEs varied greatly even within
samples of the same type of food, some trends were clear: fish had the
most PBDE contamination by weight, followed by meats and dairy foods.
But when relative consumption of these foods by Americans was taken
into account, meat contributed the most PBDEs to the diet of Americans
beyond weaning. (Nursing infants' intake of PBDEs is primarily
via breast milk.)
The analysis showed that U.S. foods are generally
more contaminated by PBDEs than foods in Japan or Spain, as reported
in earlier surveys. But these differences still are not enough to explain
the much larger blood and milk burdens observed in Americans. The authors
suggest, as others have earlier, that additional routes of exposure,
such as house dust inhalation and ingestion, also play important roles
in PBDE exposure among Americans.
Victoria McGovern
Faulty Folic Acid Assumptions
Prenatal Supplements Not Always a Good Idea
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One dose doesn't fit all? New data shows the recommendation for folate consumption for women of childbearing age may not be universal due to differences in women's folate metabolisms.
image: Shutterstock |
Dietary folic acid supplementation in women of childbearing
age has been a major public health success story, reducing the incidence
of neural tube defects (NTDs) by an estimated 50–70%. The CDC
currently recommends that all women of childbearing age eat a diet high
in folic acid or take a daily multivitamin with 0.4 mg of folic acid
each day, with higher intake from before conception through the first
three months of pregnancy. In light of a new analysis of NTDs and folate
pathway genes, however, that blanket recommendation may need to be fine-tuned
[EHP 114:1547–1552; Boyles et al.].
If these results are confirmed, it appears there
may be a subgroup of women in whom folic acid supplementation is actually
positively associated with the formation of NTDs in their offspring—a
startling finding the authors acknowledge to be counterintuitive. Counterintuitive
or not, the study may have uncovered individuals susceptible to adverse
outcomes stemming from overactivity in the folate metabolism pathway
during a critical stage of embryonic neurodevelopment.
The researchers analyzed the genomes of 304 families
where at least one individual had an NTD. They focused their analysis
on 28 single-nucleotide polymorphisms (SNPs) in 11 genes known to be
involved in the folate metabolism pathway, and stratified the genomic
results by potential gene–gene interactions and by whether the
mothers had taken folate-containing nutritional supplements prior to
conception.
The results showed that certain SNPs in the βine-homocysteine
methyltransferase (BHMT) gene were significantly associated with
NTDs, and that the significance was strongest with mothers who took
folate supplements before conception. The group also found an associative
gene–gene interaction: significance increased in the BHMT
rs3733890 SNP when the data were stratified by preferential transmission
of one particular MTHFR allele from parent to offspring. However,
MTHFR, the most widely studied gene implicated in NTD research,
was not found to be a significant single risk factor.
The authors speculate that the stratification method
they employed may have inadvertently grouped families by one or more
unidentified cofactors correlated with folate supplementation, or that
the BHMT polymorphism may create a genetic variant that
promotes overactivity of the folate metabolic cycle, given the high
folate levels achieved during supplementation. This overactivity may
inappropriately silence growth factors necessary for proper neural tube
closure. Whether this potentially important polymorphic anomaly is grounded
in analytic methodology or in actual biology, further research is clearly
indicated.
NTDs are known to be complex multifactorial disorders
arising from an array of genetic and environmental interactions. In
their various physiologic manifestations, they are either profoundly
disabling or fatal. Although the preventive effect of folic acid supplementation
is undeniable, its protective mechanism of action is still poorly understood.
And if the results of this study are replicated and confirmed, the public
health directives concerning folic acid supplementation may need to
be revised.
Ernie Hood
A Backpack's Worth of Data
Elevated Teen Cancer Risks Linked to Air Pollution
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It goes where they go. A new backpack monitor records teens' personal exposures to pollutants.
image: Sonja Sax |
It is difficult to assess the cancer risks associated
with exposures to air pollutants because much of the health focus has
been on the major outdoor pollutants; far less is known about exposures
inside homes and buildings, where pollutants may be far more concentrated.
Better assessments would measure personal exposures to inhaled pollutants,
but such measurements are both costly and challenging to collect. Now
a research team has developed an effective method to monitor personal
exposures to air pollution with the goal of estimating cancer risks
for indoor and outdoor exposures in urban areas
[EHP 114:1558–1566; Sax et al.].
The team recruited 87 high school students from
Los Angeles and New York City. Three types of measurements were obtained:
indoor home samples, outdoor home samples, and personal exposure samples.
To obtain personal exposure samples, each teenager wore a regular backpack
modified to carry sampling equipment and various types of samplers for
aldehydes, particles, and volatile organic compounds (VOCs). This enabled
sampling of air wherever the teenager spent time over a 48-hour period,
providing an integrated measurement of the air exposures from all indoor
and outdoor environments. The personal, ambient, and modeled concentrations
were used together with EPA data and other toxicological information
to determine excess cancer risks associated with the exposure levels.
In both cities, median cancer risks from personal
VOC exposures were much greater than from ambient exposures. Of the
VOCs measured, formaldehyde carried the greatest cancer risk (more than
1 in 1 million, based on current EPA data), despite the decline of indoor
levels since the banning of formaldehyde foam insulation. Levels of
1,4-dichlorobenzene also posed a substantial risk, though the carcinogenicity
of the compound is uncertain, and the risk applied only to teenagers
who had sources of this compound (e.g., toilet bowl deodorizers) in
their homes. Benzene, the only known human carcinogen in the group of
VOCs, posed the greatest risk from outdoor sources. Automobile exhaust
and tobacco smoke are two major sources of this pollutant.
This study is unique in its focus on teenage groups
in two of the nation's largest and most polluted cities. The two
cities have different climates and different housing and commuting options,
all factors that can influence exposures to both outdoor and indoor
pollutants. Surprisingly, however, the two cities differed little in
terms of overall cancer risks. In both cities, indoor exposures were
a large determinant of cancer risks.
It is unclear whether the results of this study
can be generalized to teens living in other urban areas. Large cancer
risks were associated with exposures to many of the VOCs studied, but
the toxicological data used to determine these risks have substantial
uncertainty. Still, the findings provide valuable assessments of the
risks associated with inhaling a suite of pollutants, both gaseous and
particle-bound, based on personal exposure measurements that can be
used to improve modeled estimates.
M. Nathaniel Mead